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 VR 1.0
 PT J
 AU He, DH
    Chen, TY
    Yang, MJ
    Han, CF
    Yang, Y
    Cao, XT
    Cai, Z
 AF He, Donghua
    Chen, Taoyong
    Yang, Mingjin
    Han, Chaofeng
    Yang, Yang
    Cao, Xuetao
    Cai, Zhen
 TI Rab7b Promotes Megakaryocytic Differentiation of K562 Cells by
    Activating the Protein Kinase C/Extracellular Signal-Regulated Kinase
    Dependent Pathway.
 SO BLOOD
 LA English
 DT Meeting Abstract
 CT 51st Annual Meeting of the American-Society-of-Hematology
 CY DEC 05-08, 2009
 CL New Orleans, LA
 SP Amer Soc Hematol
 C1 [He, Donghua; Yang, Yang; Cai, Zhen] Zhejiang Univ, Affiliated Hosp 1, Dept Hematol, Hangzhou 310003, Zhejiang, Peoples R China.
    [Cao, Xuetao] Mil Med Coll 2, Inst Immunol, Shanghai, Peoples R China.
 NR 0
 TC 0
 PU AMER SOC HEMATOLOGY
 PI WASHINGTON
 PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
 SN 0006-4971
 J9 BLOOD
 JI Blood
 PD NOV 20
 PY 2009
 VL 114
 IS 22
 BP 1397
 EP 1397
 PG 1
 SC Hematology
 GA 532DS
 UT ISI:000272725804276
 ER
 
 PT J
 AU Racke, FK
    Baird, ME
    Barth, R
    Huo, TY
    Yang, WL
    Weldon, M
    Gupta, N
 AF Racke, Frederick Karl
    Baird, Maureen E.
    Barth, Rolf
    Huo, Tianyao
    Yang, Weilian
    Weldon, Michael
    Gupta, Nilendu
 TI Unique Thrombopoietic Activity of Novel PKC Agonist Ingenol 3,20
    Dibenzoate.
 SO BLOOD
 LA English
 DT Meeting Abstract
 CT 51st Annual Meeting of the American-Society-of-Hematology
 CY DEC 05-08, 2009
 CL New Orleans, LA
 SP Amer Soc Hematol
 C1 [Racke, Frederick Karl; Baird, Maureen E.; Barth, Rolf; Huo, Tianyao; Yang, Weilian; Weldon, Michael; Gupta, Nilendu] Ohio State Univ, Med Ctr, Columbus, OH 43210 USA.
 NR 0
 TC 0
 PU AMER SOC HEMATOLOGY
 PI WASHINGTON
 PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
 SN 0006-4971
 J9 BLOOD
 JI Blood
 PD NOV 20
 PY 2009
 VL 114
 IS 22
 BP 1400
 EP 1400
 PG 1
 SC Hematology
 GA 532DS
 UT ISI:000272725804286
 ER
 
 PT J
 AU Li, Y
    Chen, S
    He, YZ
    Li, XH
    Yang, FC
 AF Li, Yan
    Chen, Shi
    He, Yongzheng
    Li, Xiaohong
    Yang, Fengchun
 TI Impaired Bone Marrow Microenvironment in Fanconi Anemia Murine Model Is
    Responsible for the Defective Hematopoietic Stem Progenitor Cell
    Mobilization
 SO BLOOD
 LA English
 DT Meeting Abstract
 CT 51st Annual Meeting of the American-Society-of-Hematology
 CY DEC 05-08, 2009
 CL New Orleans, LA
 SP Amer Soc Hematol
 C1 [Li, Yan; Chen, Shi; He, Yongzheng; Li, Xiaohong] Indiana Univ Sch Med, Indianapolis, IN USA.
    [Yang, Fengchun] Indiana Univ, Inst Canc Res, Indianapolis, IN 46204 USA.
 NR 0
 TC 0
 PU AMER SOC HEMATOLOGY
 PI WASHINGTON
 PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
 SN 0006-4971
 J9 BLOOD
 JI Blood
 PD NOV 20
 PY 2009
 VL 114
 IS 22
 BP 1402
 EP 1402
 PG 1
 SC Hematology
 GA 532DS
 UT ISI:000272725804293
 ER
 
 PT J
 AU Singh, A
    Evens, AM
    Anderson, R
    Beckstead, J
    Sankar, N
    Bhalla, S
    Yang, S
    Forte, T
    Ryan, R
    Gordon, LI
 AF Singh, Amareshwar
    Evens, Andrew M.
    Anderson, Reilly
    Beckstead, Jennifer
    Sankar, Natesan
    Bhalla, Savita
    Yang, Shuo
    Forte, Trudy
    Ryan, Robert
    Gordon, Leo I.
 TI All Trans Retinoic Acid Nanodisks Enhance Retinoic Acid
    Receptor-Mediated Apoptosis and Cell Cycle Arrest in Mantle Cell
    Lymphoma
 SO BLOOD
 LA English
 DT Meeting Abstract
 CT 51st Annual Meeting of the American-Society-of-Hematology
 CY DEC 05-08, 2009
 CL New Orleans, LA
 SP Amer Soc Hematol
 C1 [Beckstead, Jennifer; Forte, Trudy; Ryan, Robert] Childrens Hosp Oakland, Res Inst, Oakland, CA 94609 USA.
    [Bhalla, Savita; Gordon, Leo I.] Northwestern Univ, Feinberg Sch Med, Div Hematol Oncol, Dept Med, Chicago, IL 60611 USA.
    [Yang, Shuo] Robert H Lurie Comprehens Canc Ctr, Chicago, IL USA.
 NR 0
 TC 0
 PU AMER SOC HEMATOLOGY
 PI WASHINGTON
 PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
 SN 0006-4971
 J9 BLOOD
 JI Blood
 PD NOV 20
 PY 2009
 VL 114
 IS 22
 BP 1433
 EP 1434
 PG 2
 SC Hematology
 GA 532DS
 UT ISI:000272725804386
 ER
 
 PT J
 AU Xu, L
    Patterson, CJ
    Sun, J
    Yang, G
    Zhou, YS
    Hunter, Z
    Hatjiharissi, E
    Ciccarelli, B
    Gong, P
    Liu, X
    Tseng, H
    Ioakimidis, T
    Manning, R
    Hanzis, C
    Cao, Y
    Lewicki, M
    Treon, S
 AF Xu, Lian
    Patterson, Christopher J.
    Sun, Jenny
    Yang, Guang
    Zhou, Yangsheng
    Hunter, Zachary
    Hatjiharissi, Evdoxia
    Ciccarelli, Bryan
    Gong, Ping
    Liu, Xia
    Tseng, Hsiuyi
    Ioakimidis, Thea
    Manning, Robert
    Hanzis, Christina
    Cao, Yang
    Lewicki, Megan
    Treon, Steven
 TI Involvement of Fatty Acid Synthase in Azacytidine-Induced Cytotoxicity
    in Waldenstrom's Macroglobulinemia.
 SO BLOOD
 LA English
 DT Meeting Abstract
 CT 51st Annual Meeting of the American-Society-of-Hematology
 CY DEC 05-08, 2009
 CL New Orleans, LA
 SP Amer Soc Hematol
 C1 [Patterson, Christopher J.] Dana Farber Canc Inst, Waldenstroms Macroflublinemia Ctr, Boston, MA 02115 USA.
    [Sun, Jenny; Zhou, Yangsheng; Liu, Xia; Tseng, Hsiuyi] Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA.
 NR 0
 TC 0
 PU AMER SOC HEMATOLOGY
 PI WASHINGTON
 PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
 SN 0006-4971
 J9 BLOOD
 JI Blood
 PD NOV 20
 PY 2009
 VL 114
 IS 22
 BP 1437
 EP 1437
 PG 1
 SC Hematology
 GA 532DS
 UT ISI:000272725804395
 ER
 
 PT J
 AU Yang, G
    Gong, P
    Xu, L
    Hunter, Z
    Sun, J
    Ciccarelli, B
    Zhou, YS
    Liu, X
    Tseng, H
    Cao, Y
    Manning, R
    Lewicki, M
    Hanzis, C
    Ioakimidis, T
    Sheehy, P
    Patterson, CJ
    Treon, S
 AF Yang, Guang
    Gong, Ping
    Xu, Lian
    Hunter, Zachary
    Sun, Jenny
    Ciccarelli, Bryan
    Zhou, Yangsheng
    Liu, Xia
    Tseng, Hsiuyi
    Cao, Yang
    Manning, Robert
    Lewicki, Megan
    Hanzis, Christina
    Ioakimidis, Thea
    Sheehy, Patricia
    Patterson, Christopher J.
    Treon, Steven
 TI The Inhibitory Receptor FcgRIIB Is Overexpressed, and Its Ligation by
    Anti- FcgRIIB Antibodies Suppresses IgM Production and Induces
    Apoptosis in Waldenstrom's Macroglobulinemia.
 SO BLOOD
 LA English
 DT Meeting Abstract
 CT 51st Annual Meeting of the American-Society-of-Hematology
 CY DEC 05-08, 2009
 CL New Orleans, LA
 SP Amer Soc Hematol
 C1 [Xu, Lian; Hunter, Zachary; Ciccarelli, Bryan; Hanzis, Christina] Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA.
    [Patterson, Christopher J.] Dana Farber Canc Inst, Waldenstroms Macroglubulinemia Ctr, Boston, MA 02115 USA.
 NR 0
 TC 0
 PU AMER SOC HEMATOLOGY
 PI WASHINGTON
 PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
 SN 0006-4971
 J9 BLOOD
 JI Blood
 PD NOV 20
 PY 2009
 VL 114
 IS 22
 BP 1438
 EP 1439
 PG 2
 SC Hematology
 GA 532DS
 UT ISI:000272725804400
 ER
 
 PT J
 AU Sun, J
    Tseng, H
    Xu, L
    Hunter, Z
    Ciccarelli, B
    Fulciniti, M
    Yang, G
    Gong, P
    Zhou, YS
    Liu, X
    Munshi, NC
    Patterson, CJ
    Treon, S
 AF Sun, Jenny
    Tseng, Hsiuyi
    Xu, Lian
    Hunter, Zachary
    Ciccarelli, Bryan
    Fulciniti, Mariateresa
    Yang, Guang
    Gong, Ping
    Zhou, Yangsheng
    Liu, Xia
    Munshi, Nikhil C.
    Patterson, Christopher J.
    Treon, Steven
 TI Vorinostat Induced Cellular Stress Disrupts the Balance Between p38
    MAPK and Erk Pathways Leading to Apoptosis in WM Cells
 SO BLOOD
 LA English
 DT Meeting Abstract
 CT 51st Annual Meeting of the American-Society-of-Hematology
 CY DEC 05-08, 2009
 CL New Orleans, LA
 SP Amer Soc Hematol
 C1 [Sun, Jenny; Tseng, Hsiuyi; Fulciniti, Mariateresa; Zhou, Yangsheng; Liu, Xia] Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA.
    [Munshi, Nikhil C.] Harvard Univ, Sch Med, Dana Farber Canc Inst, Boston VA Healthcare Syst, Boston, MA 02115 USA.
    [Patterson, Christopher J.] Dana Farber Canc Inst, Waldenstroms Macroglubulinemia Ctr, Boston, MA 02115 USA.
 NR 0
 TC 0
 PU AMER SOC HEMATOLOGY
 PI WASHINGTON
 PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
 SN 0006-4971
 J9 BLOOD
 JI Blood
 PD NOV 20
 PY 2009
 VL 114
 IS 22
 BP 1440
 EP 1440
 PG 1
 SC Hematology
 GA 532DS
 UT ISI:000272725804404
 ER
 
 PT J
 AU Yang, DH
    Kim, WS
    Suh, C
    Kwak, JY
    Jung, JS
    Kim, SH
    Kim, JS
    Lee, JJ
    Kim, HJ
 AF Yang, Deok-Hwan
    Kim, Won Seog
    Suh, Cheolwon
    Kwak, Jae-Yong
    Jung, Joo-Sep
    Kim, Sung Hyun
    Kim, Jin Seok
    Lee, Je-Jung
    Kim, Hyeoung-Joon
 TI Phase II Trial of (90)y-Ibritumomab Tiuxetan Treatment as Consolidation
    After 6th R-CHOP Chemotherapy in Patients with Limited-Stage, Bulky
    Diffuse Large B Cell Lymphoma
 SO BLOOD
 LA English
 DT Meeting Abstract
 CT 51st Annual Meeting of the American-Society-of-Hematology
 CY DEC 05-08, 2009
 CL New Orleans, LA
 SP Amer Soc Hematol
 C1 [Yang, Deok-Hwan] Chonnam Natl Univ, Hwasun Hosp, Jeollanam Do, South Korea.
    [Kim, Won Seog] Sungkyunkwan Univ, Sch Med, Samsung Med Ctr, Seoul, South Korea.
    [Suh, Cheolwon] Univ Ulsan, Coll Med, Dept Oncol, Asan Med Ctr, Seoul, South Korea.
    [Kwak, Jae-Yong] Chonbuk Natl Univ Hosp, Dept Internal Med, Jeonju, South Korea.
    [Jung, Joo-Sep] Busan Natl Univ Hosp, Pusan, South Korea.
    [Kim, Sung Hyun] Dong A Univ, Coll Med, Dept Internal Med, Pusan, South Korea.
    [Kim, Jin Seok] Yonsei Univ, Coll Med, Dept Internal Med, Seoul, South Korea.
    [Kim, Hyeoung-Joon] Chonnam Natl Univ, Hwasun Hosp, Coll Med, Hwasun, Jellanamdo, South Korea.
 NR 0
 TC 0
 PU AMER SOC HEMATOLOGY
 PI WASHINGTON
 PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
 SN 0006-4971
 J9 BLOOD
 JI Blood
 PD NOV 20
 PY 2009
 VL 114
 IS 22
 BP 1444
 EP 1444
 PG 1
 SC Hematology
 GA 532DS
 UT ISI:000272725804415
 ER
 
 PT J
 AU Kim, M
    Oh, B
    Kim, SY
    Park, HK
    Hwang, SM
    Moon, HW
    She, CJ
    Yang, I
    Yoon, SS
    Yoon, JH
    Lee, DS
 AF Kim, Miyoung
    Oh, Bora
    Kim, Song-yee
    Park, Hyun-Kyung
    Hwang, Sang Mee
    Moon, Hee Won
    She, Cha Ja
    Yang, Inchul
    Yoon, Sung-Soo
    Yoon, Jong Hyun
    Lee, Dong Soon
 TI p15INK4b Methylation is Related to Blast Percentage, Thrombocytopenia,
    the Number of Lineages Involved in Cytopenia and Survival in
    Myelodysplastic Syndrome at the Time of Diagnosis: a Pyrosequencing
    Study
 SO BLOOD
 LA English
 DT Meeting Abstract
 CT 51st Annual Meeting of the American-Society-of-Hematology
 CY DEC 05-08, 2009
 CL New Orleans, LA
 SP Amer Soc Hematol
 C1 [Kim, Miyoung; Kim, Song-yee] Seoul Natl Univ Hosp, Dept Lab Med, Seoul 110744, South Korea.
    [Oh, Bora] Seoul Natl Univ, Coll Med, Dept Mol & Clin Oncol, Seoul, South Korea.
    [Park, Hyun-Kyung] Seoul Clin Lab, Seoul, South Korea.
    [Moon, Hee Won] Konkuk Univ, Coll Med, Dept Lab Med, Seoul, South Korea.
    [She, Cha Ja; Lee, Dong Soon] Seoul Natl Univ, Coll Med, Dept Lab Med, Seoul, South Korea.
    [Yang, Inchul] Korea Res Inst Stand & Sci, Organ & Bioanal Grp, Taejon, South Korea.
    [Yoon, Sung-Soo] Seoul Natl Univ, Coll Med, Dept Internal Med, Seoul 151, South Korea.
    [Yoon, Jong Hyun] Seoul Natl Univ, Boramae Hosp, Dept Lab Med, Seoul, South Korea.
 NR 0
 TC 0
 PU AMER SOC HEMATOLOGY
 PI WASHINGTON
 PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
 SN 0006-4971
 J9 BLOOD
 JI Blood
 PD NOV 20
 PY 2009
 VL 114
 IS 22
 BP 1458
 EP 1459
 PG 2
 SC Hematology
 GA 532DS
 UT ISI:000272725804457
 ER
 
 PT J
 AU Hunter, Z
    Hatjiharissi, E
    Sun, J
    Cao, Y
    Tseng, H
    Lewicki, M
    Xu, L
    Yang, G
    Zhou, YS
    Liu, X
    Gong, P
    Hanzis, C
    Ioakimidis, T
    Patterson, CJ
    Sheehy, P
    Barlogie, B
    Shaughnessy, JD
    Treon, S
 AF Hunter, Zachary
    Hatjiharissi, Evdoxia
    Sun, Jenny
    Cao, Yang
    Tseng, Hsiuyi
    Lewicki, Megan
    Xu, Lian
    Yang, Guang
    Zhou, Yangsheng
    Liu, Xia
    Gong, Ping
    Hanzis, Christina
    Ioakimidis, Thea
    Patterson, Christopher J.
    Sheehy, Patricia
    Barlogie, Bart
    Shaughnessy, John D., Jr.
    Treon, Steven
 TI Gene Expression Profiling Distinguishes Waldenstrom's Macroglobulinemia
    Patients Presenting with Familial Disease, Advanced IPSS Prognostic
    Score, and Previous Treatment with Rituximab.
 SO BLOOD
 LA English
 DT Meeting Abstract
 CT 51st Annual Meeting of the American-Society-of-Hematology
 CY DEC 05-08, 2009
 CL New Orleans, LA
 SP Amer Soc Hematol
 C1 [Sun, Jenny; Tseng, Hsiuyi; Zhou, Yangsheng; Liu, Xia; Sheehy, Patricia] Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA.
    [Patterson, Christopher J.] Dana Farber Canc Inst, Waldenstroms Macroglubulinemia Ctr, Boston, MA 02115 USA.
    [Barlogie, Bart; Shaughnessy, John D., Jr.] Univ Arkansas Med Sci, Myeloma Inst Res & Therapy, Little Rock, AR 72205 USA.
 NR 0
 TC 0
 PU AMER SOC HEMATOLOGY
 PI WASHINGTON
 PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
 SN 0006-4971
 J9 BLOOD
 JI Blood
 PD NOV 20
 PY 2009
 VL 114
 IS 22
 BP 1511
 EP 1511
 PG 1
 SC Hematology
 GA 532DS
 UT ISI:000272725804594
 ER
 
 PT J
 AU Zhou, YS
    Liu, X
    Gong, P
    Xu, L
    Ciccarelli, B
    Yang, G
    Patterson, CJ
    Treon, S
 AF Zhou, Yangsheng
    Liu, Xia
    Gong, Ping
    Xu, Lian
    Ciccarelli, Bryan
    Yang, Guang
    Patterson, Christopher J.
    Treon, Steven
 TI Metalloproteinase Inhibitors Inhibit the Release of Soluble CD27 by
    Waldenstrom's Macroglobulinemia Cells.
 SO BLOOD
 LA English
 DT Meeting Abstract
 CT 51st Annual Meeting of the American-Society-of-Hematology
 CY DEC 05-08, 2009
 CL New Orleans, LA
 SP Amer Soc Hematol
 C1 [Zhou, Yangsheng; Liu, Xia] Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA.
    [Patterson, Christopher J.] Dana Farber Canc Inst, Waldenstroms Macroglubulinemia Ctr, Boston, MA 02115 USA.
 NR 0
 TC 0
 PU AMER SOC HEMATOLOGY
 PI WASHINGTON
 PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
 SN 0006-4971
 J9 BLOOD
 JI Blood
 PD NOV 20
 PY 2009
 VL 114
 IS 22
 BP 1516
 EP 1516
 PG 1
 SC Hematology
 GA 532DS
 UT ISI:000272725804606
 ER
 
 PT J
 AU Goodwin, CB
    Yang, ZY
    Vemula, S
    Yin, FQ
    Kapur, R
    Chan, RJ
 AF Goodwin, Charles B.
    Yang, Zhenyun
    Vemula, Sasidhar
    Yin, Fuqin
    Kapur, Reuben
    Chan, Rebecca J.
 TI Genetic Disruption of the PI3K Regulatory Subunit, p85 alpha Partially
    Normalizes Gain-of-Function PTPN11-Induced Hypersensitivity to GM-CSF
    in Hematopoietic Progenitors
 SO BLOOD
 LA English
 DT Meeting Abstract
 CT 51st Annual Meeting of the American-Society-of-Hematology
 CY DEC 05-08, 2009
 CL New Orleans, LA
 SP Amer Soc Hematol
 C1 [Goodwin, Charles B.; Yang, Zhenyun; Vemula, Sasidhar; Yin, Fuqin; Kapur, Reuben; Chan, Rebecca J.] Indiana Univ, Sch Med, Indianapolis, IN 46204 USA.
 NR 0
 TC 0
 PU AMER SOC HEMATOLOGY
 PI WASHINGTON
 PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
 SN 0006-4971
 J9 BLOOD
 JI Blood
 PD NOV 20
 PY 2009
 VL 114
 IS 22
 BP 1526
 EP 1526
 PG 1
 SC Hematology
 GA 532DS
 UT ISI:000272725804632
 ER
 
 PT J
 AU Yang, JF
    Chen, Z
    Zhu, WL
    Ruan, CG
 AF Yang, Jianfeng
    Chen, Zhi
    Zhu, Weiliang
    Ruan, Changgeng
 TI A Novel Platelet Small-Molecule Agonist Targeting Glycoprotein Ibalpha
 SO BLOOD
 LA English
 DT Meeting Abstract
 CT 51st Annual Meeting of the American-Society-of-Hematology
 CY DEC 05-08, 2009
 CL New Orleans, LA
 SP Amer Soc Hematol
 C1 [Yang, Jianfeng] Soochow Univ, Jiangsu Inst Hematol, Affiliated Hosp 1, Suzhou, Peoples R China.
    [Chen, Zhi; Zhu, Weiliang] Chinese Acad Sci, Shanghai Inst Mat Med, Drug Discovery & Design Ctr, Shanghai 200031, Peoples R China.
 NR 0
 TC 0
 PU AMER SOC HEMATOLOGY
 PI WASHINGTON
 PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
 SN 0006-4971
 J9 BLOOD
 JI Blood
 PD NOV 20
 PY 2009
 VL 114
 IS 22
 BP 1540
 EP 1540
 PG 1
 SC Hematology
 GA 532DS
 UT ISI:000272725804674
 ER
 
 PT J
 AU Clapp, DW
    Yang, FC
    Ingram, DA
    Robertson, KA
    Hutchins, GD
    Parada, LF
 AF Clapp, D. Wade
    Yang, Fengchun
    Ingram, David A., Jr.
    Robertson, Kent A.
    Hutchins, Gary D.
    Parada, Luis F.
 TI Mast Cells and Tumor Progression
 SO BLOOD
 LA English
 DT Meeting Abstract
 CT 51st Annual Meeting of the American-Society-of-Hematology
 CY DEC 05-08, 2009
 CL New Orleans, LA
 SP Amer Soc Hematol
 C1 [Clapp, D. Wade; Yang, Fengchun; Ingram, David A., Jr.; Hutchins, Gary D.] Indiana Univ, Sch Med, Canc Res Inst, Indianapolis, IN USA.
    [Robertson, Kent A.] Indiana Univ, James Whitcomb Riley Hosp Children, Med Ctr, Indianapolis, IN 46223 USA.
    [Parada, Luis F.] Univ Texas SW Med Ctr Dallas, Dept Dev Biol, Dallas, TX 75390 USA.
 NR 0
 TC 0
 PU AMER SOC HEMATOLOGY
 PI WASHINGTON
 PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
 SN 0006-4971
 J9 BLOOD
 JI Blood
 PD NOV 20
 PY 2009
 VL 114
 IS 22
 BP 1582
 EP 1582
 PG 1
 SC Hematology
 GA 532DS
 UT ISI:000272725804793
 ER
 
 PT J
 AU Yang, D
    Zeng, Y
    Tian, C
    Liu, J
    Guo, SB
    Zheng, YH
    Li, HH
 AF Yang, Dan
    Zeng, Yong
    Tian, Cui
    Liu, Jing
    Guo, Shu-Bin
    Zheng, Yue-Hong
    Li, Hui-Hua
 TI Transcriptomic Analysis of Mild Hypothermia-dependent Alterations
    during Endothelial Reperfusion Injury
 SO CELLULAR PHYSIOLOGY AND BIOCHEMISTRY
 LA English
 DT Article
 DE Mild hypothermia; Ischemia-Reperfusion; Endothelial cells; Microarray
 ID CELL-PROLIFERATION; SIGNALING PATHWAYS; THERAPEUTIC HYPOTHERMIA;
    MODERATE HYPOTHERMIA; CEREBRAL-ISCHEMIA; NERVOUS-SYSTEM; FOCAL
    ISCHEMIA; PROTEIN-KINASE; CARDIAC-ARREST; BRAIN
 AB Background: Mild hypothermia (32-34 C) improves resistance to
    ischemia-reperfusion (I/R) injury. However, the mechanisms by which it
    affects human cellular function are not fully elucidated. To further
    test for hypothermic modulation of global biological processes, we used
    DNA microarray technique to detect the overall gene expression profile.
    Methods: Human umbilical endothelial cells (HUVECs) were incubated
    under control condition (37 degrees C) or mild hypothermia (33 degrees
    C) for 2 hours after stimulated ischemia. Detection of differentially
    expressed genes was performed with Affymetrix U133 plus 2.0 arrays and
    PARTEK software. We used DAVID and KEGG Pathways database to identify
    global trends in gene expression data. Results: Our analysis has
    identified numerous interesting genes and processes that are
    differentially presented in hypothermic group when compared with
    normothermic control. The cell cycle was the most prominent process;
    several genes involved in cell apoptosis and proliferation displayed
    significantly differential expression; lower transcriptional level was
    observed for genes involved in chemokine and cell adhesion processes;
    genes associated with activity of transmembrane transporter and lipase
    were also under-expressed. Conclusion: Our data indicated that mild
    hypothermia altered endothelial expression pattern under the condition
    of I/R, preferably through varying the expression of genes associated
    with cell cycle, apoptosis, proliferation, and inflammatory response.
    Copyright (C) 2010 S. Karger AG, Basel
 C1 [Yang, Dan; Tian, Cui; Liu, Jing; Li, Hui-Hua] Capital Med Univ, Sch Basic Med Sci, Dept Pathol, Beijing 100069, Peoples R China.
    [Zheng, Yue-Hong] Peking Union Med Hosp, Dept Vasc Surg, Beijing 100730, Peoples R China.
    [Guo, Shu-Bin] Peking Union Med Hosp, Dept Emergency Med, Beijing 100730, Peoples R China.
    [Zeng, Yong] Peking Union Med Hosp, Dept Cardiol, Beijing 100730, Peoples R China.
 RP Li, HH, Capital Med Univ, Sch Basic Med Sci, Dept Pathol, 10 Xitoutiao,
    Beijing 100069, Peoples R China.
 EM yuehongzheng@yahoo.com
    hhli1935@yahoo.cn
 FU China Natural Science Foundation [2006CB910306]; 111 project [B08007]
 FX This work was supported by grants from China Natural Science Foundation
    (H. L., 2006CB910306) and the 111 project (H. L., B08007). We thank Dr.
    Ran Zhang (Central Laboratory, Institute of Basic Medical Sciences,
    Chinese Academy of Medical Sciences and Peking Union Medical College)
    for helpful assistance of microarray technique.
 CR ARMSTRONG SC, 2004, CARDIOVASC RES, V61, P427, DOI
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    GANTA CK, 2006, AM J PHYSIOL-REG I, V291, R558, DOI
    10.1152/ajpregu.00846.2005
    GONZALEZNICOLINI V, 2004, INVEST NEW DRUG, V22, P253
    GRESSENS P, 2008, BRAIN PATHOL, V18, P10, DOI
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 NR 32
 TC 0
 PU KARGER
 PI BASEL
 PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND
 SN 1015-8987
 J9 CELL PHYSIOL BIOCHEM
 JI Cell. Physiol. Biochem.
 PY 2010
 VL 25
 IS 6
 BP 605
 EP 614
 DI 10.1159/000315079
 PG 10
 SC Cell Biology; Physiology
 GA 599DI
 UT ISI:000277890000005
 ER
 
 PT J
 AU Rotte, A
    Pasham, V
    Bhandaru, M
    Eichenmuller, M
    Yang, W
    Qadri, SM
    Kempe, DS
    Puchchakayala, G
    Pearce, D
    Birnbaum, MJ
    Lang, F
 AF Rotte, Anand
    Pasham, Venkanna
    Bhandaru, Madhuri
    Eichenmueller, Melanie
    Yang, Wenting
    Qadri, Syed M.
    Kempe, Daniela S.
    Puchchakayala, Goverdhan
    Pearce, David
    Birnbaum, Morris J.
    Lang, Florian
 TI Regulation of Gastric Acid Secretion by PKB/Akt2
 SO CELLULAR PHYSIOLOGY AND BIOCHEMISTRY
 LA English
 DT Article
 DE PI3 kinase; PKB/Akt2; Stomach; H+/K+ ATPase; K+ recycling; H+ secretion
 ID INDUCIBLE KINASE SGK; PROTEIN-KINASE; POTASSIUM CHANNELS;
    PHOSPHOINOSITIDE 3-KINASE; SERUM; PDK1; MICE; CELL; DEXAMETHASONE;
    STIMULATION
 AB Pharmacological inhibition of phosphoinositol 3 kinase (PI3K) and
    partial deficiency of phosphoinositide dependent kinase PDK1 have
    previously been shown to enhance basal gastric acid secretion.
    PI3K/PDK1 dependent signaling involves activation of protein kinase
    B/Akt, which may thus be similarly involved in the regulation of
    gastric acid secretion. To test that hypothesis, gastric acid secretion
    was determined in isolated glands from gene targeted mice lacking
    functional Akt2 (akt2(-/-)) or from their wild type littermates
    (akt2(+/+)). According to BCECF-fluorescence cytosolic pH in isolated
    gastric glands was similar in akt2(-/-) and akt2(+/+) mice.
    Na+-independent pH recovery (Delta pH/min) following an ammonium pulse,
    a measure of H+/K+ ATPase activity, was, however, significantly faster
    in akt2(-/-) than in akt2(+/+) mice. In both genotypes, Delta pH/min
    was virtually abolished by H+/K+ ATPase inhibitor omeprazole (100 mu
    M). Increase of extracellular K+ concentrations to 35 mM (replacing
    Na+) increased Delta pH/min to a significantly larger extent in
    akt2(+/+) than in akt2(-/-) mice and dissipated the differences between
    the genotypes. Similarly, treatment with 5 mu M forskolin enhanced
    Delta pH/min significantly only in akt2(+/+) mice and abolished the
    differences between the genotypes. Conversely, protein kinase A
    inhibitor H89 (50 nM) decreased Delta pH/min to similarly low values in
    both genotypes. In conclusion, Akt2 suppresses gastric acid secretion
    and contributes to or even accounts for the inhibition of gastric acid
    secretion by PI3K. Copyright (C) 2010 S. Karger AG, Basel
 C1 [Rotte, Anand; Pasham, Venkanna; Bhandaru, Madhuri; Eichenmueller, Melanie; Yang, Wenting; Qadri, Syed M.; Kempe, Daniela S.; Puchchakayala, Goverdhan; Lang, Florian] Univ Tubingen, Dept Physiol, D-72076 Tubingen, Germany.
    [Birnbaum, Morris J.] Univ Penn, Div Endocrinol Diabet & Metab, Philadelphia, PA 19104 USA.
    [Pearce, David] Univ Calif San Francisco, Dept Med Nephrol, San Francisco, CA 94143 USA.
 RP Lang, F, Univ Tubingen, Dept Physiol, Gmelinstr 5, D-72076 Tubingen,
    Germany.
 EM florian.lang@uni-tuebingen.de
 FU DFG [SFB 773]
 FX The authors gratefully acknowledge the meticulous preparation of the
    manuscript by Tanja Loch. This work was supported by grants from the
    DFG (SFB 773).
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 NR 44
 TC 4
 PU KARGER
 PI BASEL
 PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND
 SN 1015-8987
 J9 CELL PHYSIOL BIOCHEM
 JI Cell. Physiol. Biochem.
 PY 2010
 VL 25
 IS 6
 BP 695
 EP 704
 DI 10.1159/000315089
 PG 10
 SC Cell Biology; Physiology
 GA 599DI
 UT ISI:000277890000015
 ER
 
 PT J
 AU Kuebler, WM
    Yang, Y
    Samapati, R
    Uhlig, S
 AF Kuebler, Wolfgang M.
    Yang, Yang
    Samapati, Rudi
    Uhlig, Stefan
 TI Vascular Barrier Regulation by PAF, Ceramide, Caveolae, and NO - an
    Intricate Signaling Network with Discrepant Effects in the Pulmonary
    and Systemic Vasculature
 SO CELLULAR PHYSIOLOGY AND BIOCHEMISTRY
 LA English
 DT Review
 DE Permeability; Endothelium; aveolae; Acid sphingomyelinase; Ceramide;
    Nitric oxide
 ID NITRIC-OXIDE SYNTHASE; HYDROSTATIC LUNG EDEMA; ENDOTHELIAL-CELLS;
    MICROVASCULAR PERMEABILITY; TYROSINE PHOSPHORYLATION; ACID
    SPHINGOMYELINASE; IN-VIVO; INDUCED HYPERPERMEABILITY; FILTRATION
    COEFFICIENT; DEPENDENT ACTIVATION
 AB Increased endothelial permeability and vascular barrier failure are
    hallmarks of inflammatory responses in both the pulmonary and the
    systemic circulation. Platelet-activating factor (PAF) has been
    implicated as an important lipid mediator in the formation of pulmonary
    and extrapulmonary edema. Ostensibly, the PAF-induced signaling
    pathways in endothelial cells utilize similar structures and molecules
    including acid sphingomyelinase, ceramide, caveolae, endothelial nitric
    oxide synthase, and nitric oxide, in pulmonary and systemic
    microvessels. Yet, the constituents of these signaling pathways act and
    respond in distinctly different and frequently opposing ways in the
    lung versus organs of the systemic circulation. By confronting
    seemingly discrepant findings from the literature, we reconstruct the
    differential signaling pathways by which PAF regulates edema formation
    in the systemic and the pulmonary vascular bed, and trace this
    dichotomy from the level of myosin light chain kinase via the
    regulation of endothelial nitric oxide synthase and sphingomyelinase
    signaling to the level of caveolar trafficking. Here, we propose that
    PAF regulates vascular barrier function in individual organs by
    opposing signaling pathways that culminate in increased respectively
    decreased nitric oxide synthesis in the systemic and the pulmonary
    endothelium. The present review may provide a physiological explanation
    for the overall disappointing results of previous pharmacological
    strategies in conditions of generalized barrier failure such as sepsis,
    and instead advertises the development of organ-specific interventions
    by targeting the individual composition or trafficking of endothelial
    caveolae. Copyright (C) 2010 S. Karger AG, Basel
 C1 [Yang, Yang; Uhlig, Stefan] Rhein Westfal TH Aachen, Inst Pharmacol & Toxicol, Fac Med, D-52074 Aachen, Germany.
    [Kuebler, Wolfgang M.] St Michaels Hosp, Keenan Res Ctr, Li Ka Shing Knowledge Inst, Toronto, ON M5B 1W8, Canada.
    [Kuebler, Wolfgang M.; Samapati, Rudi] Charite Univ Med Berlin, Inst Physiol, Berlin, Germany.
 RP Uhlig, S, Rhein Westfal TH Aachen, Inst Pharmacol & Toxicol, Fac Med,
    Wendlingweg 2, D-52074 Aachen, Germany.
 EM suhlig@ukaachen.de
 FU Deutsche Forschungsgemeinschaft [KU 1218/5-1, UH 88/8-1]
 FX This study was funded by the Deutsche Forschungsgemeinschaft within the
    SPP1267 "Sphingolipids and disease" (KU 1218/5-1, UH 88/8-1).
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 NR 87
 TC 1
 PU KARGER
 PI BASEL
 PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND
 SN 1015-8987
 J9 CELL PHYSIOL BIOCHEM
 JI Cell. Physiol. Biochem.
 PY 2010
 VL 26
 IS 1
 BP 29
 EP 40
 DI 10.1159/000315103
 PG 12
 SC Cell Biology; Physiology
 GA 599DL
 UT ISI:000277890300004
 ER
 
 PT J
 AU Duncan, DJ
    Yang, ZK
    Hopkins, PM
    Steele, DS
    Harrison, SM
 AF Duncan, David J.
    Yang, Zhaokang
    Hopkins, Philip M.
    Steele, Derek S.
    Harrison, Simon M.
 TI TNF-alpha and IL-1 beta increase Ca2+ leak from the sarcoplasmic
    reticulum and susceptibility to arrhythmia in rat ventricular myocytes
 SO CELL CALCIUM
 LA English
 DT Article
 DE Sepsis; Cytokines; Sarcoplasmic reticulum; Myocardial contraction;
    Calcium; Arrhythmia
 ID NECROSIS-FACTOR-ALPHA; NITRIC-OXIDE; RYANODINE RECEPTORS; CALCIUM
    SPARKS; SEPTIC SHOCK; SEPSIS; DYSFUNCTION; SKELETAL; RELEASE;
    INTERLEUKIN-1-BETA
 AB Sepsis is associated with ventricular dysfunction and increased
    incidence of atrial and ventricular arrhythmia however the underlying
    pro-arrhythmic mechanisms are unknown. Serum levels of tumour necrosis
    factor-alpha (TNF-alpha) and interleukin-1 beta (IL-1 beta) are
    elevated during sepsis and affect Ca2+ regulation. We investigated
    whether pro-inflammatory cytokines disrupt cellular Ca2+ cycling
    leading to reduced contractility, but also increase the probability of
    pro-arrhythmic spontaneous Ca2+ release from the sarcoplasmic reticulum
    (SR). Isolated rat ventricular myocytes were exposed to TNF-alpha (0.05
    ng ml(-1)) and IL-1 beta (2 ng ml(-1)) for 3 hr and then loaded with
    fura-2 or fluo-3 to record the intracellular Ca2+ concentration
    ([Ca2+](i)). Cytokine treatment decreased the amplitude of the
    spatially averaged Ca2+ transient and the associated contraction,
    induced asynchronous Ca2+ release during electrical stimulation,
    increased the frequency of localized Ca2+ release events, decreased the
    SR Ca2+ content and increased the frequency of spontaneous Ca2+ waves
    at any given cytoplasmic Ca2+. These data suggest that INF-alpha and
    IL-1 beta increase the SR Ca2+ leak from the SR, which contributes to
    the depressed Ca2+ transient and contractility. Increased
    susceptibility to spontaneous SR Ca2+ release may contribute to
    arrhythmias in sepsis as the resulting Ca2+ extrusion via NCX is
    electrogenic, leading to cell depolarisation. (C) 2010 Elsevier Ltd.
    All rights reserved.
 C1 [Duncan, David J.; Yang, Zhaokang; Steele, Derek S.; Harrison, Simon M.] Univ Leeds, Inst Membrane & Syst Biol, Multidisciplinary Cardiovasc Res Ctr, Leeds LS2 9JT, W Yorkshire, England.
    [Hopkins, Philip M.] Univ Leeds, Acad Unit Anaesthesia, Leeds LS2 9JT, W Yorkshire, England.
 RP Harrison, SM, Univ Leeds, Inst Membrane & Syst Biol, Multidisciplinary
    Cardiovasc Res Ctr, Garstang Bldg, Leeds LS2 9JT, W Yorkshire, England.
 EM S.M.Harrison@leeds.ac.uk
 FU British Heart Foundation ; White Rose Consortium 
 FX This work was supported by grants from the British Heart Foundation and
    the White Rose Consortium.
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 NR 32
 TC 2
 PU CHURCHILL LIVINGSTONE
 PI EDINBURGH
 PA JOURNAL PRODUCTION DEPT, ROBERT STEVENSON HOUSE, 1-3 BAXTERS PLACE,
    LEITH WALK, EDINBURGH EH1 3AF, MIDLOTHIAN, SCOTLAND
 SN 0143-4160
 J9 CELL CALCIUM
 JI Cell Calcium
 PD APR
 PY 2010
 VL 47
 IS 4
 BP 378
 EP 386
 DI 10.1016/j.ceca.2010.02.002
 PG 9
 SC Cell Biology
 GA 597SI
 UT ISI:000277781100008
 ER
 
 PT J
 AU Tamura, D
    Arao, T
    Tanaka, K
    Kaneda, H
    Matsumoto, K
    Kudo, K
    Aomatsu, K
    Fujita, Y
    Watanabe, T
    Saijo, N
    Kotani, Y
    Nishimura, Y
    Nishio, K
 AF Tamura, Daisuke
    Arao, Tokuzo
    Tanaka, Kaoru
    Kaneda, Hiroyasu
    Matsumoto, Kazuko
    Kudo, Kanae
    Aomatsu, Keiichi
    Fujita, Yoshihiko
    Watanabe, Takashi
    Saijo, Nagahiro
    Kotani, Yoshikazu
    Nishimura, Yoshihiro
    Nishio, Kazuto
 TI Bortezomib potentially inhibits cellular growth of vascular endothelial
    cells through suppression of G2/M transition
 SO CANCER SCIENCE
 LA English
 DT Article
 ID MULTIPLE-MYELOMA; PROTEASOME INHIBITION; PROTEIN-DEGRADATION; UBIQUITIN
    SYSTEM; APOPTOSIS; CANCER; THERAPIES; LYMPHOMA; ARREST; LINES
 AB Bortezomib, a selective 26S proteasome inhibitor, has shown clinical
    benefits against refractory multiple myeloma. The indirect
    anti-angiogenic activity of bortezomib has been widely recognized;
    however, the growth-inhibitory mechanism of bortezomib on vascular
    endothelial cells remains unclear, especially on the cell cycle. Here,
    we showed that bortezomib (2 nM of the IC50 value) potently inhibited
    the cellular growth of human umbilical vascular endothelial cells
    (HUVECs) via a vascular endothelial growth factor receptor
    (VEGFR)-independent mechanism resulting in the induction of apoptosis.
    Bortezomib significantly increased the vascular permeability of HUVECs,
    whereas a VEGFR-2 tyrosine kinase inhibitor decreased it.
    Interestingly, a cell cycle analysis using flow cytometry, the
    immunostaining of phospho-histone H3, and Giemsa staining revealed that
    bortezomib suppressed the G2/M transition of HUVECs, whereas the
    mitotic inhibitor paclitaxel induced M-phase accumulation. A further
    analysis of cell cycle-related proteins revealed that bortezomib
    increased the expression levels of cyclin B1, the cdc2/cyclin B
    complex, and the phosphorylation of all T14, Y15, and T161 residues on
    cdc2. Bortezomib also increased the ubiquitination of cyclin B1 and
    wee1, but inhibited the kinase activity of the cdc2/cyclin B complex.
    These protein modifications support the concept that bortezomib
    suppresses the G2/M transition, rather than causing M-phase arrest. In
    conclusion, we demonstrated that bortezomib potently inhibits cell
    growth by suppressing the G2/M transition, modifying G2/M-phase-related
    cycle regulators, and increasing the vascular permeability of vascular
    endothelial cells. Our findings reveal a cell cycle-related mode of
    action and strongly suggest that bortezomib exerts an additional unique
    vascular disrupting effect as a vascular targeting drug. (Cancer Sci
    2010).
 C1 [Tamura, Daisuke; Arao, Tokuzo; Tanaka, Kaoru; Kaneda, Hiroyasu; Matsumoto, Kazuko; Kudo, Kanae; Aomatsu, Keiichi; Fujita, Yoshihiko; Nishio, Kazuto] Kinki Univ, Sch Med, Dept Genome Biol, Osaka 589, Japan.
    [Tamura, Daisuke; Kotani, Yoshikazu; Nishimura, Yoshihiro] Kobe Univ, Div Resp Med, Dept Internal Med, Grad Sch Med, Kobe, Hyogo 657, Japan.
    [Watanabe, Takashi; Saijo, Nagahiro] Natl Canc Ctr Hosp, Div Med Oncol, Kashiwa, Chiba, Japan.
 RP Nishio, K, Kinki Univ, Sch Med, Dept Genome Biol, Osaka 589, Japan.
 EM knishio@med.kindai.ac.jp
 FU Third-Term Comprehensive 10-Year Strategy for Cancer Control ; National
    Institute of Biomedical Innovation (NiBio) ; funds for Health and Labor
    Scientific Research 
 FX We thank Mr Shinji Kurashimo, Mr Yoshihiro Mine, and Ms Tomoko Kitayama
    for their technical assistance. This work was supported in part by the
    Third-Term Comprehensive 10-Year Strategy for Cancer Control, the
    Program for the Promotion of Fundamental Studies in Health Sciences of
    the National Institute of Biomedical Innovation (NiBio), funds for
    Health and Labor Scientific Research Grants, and a Grant-in-Aid for
    Scientific Research (A).
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 NR 28
 TC 0
 PU WILEY-BLACKWELL PUBLISHING, INC
 PI MALDEN
 PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
 SN 1347-9032
 J9 CANCER SCI
 JI Cancer Sci.
 PD JUN
 PY 2010
 VL 101
 IS 6
 BP 1403
 EP 1408
 DI 10.1111/j.1349-7006.2010.01544.x
 PG 6
 SC Oncology
 GA 599LJ
 UT ISI:000277913800011
 ER
 
 PT J
 AU Yang, JYK
    Williams, S
    Brandao, LR
    Chan, AKC
 AF Yang, Janet Y. K.
    Williams, Suzan
    Brandao, Leonardo R.
    Chan, Anthony K. C.
 TI Neonatal and childhood right atrial thrombosis: recognition and a
    risk-stratified treatment approach
 SO BLOOD COAGULATION & FIBRINOLYSIS
 LA English
 DT Review
 DE central venous catheters; children; pediatric; right atrial thrombosis;
    right atrial thrombus
 ID TISSUE-PLASMINOGEN ACTIVATOR; CENTRAL VENOUS CATHETERS; TWO-DIMENSIONAL
    ECHOCARDIOGRAPHY; TOTAL PARENTERAL-NUTRITION; RIGHT HEART THROMBUS;
    VENA-CAVA; THROMBOEMBOLIC COMPLICATIONS; INTRACARDIAC THROMBOSIS;
    PULMONARY-EMBOLISM; PREMATURE-INFANTS
 AB Pediatric literature and guidelines of treatment options for right
    atrial thrombosis (RAT) are lacking; thus, this review summarizes the
    available literature on RAT in infants and children. Medline search
    identified 35 publications, with 27 prospective or retrospective case
    series included for data analysis. A total of 122 cases of RAT were
    identified. The mean age of patients is 3.58 years (n=86) with a strong
    predominance in the neonatal and infancy period. Ninety-one percent of
    cases were found to be associated with central venous catheters, 40.8%
    are premature neonates, 27.2% are postcardiac surgery patients, and
    19.2% have underlying malignancies. Gut failure with total parenteral
    nutrition given via the central venous catheters occurred in 45.6% of
    patients. The most frequent presenting symptoms are respiratory
    distress and arrhythmia, and 56.8% (42 of 74) were asymptomatic. Our
    study defined high-risk features on echocardiogram as large size, more
    than 2cm in any dimension, pedunculated, mobile, or snake-shaped, and
    mobile. Our result confirmed there is significant difference in the
    mortality for the high-risk group (16.7%; three of 18) versus the low
    risk group (0%; n=32; P=0.0416). Moreover, none of the asymptomatic
    patients showed progression in disease or died. Asymptomatic and
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    associated with good prognosis irrespective of treatment. We
    recommended removal of central venous line if possible, with or without
    anticoagulation for this group of patients. Systemic anticoagulation
    therapy should be given to all high-risk or symptomatic RAT patients.
    Surgical thrombectomy or thrombolytic therapy carries significant risk
    and should be considered individually. Blood Coagul Fibrinolysis
    21:301-307 (C) 2010 Wolters Kluwer Health vertical bar Lippincott
    Williams & Wilkins.
 C1 [Yang, Janet Y. K.; Chan, Anthony K. C.] McMaster Univ, Dept Pediat, Div Hematol & Oncol, Hamilton, ON, Canada.
    [Yang, Janet Y. K.] Tuen Mun Hosp, Dept Pediat & Adolescent Med, Hong Kong, Peoples R China.
    [Williams, Suzan; Brandao, Leonardo R.] Hosp Sick Children, Dept Hematol & Oncol, Toronto, ON M5G 1X8, Canada.
 RP Chan, AKC, Henderson Res Ctr, 711 Concess St, Hamilton, ON L8V 1C3,
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 EM achan@thrombosis.hhscr.org
 FU Heart and Stroke Foundation of Canada 
 FX A.C. is a career investigator funded by the Heart and Stroke Foundation
    of Canada.
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 NR 45
 TC 2
 PU LIPPINCOTT WILLIAMS & WILKINS
 PI PHILADELPHIA
 PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
 SN 0957-5235
 J9 BLOOD COAGULAT FIBRINOL
 JI Blood Coagul. Fibrinolysis
 PD JUN
 PY 2010
 VL 21
 IS 4
 BP 301
 EP 307
 DI 10.1097/MBC.0b013e3283333c7c
 PG 7
 SC Hematology
 GA 599PO
 UT ISI:000277925800001
 ER
 
 PT S
 AU Watanabe, Y
    Buckingham, M
 AF Watanabe, Yusuke
    Buckingham, Margaret
 ED Beyar, R; Landesberg, A
 TI The formation of the embryonic mouse heart Heart fields and myocardial
    cell lineages
 SO ANALYSIS OF CARDIAC DEVELOPMENT: FROM EMBRYO TO OLD AGE
 SE Annals of the New York Academy of Sciences
 LA English
 DT Proceedings Paper
 CT 6th Larry and Horti Fairberg Workshop on Analysis of Cardiac
    Development, From Embryo to Old Age
 CY MAR 30-APR 01, 2009
 CL Haifa, ISRAEL
 SP Rambam Med Ctr
 HO Tech-Israel Inst Technol
 DE cardiogenesis; mouse embryos; second heart field; myocardial cell
    lineages
 ID CARDIAC OUTFLOW TRACT; NEURAL CREST CELLS; FORKHEAD TRANSCRIPTION
    FACTORS; LEFT-RIGHT ASYMMETRY; ARTERIAL POLE; CARDIOVASCULAR
    DEVELOPMENT; VENTRICULAR MYOCARDIUM; SECONDARY HEART; PHARYNGEAL ARCH;
    SONIC HEDGEHOG
 AB During cardiogenesis in the mouse, the second heart field (SHF) is the
    source of the myocardium of the outflow tract and it contributes to
    other regions of the heart with the exception of the primitive left
    ventricle. This contribution corresponds with that of the second
    myocardial cell lineage, identified by retrospective clonal analysis.
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    myocardial progenitor cells within the first heart field. The extension
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    endothelial cells of the pharyngeal arch arteries. Knowledge about the
    origin and genetic regulation of cells that contribute to the heart and
    associated vasculature is important for the diagnosis and treatment of
    congenital heart malformations.
 C1 [Buckingham, Margaret] Inst Pasteur, CNRS, Dept Dev Biol, URA 2578, F-75015 Paris, France.
 RP Buckingham, M, Inst Pasteur, CNRS, Dept Dev Biol, URA 2578, 25 Rue Dr
    Roux, F-75015 Paris, France.
 EM margab@pasteur.fr
 FU Pasteur Institute ; Centre National de la Recherche Scientifique ;
    European Union ; Integrated Project "Heart Repair" [LHSM-CT2005-018630]
 FX We thank D. Rocancourt and S. Meilhac for help with illustrations.
    M.B.'s laboratory is supported by the Pasteur Institute, the Centre
    National de la Recherche Scientifique, and the European Union.
    Integrated Project "Heart Repair" (LHSM-CT2005-018630). Y.W. is a
    research fellow supported by the Heart Repair project.
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 NR 53
 TC 1
 PU BLACKWELL PUBLISHING
 PI OXFORD
 PA 9600 GARSINGTON RD, OXFORD OX4 2DQ, OXEN, ENGLAND
 SN 0077-8923
 BN 978-1-57331-747-4
 J9 ANN N Y ACAD SCI
 JI Ann.NY Acad.Sci.
 PY 2010
 VL 1188
 BP 15
 EP 24
 DI 10.1111/j.1749-6632.2009.05078.x
 PG 10
 SC Multidisciplinary Sciences
 GA BOV10
 UT ISI:000277731600003
 ER
 
 PT J
 AU Payne, JL
    Turchyn, AV
    Paytan, A
    DePaolo, DJ
    Lehrmann, DJ
    Yu, MY
    Wei, JY
 AF Payne, Jonathan L.
    Turchyn, Alexandra V.
    Paytan, Adina
    DePaolo, Donald J.
    Lehrmann, Daniel J.
    Yu, Meiyi
    Wei, Jiayong
 TI Calcium isotope constraints on the end-Permian mass extinction
 SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
    AMERICA
 LA English
 DT Article
 ID EARLIEST TRIASSIC MICROBIALITES; MARINE CARBONATE PLATFORMS;
    PHOTIC-ZONE EUXINIA; SOUTH CHINA; NANPANJIANG BASIN; GREAT BANK;
    GUIZHOU PROVINCE; METHANE RELEASE; CA ISOTOPES; BOUNDARY
 AB The end-Permian mass extinction horizon is marked by an abrupt shift in
    style of carbonate sedimentation and a negative excursion in the carbon
    isotope (delta C-13) composition of carbonate minerals. Several
    extinction scenarios consistent with these observations have been put
    forward. Secular variation in the calcium isotope (delta(44)/Ca-40)
    composition of marine sediments provides a tool for distinguishing
    among these possibilities and thereby constraining the causes of mass
    extinction. Here we report delta(44)/Ca-40 across the Permian-Triassic
    boundary from marine limestone in south China. The delta(44)/Ca-40
    exhibits a transient negative excursion of similar to 0.3 parts per
    thousand over a few hundred thousand years or less, which we interpret
    to reflect a change in the global delta(44)/Ca-40 composition of
    seawater. CO2-driven ocean acidification best explains the coincidence
    of the delta(44)/Ca-40 excursion with negative excursions in the delta
    C-13 of carbonates and organic matter and the preferential extinction
    of heavily calcified marine animals. Calcium isotope constraints on
    carbon cycle calculations suggest that the average delta C-13 of CO2
    released was heavier than -28 parts per thousand and more likely near
    -15 parts per thousand; these values indicate a source containing
    substantial amounts of mantle- or carbonate-derived carbon.
    Collectively, the results point toward Siberian Trap volcanism as the
    trigger of mass extinction.
 C1 [Payne, Jonathan L.] Stanford Univ, Dept Geol & Environm Sci, Stanford, CA 94305 USA.
    [Turchyn, Alexandra V.] Univ Cambridge, Dept Earth Sci, Cambridge CB2 3EQ, England.
    [Paytan, Adina] Univ Calif Santa Cruz, Inst Marine Sci, Santa Cruz, CA 95064 USA.
    [DePaolo, Donald J.] Univ Calif Berkeley, Dept Earth & Planetary Sci, Berkeley, CA 94720 USA.
    [Lehrmann, Daniel J.] Univ Wisconsin, Dept Geol, Oshkosh, WI 54901 USA.
    [Yu, Meiyi] Guizhou Univ, Coll Resource & Environm Engn, Guiyang 550003, Guizhou Prov, Peoples R China.
    [Wei, Jiayong] Guizhou Geol Survey, Guiyang 550005, Guizhou Prov, Peoples R China.
 RP Payne, JL, Stanford Univ, Dept Geol & Environm Sci, 450 Serra Mall,Bldg
    320, Stanford, CA 94305 USA.
 EM jlpayne@stanford.edu
 FU Miller Institute for Basic Research ; Canadian Institute for Advanced
    Research ; American Chemical Society [45329-G8, 40948]; National
    Geographic Society [8102-06]; National Science Foundation
    [EAR-0807377]; National Aeronautics and Space Administration
    [NNX09AN67G]
 FX We thank S. Brown, T. Owens, and A. Jost for assistance with analyses.
    This study was supported by the Miller Institute for Basic Research and
    the Canadian Institute for Advanced Research (fellowships to A. V. T.),
    the Petroleum Research Fund of the American Chemical Society [Grant
    45329-G8 (to J.L.P.); Grant 40948 (to D.J.L.), the National Geographic
    Society [Grant 8102-06 (to J.L.P.)], the National Science Foundation
    [CAREER Award (to A. P.); Grant EAR-0807377 (to J.L.P.)], and National
    Aeronautics and Space Administration [Grant NNX09AN67G (to J.L.P.)].
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 NR 68
 TC 2
 PU NATL ACAD SCIENCES
 PI WASHINGTON
 PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA
 SN 0027-8424
 J9 PROC NAT ACAD SCI USA
 JI Proc. Natl. Acad. Sci. U. S. A.
 PD MAY 11
 PY 2010
 VL 107
 IS 19
 BP 8543
 EP 8548
 DI 10.1073/pnas.0914065107
 PG 6
 SC Multidisciplinary Sciences
 GA 595DP
 UT ISI:000277591200012
 ER
 
 PT J
 AU Zhong, BL
    Chen, HH
    Zhang, JF
    Xu, HM
    Zhou, C
    Yang, F
    Song, J
    Tang, J
    Xu, Y
    Zhang, S
    Zhang, Y
    Zhou, L
 AF Zhong, Bao-liang
    Chen, Hong-hui
    Zhang, Jian-fang
    Xu, Han-ming
    Zhou, Cong
    Yang, Fan
    Song, Jin
    Tang, Jun
    Xu, Yang
    Zhang, Sheng
    Zhang, Yan
    Zhou, Lei
 TI Prevalence, correlates and recognition of depression among inpatients
    of general hospitals in Wuhan, China
 SO GENERAL HOSPITAL PSYCHIATRY
 LA English
 DT Article
 DE Depression; Prevalence; Correlates; Recognition; Inpatients
 ID OLDER MEDICAL INPATIENTS; CORONARY-ARTERY-DISEASE; MAJOR DEPRESSION;
    EPIDEMIOLOGIC SURVEY; MINOR DEPRESSION; DISORDERS; COMORBIDITY;
    DISABILITY; MORTALITY; ANXIETY
 AB Objective: To determine the prevalence, correlates and recognition of
    depression among inpatients of general hospitals in Wuhan, China.
    Method: A total of 513 patients were randomly selected from 1923
    inpatients from three general hospitals and evaluated with a Chinese
    version of the Structured Clinical Interview for Diagnostic and
    Statistical Manual-IV Axis 1 disorders by eight psychiatrists. Logistic
    regression was used to identify factors that were associated with
    depression.
    Results: The prevalence (95% confidence interval) of all current
    depressive disorders and major depressive disorder (MDD) was found to
    be 16.2% (13.0-19.4%) and 9.4% (6.8-11.9%), respectively. The
    correlates for depression include higher hospital class, divorce/being
    widowed/separation, low family income, chronic diseases, lack of
    medical insurance, dwelling in rural area, suffering from severe
    illness and multiple hospitalization history. None of the patients with
    current MDD were detected, treated or referred to psychiatric
    consultation.
    Conclusions: The prevalence of depression among inpatients of general
    hospitals in Wuhan, China, was high. None of the depressive patients
    were recognized or treated for depression, indicating a serious neglect
    of depression in general hospitals. Our studies suggest an urgent need
    to improve clinicians' ability to detect and treat depression. Crown
    Copyright (C) 2010 Published by Elsevier Inc. All rights reserved.
 C1 [Zhong, Bao-liang; Chen, Hong-hui; Zhang, Jian-fang; Xu, Han-ming; Zhou, Cong; Yang, Fan; Song, Jin; Tang, Jun; Xu, Yang; Zhang, Sheng; Zhang, Yan; Zhou, Lei] Huazhong Univ Sci & Technol, Affiliated Mental Hlth Ctr, Tongji Med Coll, Wuhan Mental Hlth Ctr, Wuhan 430074, Hubei, Peoples R China.
 RP Chen, HH, Huazhong Univ Sci & Technol, Affiliated Mental Hlth Ctr,
    Tongji Med Coll, Wuhan Mental Hlth Ctr, Wuhan 430074, Hubei, Peoples R
    China.
 EM c_honghui@hotmail.com
 FU National Natural Science Foundation of China [30770754]; Affiliated
    Mental Health Center of Tongji Medical College of the Huazhong
    University of Science and Technology 
 FX Role of funding source: This study was supported by grants from
    National Natural Science Foundation of China (Grant Number 30770754)
    and the Affiliated Mental Health Center of Tongji Medical College of
    the Huazhong University of Science and Technology.
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 NR 52
 TC 0
 PU ELSEVIER SCIENCE INC
 PI NEW YORK
 PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
 SN 0163-8343
 J9 GEN HOSP PSYCHIAT
 JI Gen. Hosp. Psych.
 PD MAY-JUN
 PY 2010
 VL 32
 IS 3
 BP 268
 EP 275
 DI 10.1016/j.genhosppsych.2010.01.016
 PG 8
 SC Psychiatry
 GA 594HT
 UT ISI:000277527900006
 ER
 
 PT J
 AU Ku, HL
    Yang, KC
    Lee, YC
    Lee, MB
    Chou, YH
 AF Ku, Hsiao-Lun
    Yang, Kai-Chun
    Lee, Ying-Chiao
    Lee, Ming-Been
    Chou, Yuan-Hwa
 TI Predictors of carbon monoxide poisoning-induced delayed
    neuropsychological sequelae
 SO GENERAL HOSPITAL PSYCHIATRY
 LA English
 DT Article
 DE Carbon monoxide; Predictors; Poisoning; Neuropsychological sequelae
 ID HYPERBARIC-OXYGEN THERAPY; TERM MORTALITY; RISK-FACTORS; INTOXICATION;
    ENCEPHALOPATHY
 AB Objective: Carbon monoxide poisoning (COP) commonly results in delayed
    neuropsychological sequelae (DNS). The aim of the article is to
    demonstrate the clinical characteristics and potential predictors of
    COP-induced DNS later.
    Method: Retrospective medical record review was performed for patients
    who had COP in the past year at a National Medical Center in Taiwan.
    Sixty patients with COP were registered during a one-year period.
    Filly-six of them (93.3%) were COP because of suicide attempt. Patients
    with COP who have a complete medical record of carboxyhemoglobin (COHb)
    and Glasgow Coma Scale (GCS) and Mini-Mental Status Examination (MMSE)
    scores were recruited. Multiple regression analysis was performed to
    search for the predictive factors of DNS.
    Results: Forty-three patients were recruited. Most had attempted
    suicide (93.0%) using CO, and thirteen developed DNS later. A longer
    duration of admission, more sessions of hyperbaric oxygen therapy, and
    positive findings in brain computed tomography (CT) scans were more
    often found in patients with DNS than those without DNS. The GCS and
    MMSE scores and positive findings in brain CT scans were associated
    with the development of DNS but COHb was not.
    Conclusions: Our results identified several potential predictors of
    DNS. This finding may help clinicians understand and treat COP patients
    efficiently. (C) 2010 Elsevier Inc. All rights reserved.
 C1 [Ku, Hsiao-Lun; Lee, Ying-Chiao; Chou, Yuan-Hwa] Natl Yang Ming Univ, Dept Psychiat, Taipei Vet Gen Hosp, Taipei 112, Taiwan.
    [Ku, Hsiao-Lun; Lee, Ying-Chiao; Chou, Yuan-Hwa] Natl Yang Ming Univ, Taipei 112, Taiwan.
    [Yang, Kai-Chun] Yuanshan Vet Hosp, Dept Psychiat, Yilan 264, Taiwan.
    [Lee, Ming-Been] Taiwan Suicide Prevent Ctr, Dept Hlth, Executive Yuan 100, Taiwan.
    [Lee, Ming-Been] Natl Taiwan Univ & Hosp, Dept Psychiat, Coll Med, Taipei 100, Taiwan.
    [Chou, Yuan-Hwa] Natl Yang Ming Univ, Inst Neurosci, Taipei 112, Taiwan.
 RP Chou, YH, Natl Yang Ming Univ, Dept Psychiat, Taipei Vet Gen Hosp,
    Taipei 112, Taiwan.
 EM c520608@ms64.hinet.net
 FU National Science Council, Taiwan [NSC 97-2314-B-075-004]; Taipei
    Veterans General Hospital [97DHA0100009]
 FX This project was supported by the National Science Council, Taiwan (NSC
    97-2314-B-075-004) and the Taipei Veterans General Hospital
    (97DHA0100009).
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 NR 36
 TC 1
 PU ELSEVIER SCIENCE INC
 PI NEW YORK
 PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
 SN 0163-8343
 J9 GEN HOSP PSYCHIAT
 JI Gen. Hosp. Psych.
 PD MAY-JUN
 PY 2010
 VL 32
 IS 3
 BP 310
 EP 314
 DI 10.1016/j.genhosppsych.2009.11.005
 PG 5
 SC Psychiatry
 GA 594HT
 UT ISI:000277527900011
 ER
 
 PT J
 AU Wu, RQ
    Li, ZX
    Yang, JP
    Xing, XH
    Shao, DY
    Xing, KL
 AF Wu, Rui-Qin
    Li, Zhi-Xi
    Yang, Jia-Ping
    Xing, Xiao-Hui
    Shao, Dong-Yan
    Xing, Kang-Lin
 TI Mutagenesis induced by high hydrostatic pressure treatment: a useful
    method to improve the bacterial cellulose yield of a Gluconoacetobacter
    xylinus strain
 SO CELLULOSE
 LA English
 DT Article
 DE Gluconoacetobacter xylinus; High hydrostatic pressure; Mutagenesis;
    Bacterial cellulose
 ID ACETOBACTER-XYLINUM; LISTERIA-MONOCYTOGENES; ESCHERICHIA-COLI; MUTANTS;
    GROWTH; ENZYME; TEMPERATURE; BLOOD; MILK
 AB Bacterial cellulose (BC) is a new biomaterial which has wide
    application potential in various industries. BC industrialization
    requires bacterial strains with high BC productivity. The objective of
    this study is to increase the BC yield of a Gluconoacetobacter xylinus
    strain through mutagenesis induced by high hydrostatic pressure (HHP)
    treatment. In this study, the parental strain in its exponential phase
    was treated at 250 MPa and 25 degrees C for 15 min to induce
    mutagenesis using a HHP machine. The HHP-treated strains were incubated
    in glucose agar plate at 30 degrees C for 4 days. After the incubation,
    50 larger colonies in these plates were randomly selected and
    cultivated to produce BC membrane in a tailor-made glass vessel, and
    wet weights of the BC membranes were tested. Compared with the parental
    strain, 29 mutants showed higher BC yields, of which eight mutants with
    BC yield >130.00 g/L were initially screened and were then cultivated
    for five generations to test their genetic stabilities for BC
    production. Among the eight mutants, M-438, a mutant which showed the
    highest average BC yield (158.56 g/L) and lowest coefficient of
    variation (2.4%) for five generations, was finally screened as
    objective mutant. HHP treatment can serve as an effective method to
    cause mutagenesis in BC-producing bacteria. The HHP-treated strains
    with significantly higher BC yield than parental strain can be screened
    from the HHP-induced mutants.
 C1 [Wu, Rui-Qin; Li, Zhi-Xi; Yang, Jia-Ping; Xing, Xiao-Hui; Shao, Dong-Yan] NW A&F Univ, Coll Food Sci & Engn, Yangling 712100, Shaanxi, Peoples R China.
    [Xing, Kang-Lin] Henan Univ Technol, Coll Mech & Elect Engn, Zhengzhou 450000, Henan, Peoples R China.
 RP Li, ZX, NW A&F Univ, Coll Food Sci & Engn, Yangling 712100, Shaanxi,
    Peoples R China.
 EM lzx580721@yahoo.com.cn
 FU Provincial Key Project for Science and Technology Development, Shaanxi,
    China [2005K03-G03]
 FX This research was financially supported by the Provincial Key Project
    for Science and Technology Development (grant number: 2005K03-G03),
    Shaanxi, China. The technical support of Dr. Xuchang Duan, associate
    professor of the College of Food Science and Engineering, Northwest A&F
    University, is also gratefully acknowledged.
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 NR 31
 TC 0
 PU SPRINGER
 PI DORDRECHT
 PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
 SN 0969-0239
 J9 CELLULOSE
 JI Cellulose
 PD APR
 PY 2010
 VL 17
 IS 2
 BP 399
 EP 405
 DI 10.1007/s10570-009-9388-8
 PG 7
 SC Materials Science, Paper & Wood; Materials Science, Textiles; Polymer
    Science
 GA 595TT
 UT ISI:000277636800017
 ER
 
 PT J
 AU Su, W
    Sun, AJ
    Xu, DL
    Zhang, HQ
    Yang, L
    Yuan, LY
    Jia, JG
    Zou, YZ
    Wu, YL
    Wang, KQ
    Ge, JB
 AF Su, Wei
    Sun, Ai-jun
    Xu, Dan-ling
    Zhang, Hong-qi
    Yang, Lin
    Yuan, Ling-yan
    Jia, Jian-guo
    Zou, Yun-zeng
    Wu, Yi-ling
    Wang, Ke-qiang
    Ge, Jun-bo
 TI Inhibiting effects of total saponins of panax ginseng on immune
    maturation of dendritic cells induced by oxidized-low density
    lipoprotein
 SO CELLULAR IMMUNOLOGY
 LA English
 DT Article
 DE Dendritic cells; Oxidized-LDL; Atherosclerosis; TSPG
 ID PPAR-GAMMA; LYMPHOID-TISSUE; ACTIVATION; MONOCYTE; RECEPTOR; LDL
 AB Total saponins of panax ginseng (TSPG) are the major active components
    in panax ginseng. Dendritic cells (DCs) play an active role in the
    immunological processes related to atherosclerosis. The purpose of this
    study was to determine the effect and possible mechanisms of TSPG on
    the maturation and immune function of DCs. Compared with those
    untreated, the DCs pre-treated with TSPG and then induced by
    oxidized-LDL exhibited a significantly lower expression of the
    maturation-associated markers of CD40, CD86, HLA-DR, and CD1a, together
    with an increased endocytosic function as well as decreased secretions
    of cytokine. However, silencing the expression of PPAR gamma in DCs,
    the inhibitory effect of TSPG on the maturation DCs was significantly
    reduced. In conclusion, TSPG could inhibit the maturation of DCs
    induced by oxidized-LDL which suggests beneficial effects on
    atherosclerosis and this effect was partly dependent on the PPAR gamma
    pathway at least. (C) 2010 Elsevier Inc. All rights reserved.
 C1 [Su, Wei; Sun, Ai-jun; Yang, Lin; Yuan, Ling-yan; Jia, Jian-guo; Zou, Yun-zeng; Wang, Ke-qiang; Ge, Jun-bo] Fudan Univ, Zhongshan Hosp, Inst Cardiovasc Dis, Shanghai 200032, Peoples R China.
    [Su, Wei] Xinxiang Med Univ, Dept Pathol, Xinxiang 453003, Henan Province, Peoples R China.
    [Xu, Dan-ling] Tongji Univ, Coll Med, Dept Anat, Shanghai 200092, Peoples R China.
    [Zhang, Hong-qi] Fudan Univ, Shanghai Med Coll, Dept Anat Histol & Embryol, Shanghai 200032, Peoples R China.
    [Wu, Yi-ling] Integrat Tradit & Western Med Res Acad Hebei Prov, Shijiazhuang 050035, Peoples R China.
 RP Ge, JB, Fudan Univ, Zhongshan Hosp, Inst Cardiovasc Dis, 180 Fenglin
    Rd, Shanghai 200032, Peoples R China.
 EM jbge@zs-hospital.sh.cn
 FU National Basic Research Program of China [2006CB503803, 2005CB523302];
    Science and Technology Ministry [2006AA0ZA406]; National Natural
    Science Foundation of China [30725036]; Key Projects in the National
    Science 82 Technology Pillar Program in the Eleventh Five-year Plan
    Period [2006BAI 01A 04]
 FX The authors thank Dr. Kai. Hu from University of Wurzburg, Germany, for
    his assistance in data analysis and article language. This study was
    funded by National Basic Research Program of China (2006CB503803 &
    2005CB523302), 863 Program of Science and Technology Ministry
    (2006AA0ZA406), Outstanding Youth Grant from National Natural Science
    Foundation of China (30725036) and Key Projects in the National Science
    82 Technology Pillar Program in the Eleventh Five-year Plan Period
    (2006BAI 01A 04).
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 NR 29
 TC 0
 PU ACADEMIC PRESS INC ELSEVIER SCIENCE
 PI SAN DIEGO
 PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
 SN 0008-8749
 J9 CELL IMMUNOL
 JI Cell. Immunol.
 PY 2010
 VL 263
 IS 1
 BP 99
 EP 104
 DI 10.1016/j.cellimm.2010.03.004
 PG 6
 SC Cell Biology; Immunology
 GA 595EL
 UT ISI:000277593400012
 ER
 
 PT J
 AU Wen, X
    Xu, GZ
    Liu, J
    Zhu, HF
    Dai, H
    Li, L
    Hong, Y
    Yang, J
    Dai, W
    Ping, L
    Shen, GX
 AF Wen, Xue
    Xu, Guozheng
    Liu, Jing
    Zhu, Huifen
    Dai, Hong
    Li, Li
    Hong, Yi
    Yang, Jing
    Dai, Wei
    Ping, Lei
    Shen, Guanxin
 TI Overexpression of programmed death-1 ligand-1 on NIT cells lead to
    negative regulation of allogeneic lymphocyte activation
 SO CELLULAR IMMUNOLOGY
 LA English
 DT Article
 DE PD-L1; Alloimmune responses; Apoptosis; Cytokine; Negative regulation;
    NIT-1 cells; PD-1; Proliferation; Immune responses; Autoimmune diseases
 ID B7 FAMILY; T-CELLS; PD-1; EXPRESSION; RESPONSES; TOLERANCE; MEMBER;
    B7-H1; ARTERIOSCLEROSIS; SUPERFAMILY
 AB PD-L1 have been identified as the ligand for PD-1, and shown to play a
    role in the regulation of immune responses. In the present study, we
    investigated whether overexpressing PD-L1 on islet beta cells could
    induce negative regulation in primary and primed allogeneic lymphocyte
    response. pPD-L1-EGFP or pEGFPn1 were transfected in NIT-1 cells, for
    establishment of pPD-L1-EGFP or pEGFPn1 stable transfectants, namely
    NIT-PD-L1 and NIT-EGFP. In mixed cells reaction, as compared with the
    controls of NIT-I or NIT-EGFP, NIT-PD-L1-primed splenocytes showed the
    lowest proliferative response but severe apoptosis when restimulated
    with NIT-PD-L1 cells in vitro. Overexpressing PD-L1 on NIT-1 cells
    could downregulate IFN-gamma but upregulate IL-4 and IL-10 production
    by the primed lymphocytes. In addition, proliferative response of
    primary reactive lymphocytes stimulated with NIT-PD-L1 was lower than
    those lymphocytes restimulated with NIT-1 cells or NIT-EGFP cells. Our
    data demonstrated that PD-L1 has down-regulative effects on alloimmune
    responses. (C) 2010 Elsevier Inc. All rights reserved.
 C1 [Wen, Xue; Liu, Jing; Zhu, Huifen; Dai, Hong; Hong, Yi; Yang, Jing; Dai, Wei; Ping, Lei; Shen, Guanxin] Huazhong Univ Sci & Technol, Tongji Med Coll, Dept Immunol, Wuhan 430030, Peoples R China.
    [Wen, Xue; Xu, Guozheng] Wuhan Gen Hosp, Guangzhou Command, Dept Neurosurg, Wuhan 430070, Peoples R China.
    [Li, Li] Wuhan Inst Biol Prod, Wuhan, Peoples R China.
    [Hong, Yi] Hubei Univ Chinese Med, Wuhan 430065, Peoples R China.
 RP Shen, GX, Huazhong Univ Sci & Technol, Tongji Med Coll, Dept Immunol,
    Wuhan 430030, Peoples R China.
 EM guanxin_shen@yahoo.com.cn
 FU National Natural Science foundation [30972734]
 FX This work was supported by Grant from the National Natural Science
    foundation (No. 30972734).
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 NR 22
 TC 0
 PU ACADEMIC PRESS INC ELSEVIER SCIENCE
 PI SAN DIEGO
 PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
 SN 0008-8749
 J9 CELL IMMUNOL
 JI Cell. Immunol.
 PY 2010
 VL 263
 IS 1
 BP 122
 EP 128
 DI 10.1016/j.cellimm.2010.03.007
 PG 7
 SC Cell Biology; Immunology
 GA 595EL
 UT ISI:000277593400015
 ER
 
 PT J
 AU Jin, HJ
    Nam, HY
    Bae, YK
    Kim, SY
    Im, IR
    Oh, W
    Yang, YS
    Choi, SJ
    Kim, SW
 AF Jin, Hye Jin
    Nam, Hae Yun
    Bae, Yun Kyong
    Kim, Soo Yeon
    Im, I. Rang
    Oh, Wonil
    Yang, Yoon Sun
    Choi, Soo Jin
    Kim, Seong Who
 TI GD2 expression is closely associated with neuronal differentiation of
    human umbilical cord blood-derived mesenchymal stem cells
 SO CELLULAR AND MOLECULAR LIFE SCIENCES
 LA English
 DT Article
 DE Umbilical cord blood; Mesenchymal stem cells; Ganglioside GD2;
    Multi-lineage differentiation; Neuronal differentiation; Basic
    helix-loop-helix
 ID NEURAL GANGLIOSIDE GD2; HUMAN BONE-MARROW; STROMAL CELLS; IN-VITRO;
    COMPLEX GANGLIOSIDES; ADIPOSE-TISSUE; SYNTHASE; BRAIN; TRANSPLANTATION;
    ACTIVATION
 AB GD2 ganglioside has been identified as a key determinant of bone
    marrow-derived mesenchymal stem cells (BM-MSCs). Here, we characterized
    GD2 ganglioside expression and its implications in umbilical cord
    blood-derived MSCs (UCB-MSCs). Using immune-selection analysis, we
    showed that both GD2-positive and GD2-negative UCB-MSCs expressed
    general stem cell markers and possessed mesodermal lineage
    differentiation potential. Although the fraction of GD2-expressing
    cells was lower in UCB-MSC than in BM-MSC populations, inhibition of
    GD2 synthesis in UCB-MSCs suppressed neuronal differentiation and
    down-regulated basic helix-loop-helix (bHLH) transcription factors,
    which are involved in early stage neuronal differentiation. In
    addition, the levels of bHLH factors in neuronally induced UCB-MSCs
    were significantly higher in GD2-positive than GD2-negative cells. Our
    data demonstrate that GD2 ganglioside expression is associated with
    regulation of bHLH factors and identify neurogenic-capable UCB-MSCs,
    providing new insights into the potential clinical applications of
    MSC-based therapy.
 C1 [Jin, Hye Jin; Nam, Hae Yun; Im, I. Rang; Kim, Seong Who] Univ Ulsan, Coll Med, Dept Biochem & Mol Biol, Seoul 136736, South Korea.
    [Jin, Hye Jin; Bae, Yun Kyong; Oh, Wonil; Yang, Yoon Sun; Choi, Soo Jin] Medipost Co Ltd, Biomed Res Inst, Seoul 136736, South Korea.
    [Kim, Soo Yeon] Mercersburg Acad, Mercersburg, PA 17236 USA.
 RP Kim, SW, Univ Ulsan, Coll Med, Dept Biochem & Mol Biol, 388-1 Pungnap 2
    Dong, Seoul 136736, South Korea.
 EM sjchoi@medi-post.co.kr
    swhokim@amc.seoul.kr
 FU Ministry of Health and Welfare, Republic of Korea [A084036]; Ministry
    of Education, Science and Technology [2009-0089589]
 FX This work was supported in part by a grant from the Korea Health 21 R&D
    Project, Ministry of Health and Welfare, Republic of Korea (A084036),
    and by Basic Science Research Program through the National Research
    Foundation of Korea funded by the Ministry of Education, Science and
    Technology (2009-0089589 to SW Kim).
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 NR 45
 TC 2
 PU BIRKHAUSER VERLAG AG
 PI BASEL
 PA VIADUKSTRASSE 40-44, PO BOX 133, CH-4010 BASEL, SWITZERLAND
 SN 1420-682X
 J9 CELL MOL LIFE SCI
 JI Cell. Mol. Life Sci.
 PD JUN
 PY 2010
 VL 67
 IS 11
 BP 1845
 EP 1858
 DI 10.1007/s00018-010-0292-z
 PG 14
 SC Biochemistry & Molecular Biology; Cell Biology
 GA 594MN
 UT ISI:000277541900007
 ER
 
 PT J
 AU Drapeau, C
    Antarr, D
    Ma, HY
    Yang, ZJ
    Tang, L
    Hoffman, RM
    Schaeffer, DJ
 AF Drapeau, Christian
    Antarr, Donna
    Ma, Huaiyu
    Yang, Zhijian
    Tang, Li
    Hoffman, Robert M.
    Schaeffer, David J.
 TI Mobilization of bone marrow stem cells with StemEnhance (R) improves
    muscle regeneration in cardiotoxin-induced muscle injury
 SO CELL CYCLE
 LA English
 DT Article
 DE bone marrow stem cell; mobilization; cardiotoxin; green fluorescent
    protein; regeneration; tissue repair
 ID ENDOTHELIAL PROGENITOR CELLS; COLONY-STIMULATING FACTOR; ACUTE
    MYOCARDIAL-INFARCTION; SKELETAL-MUSCLE; G-CSF; IN-VIVO; HEART;
    TRANSPLANTATION; STRENGTH; MICE
 AB Bone marrow-derived stem cells have the ability to migrate to sites of
    tissue damage and participate in tissue regeneration. the number of
    circulating stem cells has been shown to be a key parameter in this
    process. therefore, stimulating the mobilization of bone marrow stem
    cells may accelerate tissue regeneration in various animal models of
    injury. In this study we investigated the effect of the bone marrow
    stem cells mobilizer StemEnhance (SE), a water-soluble extract of the
    cyanophyta Aphanizomenon flos-aquae (AFA), on hematopoietic recovery
    after myeloablation as well as recovery from cardiotoxin-induced injury
    of the anterior tibialis muscle in mice. Control and SE-treated female
    mice were irradiated, and then transplanted with GFP(+) bone marrow
    stem cells and allowed to recover. Immediately after transplant,
    animals were gavaged daily with 300 mg/kg of Se in PBS or a PBS
    control. After hematopoietic recovery (23 days), mice were injected
    with cardiotoxin in the anterior tibialis muscle. Five weeks later, the
    anterior tibialis muscles were analyzed for incorporation of GFP(+)
    bone marrow-derived cells using fluorescence imaging. SE significantly
    enhanced recovery from cardiotoxin-injury. However, Stemenhance did not
    affect the growth of the animal and did not affect hematopoietic
    recovery after myeloablation, when compared to control. this study
    suggests that inducing mobilization of stem cells from the bone marrow
    is a strategy for muscle regeneration.
 C1 [Drapeau, Christian; Antarr, Donna] STEMTech HealthSci Inc, San Clemente, CA USA.
    [Ma, Huaiyu; Yang, Zhijian; Tang, Li; Hoffman, Robert M.] AntiCanc Inc, San Diego, CA USA.
    [Schaeffer, David J.] Univ Illinois, Dept Vet Biosci, Urbana, IL 61801 USA.
 RP Drapeau, C, STEMTech HealthSci Inc, San Clemente, CA USA.
 EM cdrapeau@stemtechmail.com
 FU STEMTech HealthSciences, Inc. 
 FX This study was supported by a grant from STEMTech HealthSciences, Inc.,
    to AntiCancer, Inc. This work was presented as a poster presentation at
    the Annual Meeting of the International Society of Stem Cell Research,
    Philadelphia, June 2008.
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 NR 44
 TC 0
 PU LANDES BIOSCIENCE
 PI AUSTIN
 PA 1002 WEST AVENUE, 2ND FLOOR, AUSTIN, TX 78701 USA
 SN 1538-4101
 J9 CELL CYCLE
 JI Cell Cycle
 PD MAY 1
 PY 2010
 VL 9
 IS 9
 BP 1819
 EP 1823
 PG 5
 SC Cell Biology
 GA 592TC
 UT ISI:000277402200034
 ER
 
 PT J
 AU Yu, HJ
    Chen, SL
    Yang, ZH
    Pan, A
    Zhang, G
    Shan, JJ
    Tang, XJ
    Zhou, WL
 AF Yu, Haijie
    Chen, Siliang
    Yang, Zihuan
    Pan, Ao
    Zhang, Geng
    Shan, Jiajie
    Tang, Xiaojiang
    Zhou, Wenliang
 TI Trimethyltin chloride induced chloride secretion across rat distal colon
 SO CELL BIOLOGY INTERNATIONAL
 LA English
 DT Article
 DE Cl- secretion; cystic fibrosis transmembrane conductance regulator
    (CFTR); K+ channel; rat distal colon; short circuit current;
    trimethyltin chloride
 ID RYANODINE RECEPTORS; ANION SECRETION; ION-TRANSPORT; MOUSE COLON;
    CHANNEL; EPITHELIUM; CELLS; ACTIVATION; CFTR; TIN
 AB TMT (trimethyltin chloride), an organotin, is ubiquitous in the
    environment. The consumption of contaminated food may cause exposure of
    the human diet to this toxic compound. The present study was to
    investigate the effects of TMT on the regulation of ion transport
    across the rat distal colon. The rat colonic mucosa was mounted in
    Ussing chambers. The effects of TMT were assessed using the I-SC
    (short-circuit current). Both apical and basolateral TMT induced,
    dose-dependently, an increase in I-SC, which was due to a stimulation
    of Cl- secretion as measured using ion substitution experiments and
    pharmacological manoeuvres. The secretion was also inhibited by several
    K+ channel blockers administrated at the basolateral side. When the
    apical side was permeabilized by nystatin, the TMT-induced K+
    conductance was effectively blocked by tetrapentylammonium, a
    Ca2+-sensitive K+ channel blocker. The response of TMT was sensitive to
    the basolateral Ca2+ and the intracellular Ca2+ store, which could be
    disclosed by applying the inhibitors of ryanodine receptors and
    inositol 1,4,5-trisphosphate receptors. In conclusion, TMT led to Cl-
    secretion, which was essentially regulated by basolateral
    Ca2+-sensitive K+ channels. These results suggest the importance of K+
    channels in the toxicity hazard of TMT.
 C1 [Yu, Haijie; Chen, Siliang; Yang, Zihuan; Pan, Ao; Zhang, Geng; Shan, Jiajie; Zhou, Wenliang] Sun Yat Sen Univ, Sch Life Sci, Guangzhou 510275, Guangdong, Peoples R China.
    [Tang, Xiaojiang] Guangdong Prov Ctr Occupat Dis Prevent & Treatmen, Dept Toxicol, Guangzhou, Guangdong, Peoples R China.
 RP Zhou, WL, Sun Yat Sen Univ, Sch Life Sci, Guangzhou 510275, Guangdong,
    Peoples R China.
 EM lsszwl@yahoo.com.cn
 FU Natural Science Foundation of China [30770817]; National 973 Project
    Foundation [2006CB504002, 2009CB5221027]
 FX This work was supported by the Natural Science Foundation of China
    [grant number 30770817]; and the National 973 Project Foundation [grant
    number 2006CB504002, 2009CB5221027].
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 NR 45
 TC 0
 PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
 PI LONDON
 PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
 SN 1065-6995
 J9 CELL BIOL INT
 JI Cell Biol. Int.
 PD JAN
 PY 2010
 VL 34
 IS 1
 BP 99
 EP 108
 DI 10.1042/CBI20090022
 PG 10
 SC Cell Biology
 GA 592PK
 UT ISI:000277391400015
 ER
 
 PT J
 AU Wang, TY
    Zhang, JH
    Jing, CQ
    Yang, XJ
    Lin, JT
 AF Wang, Tian-Yun
    Zhang, Jun-He
    Jing, Chang-Qin
    Yang, Xian-Jun
    Lin, Jun-Tang
 TI Positional effects of the matrix attachment region on transgene
    expression in stably transfected CHO cells
 SO CELL BIOLOGY INTERNATIONAL
 LA English
 DT Article
 DE gene silencing; mammalian expression system; matrix attachment region;
    positional effect
 ID DROSOPHILA-MELANOGASTER; GENE-EXPRESSION; RICE PLANTS; ARABIDOPSIS;
    STABILITY; ELEMENTS; MICE
 AB Previous work has shown that the MAR (matrix attachment region) could
    increase transgene expression in stably transfected CHO
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    transgene expression, three expression vectors were constructed which
    contained the human beta-globin MAR in different sites, including the
    vector with two MARs flanking the CAT (chloramphenicol
    acetyltransferase) expression cassette, one MAR at the 5' or 3' site.
    These vectors were transfected into CHO cells. The level of CAT gene
    expression was most effectively increased by two MARs flanking the CAT
    expression cassette. This increase was also seen when MAR was inserted
    at the 5' site upstream of the expression cassette, whereas the
    transgene expression level decreased when MAR was inserted at the 3'
    site downstream of the expression cassette. We have also shown that the
    transgene expression level is not directly proportional to the gene
    copy number, and gene copy number dependency does not exist.
 EM wty@xxmu.edu.cn
 FU Natural Science Foundation of Henan Province, China [511042300,
    624410041]; Science and Technology Innovation Talents in University of
    Henan Province [2008HASTIT026]
 FX This work was supported by the Natural Science Foundation of Henan
    Province, China [grant numbers 511042300, 624410041]; and Science and
    Technology Innovation Talents in University of Henan Province [grant
    number 2008HASTIT026].
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 NR 20
 TC 1
 PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
 PI LONDON
 PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
 SN 1065-6995
 J9 CELL BIOL INT
 JI Cell Biol. Int.
 PD FEB
 PY 2010
 VL 34
 IS 2
 BP 141
 EP 145
 DI 10.1042/CBI20090017
 PG 5
 SC Cell Biology
 GA 592PL
 UT ISI:000277391500001
 ER
 
 PT J
 AU Wang, TY
    Zhang, JH
    Jing, CQ
    Yang, XJ
    Lin, JT
 AF Wang, Tian-Yun
    Zhang, Jun-He
    Jing, Chang-Qin
    Yang, Xian-Jun
    Lin, Jun-Tang
 TI Positional effects of the matrix attachment region on transgene
    expression in stably transfected CHO cells (vol 34, pg 141, 2010)
 SO CELL BIOLOGY INTERNATIONAL
 LA English
 DT Correction
 CR WANG TY, 2010, CELL BIOL INT, V34, P141, DOI 10.1042/CBI20090017
 NR 1
 TC 0
 PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
 PI LONDON
 PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
 SN 1065-6995
 J9 CELL BIOL INT
 JI Cell Biol. Int.
 PD FEB
 PY 2010
 VL 34
 IS 2
 BP 235
 EP 235
 PG 1
 SC Cell Biology
 GA 592PL
 UT ISI:000277391500012
 ER
 
 PT J
 AU Huang, YC
    Yang, ZM
    Jiang, NG
    Chen, XH
    Li, XQ
    Tan, MY
    Zhou, KP
    Tang, L
    Xie, HQ
    Deng, L
 AF Huang, Yong-Can
    Yang, Zhi-Ming
    Jiang, Neng-Gang
    Chen, Xiao-He
    Li, Xiu-Qun
    Tan, Mei-Yun
    Zhou, Kun-Peng
    Tang, Li
    Xie, Hui-Qi
    Deng, Li
 TI Characterization of MSCs from human placental decidua basalis in
    hypoxia and serum deprivation
 SO CELL BIOLOGY INTERNATIONAL
 LA English
 DT Article
 DE cytokine secretion; hypoxia; metabolic activity; phenotype;
    proliferation; serum deprivation
 ID MESENCHYMAL STEM-CELLS; UMBILICAL-CORD BLOOD; BONE-MARROW; IN-VITRO;
    INDUCED APOPTOSIS; PROLIFERATION; TISSUE; NEURONS; BFGF
 AB Recently, we reported that human PDB (placental decidua basalis) is an
    excellent source of MSCs (mesenchymal stem cells), meanwhile, PDB-MSCs
    could survive under hypoxia and serum deprivation. Herein, we
    investigated the proliferation, clonogentic efficiency, phenotypes,
    metabolic activity and cytokines secretion of PDB-MSCs in hypoxia and
    serum deprivation. PDB-MSCs were cultured in four groups: normoxia (20%
    O-2) and complete medium [10% FBS (foetal bovine serum)+DMEM-HG
    (Dulbecco's modified Eagle's medium-high glucose)], hypoxia and
    complete medium, normoxia and serum deprivation (0% FBS), and hypoxia
    and serum deprivation. After 96 h of culture in the above groups,
    PDB-MSCs maintain the phenotypes stably. Interestingly, hypoxia notably
    enhanced the proliferation, colony-forming potential and
    lactate/glucose ratio in complete medium, but suppressed the secretion
    of BMP-2 (bone morphogenetic protein-2) and bFGF (basic fibroblast
    growth factor), while it did not change the quantity of VEGF (vascular
    endothelial growth factor) and bFGF in serum deprivation. Although
    PDB-MSCs grew slowly and seldom formed a colony unit in hypoxia and
    serum deprivation, they possessed a moderate metabolism. In conclusion,
    our results indicate that PDB-MSCs appear to be promising seed cells
    for ischaemia-related tissue engineering.
 C1 [Huang, Yong-Can; Yang, Zhi-Ming; Chen, Xiao-He; Li, Xiu-Qun; Tan, Mei-Yun; Zhou, Kun-Peng; Tang, Li; Xie, Hui-Qi; Deng, Li] Sichuan Univ, Div Stem Cell & Tissue Engn, State Key Lab Biotherapy, W China Hosp, Chengdu 610041, Peoples R China.
    [Huang, Yong-Can; Tang, Li] Sichuan Univ, W China Sch Pharm, Chengdu 610041, Peoples R China.
    [Jiang, Neng-Gang] Sichuan Univ, W China Hosp, Dept Lab Med, Chengdu 610041, Peoples R China.
 RP Deng, L, Sichuan Univ, Div Stem Cell & Tissue Engn, State Key Lab
    Biotherapy, W China Hosp, Chengdu 610041, Peoples R China.
 EM dengli2000@gmail.com
 FU National High Technology Research and Development Program ("863") of
    China [2007AA021900]; Science and Technology Bureau of Sichuan province
    [07SG111-004, 2008SZ0035]
 FX This work was supported by the National High Technology Research and
    Development Program ("863") of China [grant number 2007AA021900] and
    the Key Project of Science and Technology Bureau of Sichuan province
    [grant numbers 07SG111-004, 2008SZ0035).
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 NR 30
 TC 1
 PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
 PI LONDON
 PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
 SN 1065-6995
 J9 CELL BIOL INT
 JI Cell Biol. Int.
 PD MAR
 PY 2010
 VL 34
 IS 3
 BP 237
 EP 243
 DI 10.1042/CBI20090044
 PG 7
 SC Cell Biology
 GA 592PM
 UT ISI:000277391600001
 ER
 
 PT J
 AU Yang, TY
    Zaman, MH
 AF Yang, Tianyi
    Zaman, Muhammad H.
 TI Estimation of Cellular Adhesion Forces Using Mean Field Theory
 SO CELLULAR AND MOLECULAR BIOENGINEERING
 LA English
 DT Article
 DE Cell matrix interactions; Adhesion force; Mean field theory
 ID RED-BLOOD-CELLS; LARGE CONTACT AREAS; LEADING-EDGE; DETACHMENT;
    THERMODYNAMICS; PROTRUSION; MIGRATION; PHYSICS
 AB A complete understanding of the interaction of the cell with the
    surrounding substrate requires a quantitative understanding of the
    force with which they adhere to the matrix. Using mean field theory, we
    provide a new and robust method to calculate this force of cellular
    adhesion to a ligand coated substrate in a system that contains
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    conformations, long and short range interactions and solvent entropic
    effects that regulate adhesion in native environments. The results of
    our calculations provide a set of testable quantitative predictions
    that will guide future experimental endeavors.
 C1 [Zaman, Muhammad H.] Boston Univ, Dept Biomed Engn, Boston, MA 02215 USA.
    [Yang, Tianyi] Univ Texas Austin, Dept Phys, Austin, TX 78712 USA.
 RP Zaman, MH, Boston Univ, Dept Biomed Engn, Boston, MA 02215 USA.
 EM zaman@bu.edu
 FU Robert A. Welch Foundation 
 FX MHZ acknowledges the support of Robert A. Welch Foundation grant.
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 NR 18
 TC 0
 PU SPRINGER
 PI NEW YORK
 PA 233 SPRING ST, NEW YORK, NY 10013 USA
 SN 1865-5025
 J9 CELL MOL BIOENG
 JI Cell. Mol. Bioeng.
 PD JUN
 PY 2010
 VL 3
 IS 2
 BP 190
 EP 194
 DI 10.1007/s12195-010-0115-1
 PG 5
 SC Cell & Tissue Engineering; Biophysics; Cell Biology
 GA 592HK
 UT ISI:000277368900010
 ER
 
 PT J
 AU Liu, XD
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    Koblish, HK
    Yang, GJ
    Wang, Q
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    Rupar, M
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    Scherle, PA
 AF Liu, Xiangdong
    Shin, Niu
    Koblish, Holly K.
    Yang, Gengjie
    Wang, Qian
    Wang, Kathy
    Leffet, Lynn
    Hansbury, Michael J.
    Thomas, Beth
    Rupar, Mark
    Waeltz, Paul
    Bowman, Kevin J.
    Polam, Padmaja
    Sparks, Richard B.
    Yue, Eddy W.
    Li, Yanlong
    Wynn, Richard
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    Burn, Timothy C.
    Combs, Andrew P.
    Newton, Robert C.
    Scherle, Peggy A.
 TI Selective inhibition of IDO1 effectively regulates mediators of
    antitumor immunity
 SO BLOOD
 LA English
 DT Article
 ID INDOLEAMINE 2,3-DIOXYGENASE EXPRESSION; HUMAN DENDRITIC CELLS; CD8(+)
    T-CELLS; TRYPTOPHAN CATABOLISM; COLORECTAL-CANCER; POOR-PROGNOSIS;
    1-METHYL-TRYPTOPHAN; PROLIFERATION; SUPPRESSION; PROGRESSION
 AB Indoleamine 2,3-dioxygenase-1 (IDO1; IDO) mediates oxidative cleavage
    of tryptophan, an amino acid essential for cell proliferation and
    survival. IDO1 inhibition is proposed to have therapeutic potential in
    immunodeficiency-associated abnormalities, including cancer. Here, we
    describe INCB024360, a novel IDO1 inhibitor, and investigate its roles
    in regulating various immune cells and therapeutic potential as an
    anticancer agent. In cellular assays, INCB024360 selectively inhibits
    human IDO1 with IC50 values of approximately 10nM, demonstrating little
    activity against other related enzymes such as IDO2 or tryptophan
    2,3-dioxygenase (TDO). In coculture systems of human allogeneic
    lymphocytes with dendritic cells (DCs) or tumor cells, INCB024360
    inhibition of IDO1 promotes T and natural killer (NK)-cell growth,
    increases IFN-gamma production, and reduces conversion to regulatory T
    (T-reg)-like cells. IDO1 induction triggers DC apoptosis, whereas
    INCB024360 reverses this and increases the number of CD86(high) DCs,
    potentially representing a novel mechanism by which IDO1 inhibition
    activates T cells. Further-more, IDO1 regulation differs in DCs versus
    tumor cells. Consistent with its effects in vitro, administration of
    INCB024360 to tumor-bearing mice significantly inhibits tumor growth in
    a lymphocyte-dependent manner. Analysis of plasma kynurenine/tryptophan
    levels in patients with cancer affirms that the IDO pathway is
    activated in multiple tumor types. Collectively, the data suggest that
    selective inhibition of IDO1 may represent an attractive cancer
    therapeutic strategy via up-regulation of cellular immunity. (Blood.
    2010; 115(17): 3520-3530)
 C1 [Scherle, Peggy A.] Incyte Corp, Expt Stn, Wilmington, DE 19880 USA.
 RP Scherle, PA, Incyte Corp, Expt Stn, Rte 141 & Henry Clay Rd,
    Wilmington, DE 19880 USA.
 EM pscherle@incyte.com
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 NR 51
 TC 4
 PU AMER SOC HEMATOLOGY
 PI WASHINGTON
 PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
 SN 0006-4971
 J9 BLOOD
 JI Blood
 PD APR 29
 PY 2010
 VL 115
 IS 17
 BP 3520
 EP 3530
 DI 10.1182/blood-2009-09-246124
 PG 11
 SC Hematology
 GA 591WL
 UT ISI:000277335800017
 ER
 
 PT J
 AU Li, J
    Sze, DMY
    Brown, RD
    Cowley, MJ
    Kaplan, W
    Mo, SL
    Yang, SH
    Aklilu, E
    Kabani, K
    Loh, YS
    Yamagishi, T
    Chen, YL
    Ho, PJ
    Joshua, DE
 AF Li, Jia
    Sze, Daniel M. -Y.
    Brown, Ross D.
    Cowley, Mark J.
    Kaplan, Warren
    Mo, Sui-Lin
    Yang, Shihong
    Aklilu, Esther
    Kabani, Karieshma
    Loh, Yen S.
    Yamagishi, Tetsuo
    Chen, Yuling
    Ho, P. Joy
    Joshua, Douglas E.
 TI Clonal expansions of cytotoxic T cells exist in the blood of patients
    with Waldenstrom macroglobulinemia but exhibit anergic properties and
    are eliminated by nucleoside analogue therapy
 SO BLOOD
 LA English
 DT Article
 ID CHRONIC MYELOGENOUS LEUKEMIA; TYROSINE-PHOSPHATASE HEPTP; NF-KAPPA-B;
    MULTIPLE-MYELOMA; CYCLE PROGRESSION; REPERTOIRE USAGE; PROTEIN-KINASE;
    RECEPTOR; BETA; ARREST
 AB T cells contribute to host-tumor interactions in patients with
    monoclonal gammopathies. Expansions of CD8(+)CD57(+) T-cell receptor V
    beta-positive (TCRV beta(+))-restricted cytotoxic T-cell (CTL) clones
    are found in 48% of patients with multiple myeloma and confer a
    favorable prognosis. We now report that CTL clones with varying TCRV
    beta repertoire are present in 70% of patients with Waldenstrom
    macroglobulinemia (WM; n = 20). Previous nucleoside analog (NA)
    therapy, associated with increased incidence of transformation to
    aggressive lymphoma, significantly influenced the presence of TCRV beta
    expansions (chi(2) = 11.6; P < .001), as 83% of patients without (n =
    6) and only 7% with (n = 14) TCRV beta expansions had received NA.
    Clonality of CD3(+)CD8(+)CD57(+) TCRV beta(+) restricted CTLs was
    confirmed by TCRV beta CDR3 size analysis and direct sequencing. The
    differential expression of CD3(+)CD8(+)CD57(+) TCRV beta(+) cells was
    profiled using DNA microarrays and validated at mRNA and protein level.
    By gene set enrichment analysis, CTL clones expressed not only genes
    from cytotoxic pathways (GZMB, PRF1, FGFBP2) but also genes that
    suppress apoptosis, inhibit proliferation, arrest cell-cycle G1/S
    transition, and activate T cells (RAS, CSK, and TOB pathways).
    Proliferation tracking after stimulation confirmed their anergic state.
    Our studies demonstrate the incidence, NA sensitivity, and nature of
    clonal CTLs in WM and highlight mechanisms that cause anergy in these
    cells. (Blood. 2010; 115(17): 3580-3588)
 C1 [Li, Jia; Sze, Daniel M. -Y.; Mo, Sui-Lin; Loh, Yen S.; Yamagishi, Tetsuo; Chen, Yuling] Univ Sydney, Fac Pharm, Canc Immunol Grp, Sydney, NSW 2006, Australia.
    [Sze, Daniel M. -Y.; Brown, Ross D.; Yang, Shihong; Aklilu, Esther; Kabani, Karieshma; Ho, P. Joy; Joshua, Douglas E.] Royal Prince Alfred Hosp, Inst Haematol, Sydney, NSW, Australia.
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    [Cowley, Mark J.; Kaplan, Warren] Garvan Inst Med Res, Peter Wills Bioinformat Ctr, Sydney, NSW, Australia.
    [Kaplan, Warren; Chen, Yuling] Univ New S Wales, Sydney, NSW, Australia.
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 RP Brown, RD, Royal Prince Alfred Hosp, Inst Haematol, Missenden Rd,
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 EM ross.brown@sswahs.nsw.gov.au
 FU Cancer Institute NSW ; Sydney Foundation for Medical Research 
 FX This work was supported by grants from Cancer Institute NSW (D.M.-Y.S.
    and K. K.) and Sydney Foundation for Medical Research (E. A.).
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 NR 50
 TC 1
 PU AMER SOC HEMATOLOGY
 PI WASHINGTON
 PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
 SN 0006-4971
 J9 BLOOD
 JI Blood
 PD APR 29
 PY 2010
 VL 115
 IS 17
 BP 3580
 EP 3588
 DI 10.1182/blood-2009-10-246991
 PG 9
 SC Hematology
 GA 591WL
 UT ISI:000277335800023
 ER
 
 PT J
 AU Han, LQ
    Yang, GY
    Zhu, HS
    Wang, YY
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 AF Han, L. Q.
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 LA English
 DT Article
 DE geNorm; Lactation; Quantitative real-time PCR; Reference gene
 ID POLYMERASE-CHAIN-REACTION; QUANTITATIVE RT-PCR; REAL-TIME PCR;
    LACTATION CYCLE; EXPRESSION; NORMALIZATION; TISSUE
 AB Obtaining quantitative data concerning gene expression is important for
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    significantly different from the non-normalized ratio. We recommend the
    use of these three reference genes for the normalization of qRT-PCR
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 C1 [Han, L. Q.; Zhu, H. S.; Wang, Y. Y.; Wang, L. F.; Guo, Y. J.; Lu, W. F.; Li, H. J.; Wang, Y. L.] Henan Agr Univ, Coll Anim Sci & Vet Med, Zhengzhou, Peoples R China.
    [Han, L. Q.; Yang, G. Y.; Wang, Y. L.] Minist Agr, Key Lab Anim Growth & Dev, Zhengzhou, Peoples R China.
 RP Wang, YL, Henan Agr Univ, Coll Anim Sci & Vet Med, Zhengzhou, Peoples R
    China.
 EM ylwang2001@yahoo.cn
 FU Chinese National Programs for Science and Technology Development
    [2006BAD04A03-10]
 FX Research supported by Chinese National Programs for Science and
    Technology Development (#2006BAD04A03-10).
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 NR 14
 TC 0
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 PI RIBEIRAO PRETO
 PA RUA HUDSON 655, JARDIM CANADA, RIBEIRAO PRETO, SP, BRAZIL
 SN 1676-5680
 J9 GENET MOL RES
 JI Genet. Mol. Res.
 PY 2010
 VL 9
 IS 1
 BP 449
 EP 456
 DI 10.4238/vol9-1gmr724
 PG 8
 SC Biochemistry & Molecular Biology; Genetics & Heredity
 GA 591TC
 UT ISI:000277326200040
 ER
 
 PT J
 AU Yang, XY
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 TI Karyotype and genetic relationship based on RAPD markers of six wild
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 LA English
 DT Article
 DE Cultivar buckwheat; Fagopyrum; Genetic relationship; Karyotype; RAPD
    marker; Wild buckwheat
 ID PHYLOGENETIC-RELATIONSHIPS; NUCLEOTIDE-SEQUENCES; PERENNIAL BUCKWHEAT;
    POLYGONACEAE; REGION
 AB Karyotypes of six wild buckwheat species from Sichuan Pan'xi Regions of
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    tataricum clustered into a separate group. F. esculentum and F. cymosum
    clustered together in one separate group.
 C1 [Yang, Xiao-yan; Wu, Zhen-Fang; Chen, Hui; Shao, Ji-rong; Wu, Qi] Sichuan Agr Univ, Coll Life Sci, Yaan 625014, Sichuan, Peoples R China.
 RP Chen, H, Sichuan Agr Univ, Coll Life Sci, Yaan 625014, Sichuan, Peoples
    R China.
 EM samkam@126.com
    chenhui@sicau.edu.cn
 FU key scientific project of Sichuan, China [04NG001-015]
 FX This work was supported by key scientific project of Sichuan, China
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 NR 26
 TC 0
 PU SPRINGER
 PI DORDRECHT
 PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
 SN 0925-9864
 J9 GENET RESOUR CROP EVOLUTION
 JI Genet. Resour. Crop Evol.
 PD JUN
 PY 2010
 VL 57
 IS 5
 BP 649
 EP 656
 DI 10.1007/s10722-009-9500-9
 PG 8
 SC Agronomy; Plant Sciences
 GA 590QC
 UT ISI:000277241100002
 ER
 
 PT J
 AU Mei, J
    Li, Q
    Yang, X
    Qian, L
    Liu, L
    Yin, J
    Frauen, M
    Li, J
    Qian, W
 AF Mei, J.
    Li, Q.
    Yang, X.
    Qian, L.
    Liu, L.
    Yin, J.
    Frauen, M.
    Li, J.
    Qian, W.
 TI Genomic relationships between wild and cultivated Brassica oleracea L.
    with emphasis on the origination of cultivated crops
 SO GENETIC RESOURCES AND CROP EVOLUTION
 LA English
 DT Article
 DE Brassica oleracea; Cultivated form; Genomic relationships; Sicily; Wild
    taxa
 ID GENETIC DIVERSITY; LEPTOSPHAERIA-MACULANS; LENGTH POLYMORPHISMS; RAPD
    MARKERS; RELATIVES 2N; DNA; POPULATION; CHLOROPLAST; RESISTANCE;
    CRUCIFERAE
 AB Wild taxa in Brassica oleracea L. play an important role to improve
    cultivated crops, but the genomic relationships between wild and
    cultivated forms have not been well clarified. An overall survey of
    genomic relationships among 39 accessions covering 10 wild and 7
    cultivared types in B. oleracea was performed using amplified fragment
    length polymorphism and simple sequence repeat. The cultivated types
    were clustered together with B. oleracea ssp. oleracea, B. incana, B.
    bourgeaui, B. montana, B. cretica and B. hilarionis, while 4 wild taxa
    from Sicily, B. rupestris, B. insularis, B. macrocarpa and B. villosa
    formed the other group. It implies the low possibility that current B.
    oleracea crops originated in Sicily.
 C1 [Mei, J.; Li, Q.; Yang, X.; Qian, L.; Liu, L.; Yin, J.; Li, J.; Qian, W.] Southwest Univ, Coll Agron & Biotechnol, Chongqing 400716, Peoples R China.
    [Frauen, M.] Norddeutsch Pflanzenzucht Hans Georg Lembke KG, D-24363 Hohenlieth, Germany.
 RP Li, J, Southwest Univ, Coll Agron & Biotechnol, Chongqing 400716,
    Peoples R China.
 EM ljn1950@swu.edu.cn
    qianwei666@hotmail.com
 FU NPZ Company ; Natural Science Foundation [2007BB1362, 2006AA10ZIE6];
    Ministry of Education of China ; Ministry of Personnel of China Fund 
 FX We thank CGN in Netherlands, IPK in Germany, UPM in Spain, Prof.
    Snogerup S from UL in Sweden and Prof. Quiros C from UC Davis for kind
    supports in collection of materials. It is financially supported by NPZ
    Company, Natural Science Foundation Project of CQ (2007BB1362), 863
    Project (2006AA10ZIE6) and Ministry of Education of China and Ministry
    of Personnel of China Fund to W. Qian.
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 NR 34
 TC 1
 PU SPRINGER
 PI DORDRECHT
 PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
 SN 0925-9864
 J9 GENET RESOUR CROP EVOLUTION
 JI Genet. Resour. Crop Evol.
 PD JUN
 PY 2010
 VL 57
 IS 5
 BP 687
 EP 692
 DI 10.1007/s10722-009-9504-5
 PG 6
 SC Agronomy; Plant Sciences
 GA 590QC
 UT ISI:000277241100006
 ER
 
 PT J
 AU Zhang, H
    Jin, YB
    Zhang, ZX
    Yang, L
    Huang, YC
 AF Zhang, Hong
    Jin, Yin-Bin
    Zhang, Zhen-Xi
    Yang, Lin
    Huang, Ye-Cho
 TI Effects of electrical heterogeneity on transmural reentry during acute
    global ischemia
 SO GENERAL PHYSIOLOGY AND BIOPHYSICS
 LA English
 DT Article
 DE Arrhythmia; Acute ischemia; Computer simulation; Reentry; Transmural
    heterogeneity
 ID ACTION-POTENTIAL DURATION; ACUTE MYOCARDIAL-ISCHEMIA; SUDDEN CARDIAC
    DEATH; LONG-QT SYNDROME; IONIC CURRENTS; M-CELLS; SIMULATION; MODEL;
    ARRHYTHMIAS; EPICARDIUM
 AB Ventricular arrhythmias are commonly observed in patients with
    ischemia. It is reported that the electrophysiological changes evoked
    by ischemia are greater in the epicardium than in the endocardium. To
    investigate the effects of this heterogeneity on transmural reentry,
    the computer simulation method is used. A two-dimensional model which
    can reproduce the endocardial, epicardial and middle cell types,
    approximate the ischemic characteristics and distribution of the
    ischemic severity is developed by setting different ratios of the
    maximum conductance of the rapid and slow inward rectifier potassium
    currents and considering the three major component conditions of acute
    ischemia at the ionic level. The results demonstrate that action
    potentials of the ischemic cells have elevated resting potential,
    shortened duration, slowed upstroke and declined amplitude. Conduction
    velocity is much more depressed in the epicardium because of the
    ischemia-induced transmural gradient of excitability. The epicardially
    initiated activation has wider vulnerable window and more possibility
    to cause unidirectional propagation even reentry. Dispersion of the
    excitability is proposed to be the underlying mechanism.
 C1 [Zhang, Hong; Jin, Yin-Bin] Xi An Jiao Tong Univ, Sch Elect Engn, Xian 710049, Shaanxi, Peoples R China.
    [Zhang, Hong; Zhang, Zhen-Xi; Huang, Ye-Cho] Xi An Jiao Tong Univ, Sch Life Sci & Technol, Minist Educ China, Key Lab Biomed Informat Engn, Xian 710049, Shaanxi, Peoples R China.
    [Yang, Lin] Xi An Jiao Tong Univ, Hosp 1, Dept Cardiol, Xian 710061, Peoples R China.
 RP Zhang, H, Xi An Jiao Tong Univ, Sch Elect Engn, 28 W Xianning Rd, Xian
    710049, Shaanxi, Peoples R China.
 EM maxr@263.net
 FU National Natural Science Foundation of P. R. China [30870659,
    30971221]; Health Foundation of Shaanxi Province, P. R. China [08D23]
 FX This study is supported by the National Natural Science Foundation of
    P. R. China (No. 30870659 and 30971221) and the Health Foundation of
    Shaanxi Province, P. R. China (No. 08D23). We also thank Dr. Shien-Fong
    Lin (Krannert Institute of Cardiology, Indiana University School of
    Medicine, USA) for his advice and help.
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 NR 38
 TC 0
 PU GENERAL PHYSIOL AND BIOPHYSICS
 PI BRATISLAVA
 PA INST OF MOLEC PHYSIOL GENETICS SLOVAK ACAD OF SCI VLARSKA 5, 83334
    BRATISLAVA, SLOVAKIA
 SN 0231-5882
 J9 GEN PHYSIOL BIOPHYS
 JI Gen. Physiol. Biophys.
 PD MAR
 PY 2010
 VL 29
 IS 1
 BP 12
 EP 22
 DI 10.4149/gpb_2010_01_12
 PG 11
 SC Biochemistry & Molecular Biology; Biophysics; Physiology
 GA 589HD
 UT ISI:000277136800003
 ER
 
 PT J
 AU Yang, S
    Lin, G
    Tan, YQ
    Deng, LY
    Yuan, D
    Lu, GX
 AF Yang, S.
    Lin, G.
    Tan, Y. -Q.
    Deng, L. -Y.
    Yuan, D.
    Lu, G. -X.
 TI Differences between karyotypically normal and abnormal human embryonic
    stem cells
 SO CELL PROLIFERATION
 LA English
 DT Article
 ID HUMAN ES CELLS; CHROMOSOMAL-ABNORMALITIES; GENOMIC INSTABILITY;
    CULTURE; DIFFERENTIATION; FIBROBLASTS; PROTEINS; CANCER; P53
 AB Objectives:
    To compare different biological characteristics of human embryonic stem
    cells (HESCs) between those with normal and those with abnormal
    karyotype.
    Materials and methods:
    Culture-adapted HESCs (chHES-3) with abnormal karyotype were compared
    with karyotypically normal cells, with regard to pluripotency and
    differentiation capacity, ultrastructure, growth characteristics, gene
    expression profiles and signalling pathways.
    Results:
    We found a new abnormal karyotype of HESCs. We observed that chHES-3
    cells with normal and abnormal karyotypes shared similarities in
    expression markers of pluripotency; however, karyotypically abnormal
    chHES-3 cells had a tendency for differentiation towards ectoderm
    lineages and were easily maintained in suboptimal culturing conditions.
    Abnormal chHES-3 cells displayed relatively mature cell organelles
    compared to normal cells, and karyotypically abnormal chHES-3 cells had
    increased survival and population growth. Genes related to cell
    proliferation and apoptosis were up-regulated, but genes associated
    with genetic instability (p53, Rb, BRCA1) were down-regulated in the
    karyotypically abnormal cells.
    Conclusion:
    Karyotypically abnormal chHES-3 cells had a more developed capacity for
    proliferation, resistance to apoptosis and less genetic stability
    compared to normal chHES-3 cells and may be an excellent model for
    studying and characterizing initial stages that determine transition of
    embryonic stem cells into cancer stem cells.
 C1 [Lu, G. -X.] Cent S Univ, Inst Reprod & Stem Cell Engn, Changsha, Peoples R China.
    Natl Engn Res Ctr Human Stem Cells, Changsha, Peoples R China.
 RP Lu, GX, Cent S Univ, Inst Reprod & Stem Cell Engn, Changsha, Peoples R
    China.
 EM lugxdirector@yahoo.com.cn
 FU National Natural Science Foundation Major Program of China [30030070];
    Hi-Tech Research and Development of China [2003AA205181, 2006AA02A102];
    National Basic Research Program of China [00CB 51010]
 FX The authors thank Associate Prof. Jozef Lazar and Assistant Prof. Aron
    Geurts for revising and editing the manuscript. This study was
    supported by the National Natural Science Foundation Major Program of
    China (No. 30030070), the Hi-Tech Research and Development of China
    (863 program No. 2003AA205181 and 2006AA02A102) and the National Basic
    Research Program of China (973 program No. 00CB 51010).
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 NR 31
 TC 3
 PU WILEY-BLACKWELL PUBLISHING, INC
 PI MALDEN
 PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
 SN 0960-7722
 J9 CELL PROLIFERATION
 JI Cell Prolif.
 PD JUN
 PY 2010
 VL 43
 IS 3
 BP 195
 EP 206
 DI 10.1111/j.1365-2184.2010.00669.x
 PG 12
 SC Cell Biology
 GA 589PL
 UT ISI:000277164400001
 ER
 
 PT J
 AU Pan, K
    Sun, Q
    Zhang, J
    Ge, S
    Li, S
    Zhao, Y
    Yang, P
 AF Pan, K.
    Sun, Q.
    Zhang, J.
    Ge, S.
    Li, S.
    Zhao, Y.
    Yang, P.
 TI Multilineage differentiation of dental follicle cells and the roles of
    Runx2 over-expression in enhancing osteoblast/cementoblast-related gene
    expression in dental follicle cells
 SO CELL PROLIFERATION
 LA English
 DT Article
 ID MARROW STROMAL CELLS; CEMENTUM ATTACHMENT PROTEIN; OSTEOBLAST
    DIFFERENTIATION; CLEIDOCRANIAL DYSPLASIA; STEM-CELLS; IN-VITRO; CBFA1;
    TOOTH; CEMENTOGENESIS; BIOLOGY
 AB Objectives:
    Dental follicle cells (DFCs) provide the origin of periodontal tissues,
    and Runx2 is essential for bone formation and tooth development. In
    this study, pluripotency of DFCs was evaluated and effects of Runx2 on
    them were investigated.
    Materials and methods:
    The DFCs were induced to differentiate towards osteoblasts, adipocytes
    or chondrocytes, and alizarin red staining, oil red O staining or
    alcian blue staining was performed to reveal the differentiated states.
    Bone marrow stromal cells (BMSCs) and primary mouse fibroblasts served
    as controls. DFCs were also infected with recombinant retroviruses
    encoding either full-length Runx2 or mutant Runx2 without the VWRPY
    motif. Western blot analysis, real-time real time RT-PCR and in vitro
    mineralization assay were performed to evaluate the effects of
    full-length Runx2 or mutant Runx2 on osteogenic/cementogenic
    differentiation of the cells.
    Results:
    The above-mentioned staining methods demonstrated that DFCs were
    successfully induced to differentiate towards osteoblasts, adipocytes
    or chondrocytes respectively, confirming the existence of pluripotent
    mesenchymal stem cells in dental follicle tissues. However, staining
    intensity in DFC cultures was weaker than in BMSC cultures. Real-time
    PCR analysis indicated that mutant Runx2 induced a more pronounced
    increase in expression levels of OC, OPN, Col I and CP23 than
    full-length Runx2. Mineralization assay also showed that mutant Runx2
    increased mineralization nodule formation more prominently than
    full-length Runx2.
    Conclusions:
    Multipotent DFCs can be induced to differentiate towards osteoblasts,
    adipocytes or chondrocytes in vitro. Runx2 over-expression up-regulated
    expression levels of osteoblast/cementoblast-related genes and in vitro
    enhanced osteogenic differentiation of DFCs. In addition, mutant
    Runx2-induced changes in DFCs were more prominent than those induced by
    full-length Runx2.
 C1 [Pan, K.; Sun, Q.; Zhang, J.; Ge, S.; Li, S.; Yang, P.] Shandong Univ, Sch Dent, Dept Periodontol, Jinan 250012, Shandong, Peoples R China.
    [Pan, K.; Sun, Q.; Zhang, J.; Ge, S.; Li, S.; Yang, P.] Shandong Univ, Sch Dent, Inst Oral Biomed, Jinan 250012, Shandong, Peoples R China.
    [Pan, K.] Qingdao Univ, Coll Med, Affiliated Hosp, Dept Stomatol, Qingdao 266071, Peoples R China.
    [Zhao, Y.] Tianjin Med Univ, Stomatol Hosp, Dept Orthodont, Tianjin, Peoples R China.
 RP Yang, P, Shandong Univ, Sch Dent, Dept Periodontol, 44-1 Wenhuaxi Rd,
    Jinan 250012, Shandong, Peoples R China.
 EM yangps@sdu.edu.cn
 FU national Natural Science Foundation of China, Beijing, China
    [30772425]; Shandong Provincial Natural Science Foundation, Jinan,
    China [Y 2007C 091]
 FX This study was supported by grants from the national Natural Science
    Foundation of China (No. 30772425), Beijing, China, and Shandong
    Provincial Natural Science Foundation (No. Y 2007C 091), Jinan, China.
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 NR 53
 TC 0
 PU WILEY-BLACKWELL PUBLISHING, INC
 PI MALDEN
 PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
 SN 0960-7722
 J9 CELL PROLIFERATION
 JI Cell Prolif.
 PD JUN
 PY 2010
 VL 43
 IS 3
 BP 219
 EP 228
 DI 10.1111/j.1365-2184.2010.00670.x
 PG 10
 SC Cell Biology
 GA 589PL
 UT ISI:000277164400003
 ER
 
 PT J
 AU Yen, TH
    Chen, Y
    Fu, JF
    Weng, CH
    Tian, YC
    Hung, CC
    Lin, JL
    Yang, CW
 AF Yen, T. -H.
    Chen, Y.
    Fu, J. -F.
    Weng, C. -H.
    Tian, Y. -C.
    Hung, C. -C.
    Lin, J. -L.
    Yang, C. -W.
 TI Proliferation of myofibroblasts in the stroma of renal oncocytoma
 SO CELL PROLIFERATION
 LA English
 DT Article
 ID EPITHELIAL-MESENCHYMAL TRANSITION; SQUAMOUS-CELL CARCINOMA;
    BONE-MARROW-CELLS; CD34(+) FIBROCYTES; PROSTATE-CANCER; TUMOR INVASION;
    COLON-CANCER; FIBROBLASTS; SMOOTH; GROWTH
 AB Objectives:
    Myofibroblasts are a vital component of stroma of many malignant
    neoplasms, but it is not yet established whether stromal myofibroblasts
    also exist in benign tumours such as oncocytoma of the kidney.
    Materials and methods:
    Histomorphological and immunohistochemical analysis of 16 renal
    oncocytomas diagnosed at Chang Gung Memorial Hospital, Taiwan, has been
    performed.
    Results:
    Renal oncocytomas were composed of oncocytes, large cells with granular
    eosinophilic cytoplasm, arranged mostly in sheets, in tubulocystic or
    combined pattern. Few oncocytes appeared to be undergoing proliferation
    or apoptosis. MIB-1 and active caspase 3 indices were low, but higher
    in tumour than in surrounding non-tumour parenchyma (MIB-1: 0.93 +/-
    0.09 versus 0.46 +/- 0.07, P < 0.001 and active caspase 3: 0.76 +/-
    0.08 versus 0.41 +/- 0.09, P < 0.001). Wnt/beta-catenin signalling was
    not implicated in this neoplasm, as there was no loss of E-cadherin
    membranous localization or expression of intranuclear beta-catenin in
    the cells. Clumps of oncocytes were stained with periodic acid Schiff
    and had collagen I-, collagen III- and fibronectin-positive, but
    desmin- and human caldesmon-negative stromas. Importantly, alpha-smooth
    muscle actin (SMA)-immunostaining established the myofibroblastic
    nature of many of the stromal cells. Some of the myofibroblasts were
    also positive for MIB-1, indicating a proliferative role for them in
    the stroma.
    Conclusions:
    Renal oncocytomas were composed of two independent compartments: benign
    oncocytes and pronounced fibrotic stroma, which consisted of
    proliferating myofibroblasts (SMA- and MIB-1-positive) which were
    associated with excessive deposition of extracellular matrix (periodic
    acid Schiff-component, collagen I-, collagen III- and
    fibronectin-positive, and desmin- and human caldesmon-negative).
 C1 [Yen, T. -H.; Weng, C. -H.; Tian, Y. -C.; Hung, C. -C.; Lin, J. -L.; Yang, C. -W.] Chang Gung Mem Hosp, Dept Nephrol, Taipei 105, Taiwan.
    [Chen, Y.] Chang Gung Mem Hosp, Dept Urol, Taipei 105, Taiwan.
    [Fu, J. -F.] Chang Gung Mem Hosp, Dept Med Res, Taipei 105, Taiwan.
    [Yen, T. -H.; Chen, Y.; Fu, J. -F.; Weng, C. -H.; Tian, Y. -C.; Hung, C. -C.; Lin, J. -L.; Yang, C. -W.] Chang Gung Univ, Coll Med, Tao Yuan, Taiwan.
 RP Yen, TH, Chang Gung Mem Hosp, Dept Nephrol, 199 Tung Hwa N Rd, Taipei
    105, Taiwan.
 EM m19570@adm.cgmh.org.tw
 FU Chang Gung Memorial Hospital [CMRP G370601, G370602]; National Science
    Council of Taiwan [NMRP G370601]
 FX Parts of this study have been presented at the annual meeting of the
    Taiwan Society of Nephrology (12-13 December 2008, Taipei, Taiwan).
    Tzung-Hai Yen was funded by research grants from the Chang Gung
    Memorial Hospital (CMRP G370601 and G370602) and National Science
    Council of Taiwan (NMRP G370601).
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 NR 45
 TC 2
 PU WILEY-BLACKWELL PUBLISHING, INC
 PI MALDEN
 PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
 SN 0960-7722
 J9 CELL PROLIFERATION
 JI Cell Prolif.
 PD JUN
 PY 2010
 VL 43
 IS 3
 BP 287
 EP 296
 DI 10.1111/j.1365-2184.2010.00681.x
 PG 10
 SC Cell Biology
 GA 589PL
 UT ISI:000277164400009
 ER
 
 PT J
 AU Yang, YF
    Steeg, J
    Honaramooz, A
 AF Yang, Yanfei
    Steeg, Jordon
    Honaramooz, Ali
 TI The effects of tissue sample size and media on short-term hypothermic
    preservation of porcine testis tissue
 SO CELL AND TISSUE RESEARCH
 LA English
 DT Article
 DE Gonocytes; Testis tissue; Hypothermic; Leibovitz L15; HypoThermosol;
    Porcine (Yorkshire-cross)
 ID GERM-CELL TRANSPLANTATION; TESTICULAR TISSUE; STEM-CELLS; COLD-STORAGE;
    CRYOPRESERVATION; MICE; TRANSMISSION; FERTILITY; GONOCYTES; SPERM
 AB The objective of this study was to develop effective strategies for
    hypothermic preservation of immature porcine testis tissue to maintain
    structural integrity and cell viability. In Experiment 1, testes from
    1-week-old piglets were used to study the effects of tissue sample size
    (as intact testes or fragments of 100-or 30 mg) and the use of one of 9
    different media on hypothermic preservation of the testis tissue for 6
    days. The examined media included: Dulbecco's phosphate-buffered saline
    (DPBS), Dulbecco's modified Eagle's medium (DMEM), Leibovitz L15 (L15),
    L15 with fetal bovine serum (FBS, at 10%, 20% or 50%), HypoThermosol
    solution-FRS (HTS), Ham's F12, and Media 199. On days 0, 3, and 6,
    testis tissues were digested to compare the cell survival rates. Tissue
    sections were also semi-quantitatively assessed to determine the
    efficiency of different preservation strategies. There was no effect of
    testis sample size (P > 0.05), but cell survival rates of testis cells
    isolated from preserved testis tissues changed depending on the media
    and day (P < 0.05). Testis tissue within HTS did not show morphological
    changes after 6 days. In Experiment 2, two of the top performing media
    (20% FBS-L15 and HTS) were selected for immunocytochemical detection of
    gonocytes. Proportions of gonocytes (%) in isolated testis cells,
    however, did not differ between the two media on days 0, 3, or 6. These
    results show that testis tissue can be maintained for 3 days at 4A
    degrees C with high cell survival rate, and tissue morphology can be
    preserved for at least 6 days in HTS.
 C1 [Yang, Yanfei; Steeg, Jordon; Honaramooz, Ali] Univ Saskatchewan, Western Coll Vet Med, Dept Vet Biomed Sci, Saskatoon, SK S7N 5B4, Canada.
 RP Honaramooz, A, Univ Saskatchewan, Western Coll Vet Med, Dept Vet Biomed
    Sci, 52 Campus Dr, Saskatoon, SK S7N 5B4, Canada.
 EM ali.honaramooz@usask.ca
 FU University of Saskatchewan Colleges of Graduate Studies and Veterinary
    Medicine ; Natural Sciences and Engineering Research Council (NSERC) of
    Canada 
 FX We thank the University of Saskatchewan Colleges of Graduate Studies
    and Veterinary Medicine for scholarships (to Y. Yang), and the Natural
    Sciences and Engineering Research Council (NSERC) of Canada for a
    summer student scholarship (to J. Steeg) and grants (to A. Honaramooz)
    to support this project.
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 NR 34
 TC 0
 PU SPRINGER
 PI NEW YORK
 PA 233 SPRING ST, NEW YORK, NY 10013 USA
 SN 0302-766X
 J9 CELL TISSUE RES
 JI Cell Tissue Res.
 PD MAY
 PY 2010
 VL 340
 IS 2
 BP 397
 EP 406
 DI 10.1007/s00441-010-0946-z
 PG 10
 SC Cell Biology
 GA 589HE
 UT ISI:000277136900016
 ER
 
 PT J
 AU Wang, YX
    Jha, AK
    Chen, RJ
    Doonan, JH
    Yang, M
 AF Wang, Yixing
    Jha, Ajay K.
    Chen, Rujin
    Doonan, John H.
    Yang, Ming
 TI Polyploidy-Associated Genomic Instability in Arabidopsis thaliana
 SO GENESIS
 LA English
 DT Article
 DE cell cycle; flow cytometry; cyclin; aneuploid; generative cell; dyad
 ID EVOLUTION; CELLS; MEIOSIS; SENESCENCE; PATTERNS; DIVISION; TELEOSTS
 AB Formation of polyploid organisms by fertilization of unreduced gametes
    in meiotic mutants is believed to be a common phenomenon in species
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    generations due to unreduced but viable gametes in the Arabidopsis
    cyclin a1;2-2 (also named tardy asynchronous meiosis-2) mutant, but the
    resultant octaploid plants produced progeny of either the same or
    reduced ploidy via genomic reductions during meiosis and pollen
    mitosis. Ploidy reductions through sexual reproduction were also
    observed in independently generated artificial octaploid and hexaploid
    Arabidopsis plants. These results demonstrate that octaploid is likely
    the maximal ploidy produced through sexual reproduction in Arabidopsis.
    The polyploidy-associated genomic instability may be a general
    phenomenon that constrains ploidy levels in species evolution. genesis
    48:254-263,2010. (C) 2010 Wiley-Liss, Inc.
 C1 [Wang, Yixing; Jha, Ajay K.; Yang, Ming] Oklahoma State Univ, Dept Bot, Stillwater, OK 74078 USA.
    [Chen, Rujin] Samuel Roberts Noble Fdn Inc, Div Plant Biol, Ardmore, OK 73402 USA.
    [Doonan, John H.] John Innes Ctr Plant Sci Res, Dept Cell & Dev Biol, Norwich NR4 7UH, Norfolk, England.
 RP Yang, M, Oklahoma State Univ, Dept Bot, 104 Life Sci E, Stillwater, OK
    74078 USA.
 EM ming.yang@okstate.edu
 FU Underwood Fellowship ; BBSRC ; Samuel Roberts Noble Foundation ;
    Oklahoma State University 
 FX Contract grant sponsors: The Underwood Fellowship, BBSRC, The Samuel
    Roberts Noble Foundation, Oklahoma State University.
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 NR 30
 TC 2
 PU WILEY-LISS
 PI HOBOKEN
 PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA
 SN 1526-954X
 J9 GENESIS
 JI Genesis
 PD APR
 PY 2010
 VL 48
 IS 4
 BP 254
 EP 263
 DI 10.1002/dvg.20610
 PG 10
 SC Developmental Biology; Genetics & Heredity
 GA 587UF
 UT ISI:000277018300005
 ER
 
 PT J
 AU Kwon, YS
    Oh, YH
    Yi, SI
    Kim, HY
    An, JM
    Yang, SG
    Ok, SH
    Shin, JS
 AF Kwon, Yong-Sham
    Oh, You-Hwan
    Yi, Seung-In
    Kim, Hee-Yeul
    An, Jong-Moon
    Yang, Seung-Gyun
    Ok, Sung-Han
    Shin, Jeong-Sheop
 TI Informative SSR markers for commercial variety discrimination in
    watermelon (Citrullus lanatus)
 SO GENES & GENOMICS
 LA English
 DT Article
 DE Genetic characterization; Molecular fingerprinting; SSR marker;
    Watermelon
 ID GENIC MICROSATELLITE MARKERS; SIMPLE SEQUENCE REPEATS; GENETIC
    ASSESSMENT; L. VARIETIES; LINKAGE MAPS; IDENTIFICATION; CONSTRUCTION;
    UNIFORMITY; DIVERSITY; GERMPLASM
 AB SSR markers were used for variety discrimination and genetic assessment
    in watermelon varieties. Genetic characterization of 49 watermelon
    varieties was investigated using 30 SSR markers developed from melon
    and watermelon. A total of 121 polymorphic amplified fragments were
    obtained by using 30 SSR markers. The average polymorphism information
    content (PIC) was 0.502 ranging from 0.223 to 0.800. One hundred twenty
    one SSR loci were used to calculate Jaccard's distance coefficients for
    unweighted pair group method using the arithmetic averages (UPGMA)
    cluster analysis. A clustering group of varieties, based on the results
    of SSR analysis, were categorized into 5 major groups corresponding to
    morphological traits. Inheritance mode of 2 SSR markers was
    investigated to F-1 plants and F-2 populations of 2 crosses. Parental
    alleles were transmitted from F1 plants and F2 populations. Therefore,
    these marker sets may prove to be effectively applicable to genetic
    assessment of germplasm, genome mapping, and fingerprinting of
    watermelon varieties.
 C1 [Kwon, Yong-Sham; Oh, You-Hwan; Kim, Hee-Yeul] MIFAFF, Korea Seed & Variety Serv, Variety Testing Div, Suwon 443400, South Korea.
    [Yi, Seung-In] MIFAFF, Korea Seed & Variety Serv, Plant Variety Protect Div, Anyang 430016, South Korea.
    [An, Jong-Moon; Yang, Seung-Gyun] Nong Woo Bio Co, Breeding Inst, Yeoju 468885, Gyeonggi, South Korea.
    [Ok, Sung-Han; Shin, Jeong-Sheop] Korea Univ, Grad Sch Biotechnol, Div Plant Technol, Seoul 136701, South Korea.
 RP Kwon, YS, MIFAFF, Korea Seed & Variety Serv, Variety Testing Div, Suwon
    443400, South Korea.
 EM yskwon@seed.go.kr
 FU Technology Development Program for Agriculture and Forestry, Ministry
    of Agriculture and Forestry, Republic of Korea 
 FX This study was supported by the Technology Development Program for
    Agriculture and Forestry, Ministry of Agriculture and Forestry,
    Republic of Korea.
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 NR 31
 TC 0
 PU SPRINGER
 PI NEW YORK
 PA 233 SPRING ST, NEW YORK, NY 10013 USA
 SN 1976-9571
 J9 GENES GENOM
 JI Genes Genom.
 PD APR
 PY 2010
 VL 32
 IS 2
 BP 115
 EP 122
 DI 10.1007/s13258-008-0674-x
 PG 8
 SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology;
    Genetics & Heredity
 GA 587VH
 UT ISI:000277022100003
 ER
 
 PT J
 AU Sang, XC
    Fang, LK
    Vanichpakorn, Y
    Ling, YH
    Du, P
    Zhao, FM
    Yang, ZL
    He, GH
 AF Sang, Xian-chun
    Fang, Li-kui
    Vanichpakorn, Yuenyong
    Ling, Ying-hua
    Du, Peng
    Zhao, Fang-ming
    Yang, Zheng-lin
    He, Guang-hua
 TI Physiological character and molecular mapping of leaf-color mutant wyv1
    in rice (Oryza sativa L.)
 SO GENES & GENOMICS
 LA English
 DT Article
 DE Chlorophyll deficient; Fine mapping; Rice (Oryza sativa L.);
    white-yellow-virescent 1 (wyv1)
 ID CHLOROPHYLL-DEFICIENT MUTANT; CHLOROPLAST DEVELOPMENT; GENE;
    TEMPERATURE; MUTATION; IDENTIFICATION; BIOSYNTHESIS; VIRESCENT-2;
    BIOGENESIS; SUBUNITS
 AB The seed of an excellent indica restorer line Jinhui10 (Oryza sativa L.
    ssp. indica) was treated by ethyl methanesulfonate (EMS); a leaf-color
    mutant displaying distinct phenotype throughout development grown in
    paddy field was identified from the progeny. The mutant leaf showed
    white-yellow at seedling stage and then turned to yellow-green at
    tillering stage, after that, virescent color appeared until to
    maturity. The mutant was thus temporarily designed as wyv1. The
    chlorophyll contents decreased significantly and the changing was
    consistent with the chlorotic level of wyv1 leaves. Chlorophyll
    fluorescence kinetic parameters measured at the seedling stage showed
    that co-efficiency of photochemical quenching (qP), actual photosystem
    II efficiency (I broken vertical bar PS II), electron transport rate
    (ETR) and initial chlorophyll fluorescence level (Fo), net
    photosynthetic rate (Pn) and maximum photochemical efficiency (Fv / Fm)
    significantly decreased in severe chlorotic leaf of the mutant compared
    with that of wild type. However, no significant differences were
    observed for Pn and Fv/Fm between virescent leaf and normal green leaf.
    Genetic analysis suggested that the mutant phenotype was controlled by
    a single recessive nuclear gene which was finally mapped between SSR
    marker Y7 and Y6 on rice chromosome 3 based on F2 population of
    Xinong1A / wyv1. Genetic distances were 0.06 cM and 0.03 cM
    respectively, and the physical distance was 84 kb according to the
    sequence of indica rice 9311. The results must facilitate map-based
    cloning and functional analysis of WYV1 gene.
 C1 [Sang, Xian-chun; Fang, Li-kui; Vanichpakorn, Yuenyong; Ling, Ying-hua; Du, Peng; Zhao, Fang-ming; Yang, Zheng-lin; He, Guang-hua] Southwest Univ, Coll Agron & Biotechnol, Key Lab Biotechnol & Crop Qual Improvement, Minist Agr, Chongqing 400716, Peoples R China.
 RP He, GH, Southwest Univ, Coll Agron & Biotechnol, Key Lab Biotechnol &
    Crop Qual Improvement, Minist Agr, Chongqing 400716, Peoples R China.
 EM hegh1968@yahoo.com.cn
 FU National Natural Sciences Foundation of P. R. China [30800598]; Special
    Capital of Southwest University basic scientific research [XDJK
    2009B019]; Excellent Youth Foundation Project of Chongqing
    [2008BA1033]; New Century Project for Excellent Innovative Human of
    Education Ministry in P. R. China 
 FX This study was supported by the National Natural Sciences Foundation of
    P. R. China (30800598), the Special Capital of Southwest University
    basic scientific research (XDJK 2009B019), the Excellent Youth
    Foundation Project of Chongqing (CSTC, 2008BA1033), and the New Century
    Project for Excellent Innovative Human of Education Ministry in P. R.
    China
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 NR 35
 TC 0
 PU SPRINGER
 PI NEW YORK
 PA 233 SPRING ST, NEW YORK, NY 10013 USA
 SN 1976-9571
 J9 GENES GENOM
 JI Genes Genom.
 PD APR
 PY 2010
 VL 32
 IS 2
 BP 123
 EP 128
 DI 10.1007/s13258-009-0794-y
 PG 6
 SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology;
    Genetics & Heredity
 GA 587VH
 UT ISI:000277022100004
 ER
 
 PT J
 AU Liu, SH
    Yang, CN
    Pan, HC
    Sung, YJ
    Liao, KK
    Chen, WB
    Lin, WZ
    Sheu, ML
 AF Liu, Shing Hwa
    Yang, Cheng Ning
    Pan, Hung Chuan
    Sung, Yen Jen
    Liao, Ko Kaung
    Chen, Wen Bao
    Lin, Wen Zheng
    Sheu, Meei Ling
 TI IL-13 downregulates PPAR-gamma/heme oxygenase-1 via ER
    stress-stimulated calpain activation: aggravation of activated
    microglia death
 SO CELLULAR AND MOLECULAR LIFE SCIENCES
 LA English
 DT Article
 DE Microglia; Interleukin-13; Calpain; PPAR-gamma; Heme oxygenase-1
 ID ENDOPLASMIC-RETICULUM STRESS; HEME OXYGENASE-1; OXIDATIVE STRESS;
    CELL-DEATH; NEURODEGENERATIVE DISORDERS; CYCLOOXYGENASE-2 EXPRESSION;
    PARKINSONS-DISEASE; ALZHEIMERS-DISEASE; BRAIN-INJURY; MOUSE MODEL
 AB Interleukin 13 (IL-13) has been shown to induce the death of activated
    microglia. We observed that IL-13, but not IL-4 or IL-10, significantly
    enhanced endoplasmic reticulum (ER) stress induction, apoptosis and
    death in microglia activated by lipopolysaccharide (LPS). IL-13
    enhanced ER stress-regulated calpain activation and calpain-II
    expression in LPS-activated microglia. Calpain-II siRNA effectively
    reversed the IL-13 + LPS-activated caspase-12 activation. Expression of
    heme oxygenase-1 (HO-1) and peroxisome proliferator-activated
    receptor-gamma (PPAR-gamma) was also increased in activated microglia,
    and this was effectively blocked by IL-13 and recombinant calpain. Both
    HO-1 inhibitor and PPAR-gamma antagonist augmented, but calpain
    inhibitor and PPAR-gamma agonists reversed, apoptosis induction in
    activated microglia. Transfection of PPAR-gamma siRNA effectively
    inhibited HO-1 protein expression in activated microglia. LPS
    stimulated transcriptional activation of HO-1 via an increase in
    PPAR-gamma DNA binding activity, which was reversed by IL-13. These
    results indicate that an ER stress-related calpain-down-regulated
    PPAR-gamma/HO-1 pathway is involved in the IL-13-enhanced activated
    death of microglia.
 C1 [Pan, Hung Chuan; Chen, Wen Bao; Lin, Wen Zheng; Sheu, Meei Ling] Natl Chung Hsing Univ, Inst Med Technol, Taichung 402, Taiwan.
    [Liu, Shing Hwa] Natl Taiwan Univ, Coll Med, Inst Toxicol, Taipei 10764, Taiwan.
    [Yang, Cheng Ning] Natl Yang Ming Univ, Sch Life Sci, Inst Neurosci, Taipei 112, Taiwan.
    [Pan, Hung Chuan] Taichung Vet Gen Hosp, Dept Neurosurg, Taichung, Taiwan.
    [Sung, Yen Jen] Natl Yang Ming Univ, Sch Life Sci, Inst Anat & Cell Biol, Taipei 112, Taiwan.
    [Liao, Ko Kaung] Chung Shan Med Univ, Dept Anat, Taichung, Taiwan.
    [Sheu, Meei Ling] Taichung Vet Gen Hosp, Dept Educ & Res, Taichung, Taiwan.
 RP Sheu, ML, Natl Chung Hsing Univ, Inst Med Technol, 250 Kuo Kuang Rd,
    Taichung 402, Taiwan.
 EM shinghwaliu@ntu.edu.tw
    mlsheu@nchu.edu.tw
 FU Taichung Veterans General Hospital, Taiwan [TCVGH-977304B]; National
    Science Council of Taiwan [NSC96-2320-B-040-003-MY3]
 FX This work was supported by research grants from Taichung Veterans
    General Hospital, Taiwan (TCVGH-977304B), and the National Science
    Council of Taiwan (NSC96-2320-B-040-003-MY3).
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 NR 53
 TC 0
 PU BIRKHAUSER VERLAG AG
 PI BASEL
 PA VIADUKSTRASSE 40-44, PO BOX 133, CH-4010 BASEL, SWITZERLAND
 SN 1420-682X
 J9 CELL MOL LIFE SCI
 JI Cell. Mol. Life Sci.
 PD MAY
 PY 2010
 VL 67
 IS 9
 BP 1465
 EP 1476
 DI 10.1007/s00018-009-0255-4
 PG 12
 SC Biochemistry & Molecular Biology; Cell Biology
 GA 585ZJ
 UT ISI:000276869600006
 ER
 
 PT J
 AU Yang, Q
    Gong, ZJ
    Zhou, Y
    Yuan, JQ
    Cheng, JA
    Tian, L
    Li, S
    Lin, XD
    Xu, RJ
    Zhu, ZR
    Mao, CG
 AF Yang, Qiong
    Gong, Zhong-Jun
    Zhou, Ying
    Yuan, Jing-Qun
    Cheng, Jiaan
    Tian, Lin
    Li, Sheng
    Lin, Xin-Da
    Xu, Ruijuan
    Zhu, Zeng-Rong
    Mao, Cungui
 TI Role of Drosophila alkaline ceramidase (Dacer) in Drosophila
    development and longevity
 SO CELLULAR AND MOLECULAR LIFE SCIENCES
 LA English
 DT Article
 DE Alkaline ceramidase; Drosophila; Development; Lifespan
 ID KEY REGULATORY ENZYME; MOLECULAR-CLONING; LIFE-SPAN;
    SACCHAROMYCES-CEREVISIAE; PSEUDOMONAS-AERUGINOSA; NEUTRAL CERAMIDASE;
    MASS-SPECTROMETRY; C-ELEGANS; MELANOGASTER; SPHINGOSINE
 AB Ceramidases catalyze the hydrolysis of ceramides to generate
    sphingosine (SPH) and fatty acids, and ceramide metabolism is
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    Here we report the cloning, biochemical characterization, and
    functional analysis of a Drosophila alkaline ceramidase (Dacer). Dacer,
    a membrane-bound protein of 284 amino acids, shares homology with yeast
    and mammalian alkaline ceramidases. Overexpression of Dacer in High
    Five insect cells increases ceramidase activity in the alkaline pH
    range, indicating that Dacer is a bona fide alkaline ceramidase. Dacer
    mRNA is highly expressed in the midgut and at the pupal stage. An
    inactivation of Dacer by insertional mutagenesis increases the levels
    of ceramides in both Drosophila pupae and adult flies. Dacer
    inactivation increases Drosophila pre-adult development time, lifespan,
    and anti-oxidative stress capacity. Collectively, these results suggest
    that Dacer plays an important role in the Drosophila development and
    longevity by controlling the metabolism of ceramides.
 C1 [Yang, Qiong; Gong, Zhong-Jun; Zhou, Ying; Cheng, Jiaan; Zhu, Zeng-Rong] Zhejiang Univ, Inst Insect Sci, Hangzhou 310029, Zhejiang, Peoples R China.
    [Yang, Qiong; Gong, Zhong-Jun; Zhou, Ying; Cheng, Jiaan; Zhu, Zeng-Rong] Minist Agr China, Key Lab Mol Biol Crop Pathogens & Insects, State Key Lab Rice Biol, Hangzhou 310029, Zhejiang, Peoples R China.
    [Yuan, Jing-Qun] Zhejiang Univ, Ctr Chem Anal & Detect, Hangzhou 310029, Zhejiang, Peoples R China.
    [Tian, Lin; Li, Sheng] Chinese Acad Sci, Shanghai Inst Biol Sci, Inst Plant Physiol & Ecol, Shanghai 200032, Peoples R China.
    [Lin, Xin-Da] China Jiliang Univ, Coll Life Sci, Hangzhou 310018, Zhejiang, Peoples R China.
    [Xu, Ruijuan; Mao, Cungui] Med Univ S Carolina, Dept Med & Mol Biol, Charleston, SC 29425 USA.
    [Xu, Ruijuan; Mao, Cungui] Med Univ S Carolina, Dept Biochem & Mol Biol, Charleston, SC 29425 USA.
 RP Zhu, ZR, Zhejiang Univ, Inst Insect Sci, Hangzhou 310029, Zhejiang,
    Peoples R China.
 EM zrzhu@zju.edu.cn
    maoc@musc.edu
 FU China's National Basic Research 973 Program [2009CB119203]; NSFC
    [30528024]; MOE ; United States National Institutes of Health
    [R01CA104834]
 FX This work was supported by China's National Basic Research 973 Program
    2009CB119203 (ZZ), NSFC grants 30528024 (CM), and MOE project 111 (CM),
    and the United States National Institutes of Health grant R01CA104834
    (CM). We thank Qiang Li, Dongdong Niu, Weihua Wang, and Wenjuan Jiao
    for their technical assistance in fly colony maintenance. We also thank
    Dr. Jennifer Schnellmann for English proof reading and editing of the
    manuscript.
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 NR 42
 TC 2
 PU BIRKHAUSER VERLAG AG
 PI BASEL
 PA VIADUKSTRASSE 40-44, PO BOX 133, CH-4010 BASEL, SWITZERLAND
 SN 1420-682X
 J9 CELL MOL LIFE SCI
 JI Cell. Mol. Life Sci.
 PD MAY
 PY 2010
 VL 67
 IS 9
 BP 1477
 EP 1490
 DI 10.1007/s00018-010-0260-7
 PG 14
 SC Biochemistry & Molecular Biology; Cell Biology
 GA 585ZJ
 UT ISI:000276869600007
 ER
 
 PT J
 AU Liu, YS
    Teng, XH
    Yang, XX
    Song, Q
    Lu, R
    Xiong, JX
    Liu, B
    Zeng, NJ
    Zeng, Y
    Long, J
    Cao, R
    Lin, Y
    He, QZ
    Chen, P
    Lu, M
    Liang, SP
 AF Liu, Yisong
    Teng, Xiaohua
    Yang, Xiaoxu
    Song, Qing
    Lu, Rong
    Xiong, Jixian
    Liu, Bo
    Zeng, Nianju
    Zeng, Yu
    Long, Jia
    Cao, Rui
    Lin, Yong
    He, Quanze
    Chen, Ping
    Lu, Ming
    Liang, Songping
 TI Shotgun Proteomics and Network Analysis Between Plasma Membrane and
    Extracellular Matrix Proteins From Rat Olfactory Ensheathing Cells
 SO CELL TRANSPLANTATION
 LA English
 DT Article
 DE Olfactory ensheathing cells; Neural repair; 1D-shotgun proteomics;
    Plasma membrane; Extracellular matrix
 ID CENTRAL-NERVOUS-SYSTEM; APOLIPOPROTEIN-E-GENOTYPE; SPINAL-CORD
    INJURIES; GROWTH-FACTOR; BINDING PROTEIN-2; SIGNAL PEPTIDES; GENE
    ONTOLOGY; SCHWANN-CELLS; STEM-CELLS; IN-VITRO
 AB Olfactory ensheathing cells (OECs) are a special type of dial cells
    that have characteristics of both astrocytes and Schwann cells.
    Evidence suggests that the regenerative capacity of OECs is induced by
    soluble, secreted factors that influence their microenvironment These
    factors may regulate OECs self-renewal and/or induce their capacity to
    augment spinal cord regeneration Profiling of plasma membrane and
    extracellular matrix through a high-throughput expression proteomics
    approach was undertaken to identify plasma membrane and extracellular
    matrix proteins of OECs under serum-free conditions 1D-shotgun
    proteomics followed with gene ontology (GO) analysis was used to screen
    proteins from primary culture rat OECs Four hundred and seventy
    nonredundant plasma membrane proteins and 168 extracellular matrix
    proteins were identified, the majority of which were never before
    reported to be produced by OECs Furthermore. plasma membrane and
    extracellular proteins were classified based on their protein protein
    interaction predicted by STRING quantitatively integrates interaction
    data The proteomic profiling of the OECs plasma membrane proteins and
    their connection with the secretome in serum-free culture conditions
    provides new insights into the nature of their in vivo
    microenvironmental niche Proteomic analysis for the discovery of
    clinical biomarkers of OECs mechanism warrants further study
 C1 [Liu, Yisong; Yang, Xiaoxu; Song, Qing; Lu, Rong; Xiong, Jixian; Long, Jia; Cao, Rui; Lin, Yong; He, Quanze; Chen, Ping; Liang, Songping] Hunan Normal Univ, Key Lab Prot Chem & Dev Biol, Minist Educ, Coll Life Sci, Changsha 410081, Hunan, Peoples R China.
    [Teng, Xiaohua; Liu, Bo; Zeng, Nianju; Zeng, Yu; Lu, Ming] Hunan Normal Univ, Hosp PLA 163, Affiliated Hosp 2, Dept Neurosurg, Changsha 410081, Hunan, Peoples R China.
 RP Chen, P, Hunan Normal Univ, Key Lab Prot Chem & Dev Biol, Minist Educ,
    Coll Life Sci, Changsha 410081, Hunan, Peoples R China.
 FU National 973 Project of China [2007CB516809, 200703914203]; National
    Natural Science Foundation of China [30770437]
 FX The authors thank all the members of our group for kindly help and
    suggestions This work was supported by a grant from National 973
    Project of China (2007CB516809, 200703914203), and National Natural
    Science Foundation of China (30770437)
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 NR 62
 TC 4
 PU COGNIZANT COMMUNICATION CORP
 PI ELMSFORD
 PA 3 HARTSDALE ROAD, ELMSFORD, NY 10523-3701 USA
 SN 0963-6897
 J9 CELL TRANSPLANT
 JI Cell Transplant.
 PY 2010
 VL 19
 IS 2
 BP 133
 EP 146
 DI 10.3727/096368910X492607
 PG 14
 SC Cell & Tissue Engineering; Medicine, Research & Experimental;
    Transplantation
 GA 587BI
 UT ISI:000276961300002
 ER
 
 PT J
 AU Wu, MM
    Fan, DG
    Tadmori, I
    Yang, H
    Furman, M
    Jiao, XY
    Young, W
    Sun, DM
    You, SW
 AF Wu, Ming-Mei
    Fan, De-Gang
    Tadmori, Iman
    Yang, Hao
    Furman, Maya
    Jiao, Xi-Ying
    Young, Wise
    Sun, Dongming
    You, Si-Wei
 TI Death of Axotomized Retinal Ganglion Cells Delayed After Intraoptic
    Nerve Transplantation of Olfactory Ensheathing Cells in Adult Rats
 SO CELL TRANSPLANTATION
 LA English
 DT Article
 DE Olfactory ensheathing cell transplantation; Optic nerve transection;
    Retinal ganglion cells; Neuroprotection
 ID NEUROTROPHIC FACTOR; OPTIC-NERVE; SPINAL-CORD; AXONAL REGENERATION;
    GLIA TRANSPLANTS; PC12 CELLS; IN-VIVO; SURVIVAL; TRANSECTION; GDNF
 AB Intraorbital transection of the optic nerve (ON) always induces
    ultimate apoptosis of retinal ganglion cells (RGCs) and consequently
    irreversible defects of vision function It was demonstrated that
    transplanted olfactory ensheathing cells (OECs) in partially injured
    spinal cord have a distant in vivo neuroprotective effect on descending
    cortical and brain stein neurons However, this study gave no answers to
    the question whether OECs can protect the central sensitive neurons
    with a closer axonal injury because different neurons respond variously
    to similar axonal injury and the distance between the neuronal soma and
    axonal injury site has a definite effect on the severity of neuronal
    response and apoptosis In the present study, we investigated the effect
    of transplanted OECs on RGCs after intraorbital ON transection in adult
    rats Green fluorescent protein (GFP)-OECs were injected into the ocular
    stumps of transected ON and a significantly higher number of surviving
    RGCs was found together with a consistent marked increase in the mRNA
    and protein levels of BDNF in the ON stump and retina in the
    OEC-treated group at 7 days, but not 2 and 14 days, time point when
    complied to the control group Our findings suggest that OEC
    transplantation induces the expression of BDNF in the ocular ON stump
    and retina and delays the death of axotomized RGCs at a certain
    survival period.
 C1 [Wu, Ming-Mei; Yang, Hao; Jiao, Xi-Ying; You, Si-Wei] Fourth Mil Med Univ, Inst Neurosci, Xian 710032, Peoples R China.
    [Fan, De-Gang] Fourth Mil Med Univ, Inst Orthoped Oncol, Tangdu Hosp, Xian 710032, Peoples R China.
    [Tadmori, Iman; Furman, Maya; Young, Wise; Sun, Dongming] Rutgers State Univ, Dept Cell Biol & Neurosci, WM Keck Ctr Collaborat Neurosci, Piscataway, NJ USA.
 RP You, SW, Fourth Mil Med Univ, Inst Neurosci, Xian 710032, Peoples R
    China.
 FU Natural Science Foundations of China [30872829, 30571998, 30901049];
    Army Medical Research Foundation of China [06H039]
 FX Supported by Natural Science Foundations of China (Grant numbers
    30872829, 30571998, and 30901049) and Army Medical Research Foundation
    of China (Grant number 06H039)
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 NR 33
 TC 10
 PU COGNIZANT COMMUNICATION CORP
 PI ELMSFORD
 PA 3 HARTSDALE ROAD, ELMSFORD, NY 10523-3701 USA
 SN 0963-6897
 J9 CELL TRANSPLANT
 JI Cell Transplant.
 PY 2010
 VL 19
 IS 2
 BP 159
 EP 166
 DI 10.3727/096368910X492625
 PG 8
 SC Cell & Tissue Engineering; Medicine, Research & Experimental;
    Transplantation
 GA 587BI
 UT ISI:000276961300004
 ER
 
 PT J
 AU Kawase, T
    Matsuo, K
    Suzuki, T
    Hirose, K
    Hosono, S
    Watanabe, M
    Inagaki, M
    Iwata, H
    Tanaka, H
    Tajima, K
 AF Kawase, Takakazu
    Matsuo, Keitaro
    Suzuki, Takeshi
    Hirose, Kaoru
    Hosono, Satoyo
    Watanabe, Miki
    Inagaki, Masaki
    Iwata, Hiroji
    Tanaka, Hideo
    Tajima, Kazuo
 TI Association between vitamin D and calcium intake and breast cancer risk
    according to menopausal status and receptor status in Japan
 SO CANCER SCIENCE
 LA English
 DT Article
 ID FOOD FREQUENCY QUESTIONNAIRE; DIETARY CALCIUM; GENERAL-POPULATION;
    ESTROGEN-RECEPTOR; NUTRIENT INTAKE; DAIRY-PRODUCTS; CHINESE WOMEN;
    CELL-GROWTH; IN-VITRO; MICRONUTRIENTS
 AB (Cancer Sci 2010; 101: 1234-1240).
 C1 [Kawase, Takakazu; Matsuo, Keitaro; Hosono, Satoyo; Watanabe, Miki; Tanaka, Hideo; Tajima, Kazuo] Aichi Canc Ctr, Res Inst, Div Epidemiol & Prevent, Nagoya, Aichi 464, Japan.
    [Matsuo, Keitaro; Tanaka, Hideo] Nagoya Univ, Grad Sch Med, Dept Epidemiol, Nagoya, Aichi 4648601, Japan.
    [Suzuki, Takeshi] Nagoya City Univ, Grad Sch Med Sci, Dept Med Oncol & Immunol, Nagoya, Aichi, Japan.
    [Inagaki, Masaki] Aichi Canc Ctr, Res Inst, Div Biochem, Nagoya, Aichi 464, Japan.
    [Iwata, Hiroji] Aichi Canc Ctr Hosp, Dept Breast Oncol, Nagoya, Aichi 464, Japan.
 RP Matsuo, K, Aichi Canc Ctr, Res Inst, Div Epidemiol & Prevent, Nagoya,
    Aichi 464, Japan.
 EM kmatsuo@aichi-cc.jp
 FU Ministry of Education, Science, Sports, Culture and Technology of Japan
    ; Ministry of Health, Labour and Welfare of Japan 
 FX This study was supported by a Grant-in-Aid for Scientific Research from
    the Ministry of Education, Science, Sports, Culture and Technology of
    Japan, by a Grant-in-Aid for Cancer Research from the Ministry of
    Health, Labour and Welfare of Japan, and by a Grant-in-Aid for the
    Third Term Comprehensive 10-Year Strategy for Cancer Control from the
    Ministry of Health. The authors are grateful to all of the doctors,
    nurses, technical staff, and hospital business staff of Aichi Cancer
    Center Hospital for daily administration of the HERPACC study.
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 NR 49
 TC 1
 PU WILEY-BLACKWELL PUBLISHING, INC
 PI MALDEN
 PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
 SN 1347-9032
 J9 CANCER SCI
 JI Cancer Sci.
 PD MAY
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 BP 1234
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 GA 585UD
 UT ISI:000276853900024
 ER
 
 PT J
 AU Yang, XY
 AF Yang, Xiaoyong
 TI A wheel of time: the circadian clock, nuclear receptors, and physiology
 SO GENES & DEVELOPMENT
 LA English
 DT Article
 DE Circadian oscillator; transcription; protein-protein interaction
 ID REV-ERB-ALPHA; ARNT-LIKE PROTEIN-1; SUPRACHIASMATIC NUCLEUS; RECIPROCAL
    REGULATION; PERIPHERAL-TISSUES; MAMMALIAN CLOCK; BLOOD-PRESSURE;
    PPAR-GAMMA; IN-VIVO; EXPRESSION
 AB It is a long-standing view that the circadian clock functions to
    proactively align internal physiology with the 24-h rotation of the
    earth. Recent studies, including one by Schmutz and colleagues (pp.
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    of physiological processes to maintain dynamic homeostasis.
 C1 Yale Univ, Sch Med, Program Integrat Cell Signaling & Neurobiol Metab, Dept Cellular & Mol Physiol,Sect Comparat Med, New Haven, CT 06519 USA.
 RP Yang, XY, Yale Univ, Sch Med, Program Integrat Cell Signaling &
    Neurobiol Metab, Dept Cellular & Mol Physiol,Sect Comparat Med, 333
    Cedar St, New Haven, CT 06519 USA.
 EM xiaoyong.yang@yale.edu
 FU Yale start-up package ; American Diabetes Association [1-10-JF-56]
 FX I thank Hai-Bin Ruan for preparation of the artwork, and Mindian Li for
    inspiring discussions. Research in my laboratory is supported by the
    Yale start-up package and American Diabetes Association Junior Faculty
    Award (1-10-JF-56).
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 NR 74
 TC 4
 PU COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT
 PI WOODBURY
 PA 500 SUNNYSIDE BLVD, WOODBURY, NY 11797-2924 USA
 SN 0890-9369
 J9 GENE DEVELOP
 JI Genes Dev.
 PD APR 15
 PY 2010
 VL 24
 IS 8
 BP 741
 EP 747
 DI 10.1101/gad.1920710
 PG 7
 SC Cell Biology; Developmental Biology; Genetics & Heredity
 GA 584DK
 UT ISI:000276730300003
 ER
 
 PT J
 AU de la Torre-Ubieta, L
    Gaudilliere, B
    Yang, Y
    Ikeuchi, Y
    Yamada, T
    DiBacco, S
    Stegmuller, J
    Schuller, U
    Salih, DA
    Rowitch, D
    Brunet, A
    Bonni, A
 AF de la Torre-Ubieta, Luis
    Gaudilliere, Brice
    Yang, Yue
    Ikeuchi, Yoshiho
    Yamada, Tomoko
    DiBacco, Sara
    Stegmueller, Judith
    Schueller, Ulrich
    Salih, Dervis A.
    Rowitch, David
    Brunet, Anne
    Bonni, Azad
 TI A FOXO-Pak1 transcriptional pathway controls neuronal polarity
 SO GENES & DEVELOPMENT
 LA English
 DT Article
 DE FOXO; neuronal polarity; Pak1; transcription; axons; dendrites
 ID P21-ACTIVATED KINASE; POSTMITOTIC NEURONS; SAD KINASES; CELL-CYCLE;
    FOXO; AXON; MORPHOLOGY; CDH1-APC; PHOSPHORYLATION; POLARIZATION
 AB Neuronal polarity is essential for normal brain development and
    function. However, cell-intrinsic mechanisms that govern the
    establishment of neuronal polarity remain to be identified. Here, we
    report that knockdown of endogenous FOXO proteins in hippocampal and
    cerebellar granule neurons, including in the rat cerebellar cortex in
    vivo, reveals a requirement for the FOXO transcription factors in the
    establishment of neuronal polarity. The FOXO transcription factors,
    including the brain-enriched protein FOXO6, play a critical role in
    axo-dendritic polarization of undifferentiated neurites, and hence in a
    switch from unpolarized to polarized neuronal morphology. We also
    identify the gene encoding the protein kinase Pak1, which acts locally
    in neuronal processes to induce polarity, as a critical direct target
    gene of the FOXO transcription factors. Knockdown of endogenous Pak1
    phenocopies the effect of FOXO knockdown on neuronal polarity.
    Importantly, exogenous expression of Pak1 in the background of FOXO
    knockdown in both primary neurons and postnatal rat pups in vivo
    restores the polarized morphology of neurons. These findings define the
    FOXO proteins and Pak1 as components of a cell-intrinsic
    transcriptional pathway that orchestrates neuronal polarity, thus
    identifying a novel function for the FOXO transcription factors in a
    unique aspect of neural development.
 C1 [de la Torre-Ubieta, Luis; Gaudilliere, Brice; Yang, Yue; Ikeuchi, Yoshiho; Yamada, Tomoko; DiBacco, Sara; Stegmueller, Judith; Bonni, Azad] Harvard Univ, Sch Med, Dept Pathol, Boston, MA 02115 USA.
    [de la Torre-Ubieta, Luis; Yang, Yue; Bonni, Azad] Harvard Univ, Sch Med, Program Neurosci, Boston, MA 02115 USA.
    [Schueller, Ulrich; Rowitch, David] Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Pediat Oncol, Boston, MA 02115 USA.
    [Salih, Dervis A.; Brunet, Anne] Stanford Univ, Dept Genet, Stanford, CA 94305 USA.
 RP Bonni, A, Harvard Univ, Sch Med, Dept Pathol, Boston, MA 02115 USA.
 EM azad_bonni@hms.harvard.edu
 FU NIH [NS041021, NS051255]; A. Brunet [AG026648]; National Science
    Foundation ; Albert J. Ryan Foundation ; Edward and Anne Lefler
    Fellowship ; Human Frontier Science Program Long-term Fellowship ;
    Japan Society for the Promotion of Science Fellowship ; Deutsche
    Forschungsgemeinschaft 
 FX We thank Constance Cepko, Gabriel Corfas, and David van Vactor for
    helpful discussions; Marten P. Smidt for the FOXO1-GFP, FOXO3-GFP, and
    FOXO6-GFP plasmids; Jonathan Chernoff for the Pak1 plasmid; Margareta
    Nikolic for the Pak1 shRNA; and members of the Bonni laboratory for
    helpful discussions and critical reading of the manuscript. This work
    was supported by NIH grants to A. Bonni (NS041021 and NS051255), A.
    Brunet (AG026648), the National Science Foundation (L. T. U. and Y.
    Y.), the Albert J. Ryan Foundation (L. T. U. and Y. Y.) the Edward and
    Anne Lefler Fellowship (Y. Y.), the Human Frontier Science Program
    Long-term Fellowship (Y. I.), the Japan Society for the Promotion of
    Science Fellowship (T. Y.), and the Deutsche Forschungsgemeinschaft (J.
    S.).
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 NR 58
 TC 2
 PU COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT
 PI WOODBURY
 PA 500 SUNNYSIDE BLVD, WOODBURY, NY 11797-2924 USA
 SN 0890-9369
 J9 GENE DEVELOP
 JI Genes Dev.
 PD APR 15
 PY 2010
 VL 24
 IS 8
 BP 799
 EP 813
 DI 10.1101/gad.1880510
 PG 15
 SC Cell Biology; Developmental Biology; Genetics & Heredity
 GA 584DK
 UT ISI:000276730300008
 ER
 
 PT J
 AU Barbon, CM
    Yang, M
    Wands, GD
    Ramesh, R
    Slusher, BS
    Hedley, ML
    Luby, TM
 AF Barbon, Christine M.
    Yang, Min
    Wands, Gregory D.
    Ramesh, Radha
    Slusher, Barbara S.
    Hedley, Mary Lynne
    Luby, Thomas M.
 TI Consecutive low doses of cyclophosphamide preferentially target T-regs
    and potentiate T cell responses induced by DNA PLG microparticle
    immunization
 SO CELLULAR IMMUNOLOGY
 LA English
 DT Article
 DE Poly(lactide-co-glycolide); PLG; Regulatory T cell; Avidity;
    Epitope-spreading; CYP1B1; Cyclophosphamide; Vaccine; Immunization; Treg
 ID IMMUNOLOGICAL SELF-TOLERANCE; CO-GLYCOLIDE MICROPARTICLES; ANTIGEN
    CYTOCHROME P4501B1; MURINE MELANOMA MODEL; GROWTH-FACTOR-BETA;
    REGULATORY-CELLS; IMMUNE-RESPONSE; IN-VIVO; TUMOR-IMMUNITY;
    CANCER-IMMUNOTHERAPY
 AB Cyclophosphamide in combination with immunotherapeutic approaches
    preferentially impinges on T-reg activity and allows for robust
    generation of T cell effectors. Reduced dosages of cyclophosphamide are
    necessary to restrict its cytotoxic effects to the negative regulatory
    cell populations while sparing effector lymphocytes. We investigated
    cyclophosphamide dosing in combination with ZYC300, a PLG-encapsulated
    plasmid DNA vaccine which encodes the cytochrome P450 family member,
    CYP1B1, a known human tumor-associated antigen. In mice, three
    consecutive, low doses of cyclophosphamide comprised a superior regimen
    in enhancing the magnitude, diversity of epitopes, and avidity to
    individual epitopes of specific T cell responses when compared to
    regimens that used either a single low or a single high dose.
    Consecutive low doses of cyclophosphamide predominantly targeted T-regs
    while sparing overall T lymphocyte counts. Thus, we report the
    synergistic activity of pharmacologic T-reg depletion with
    cyclophosphamide on quantitatively and qualitatively increasing T cell
    responses to a known human tumor-associated antigen. (C) 2010 Elsevier
    Inc. All rights reserved.
 C1 [Barbon, Christine M.] Dana Farber Canc Inst, Boston, MA 02115 USA.
    [Yang, Min; Wands, Gregory D.; Ramesh, Radha; Slusher, Barbara S.; Hedley, Mary Lynne; Luby, Thomas M.] Eisai Res Inst Inc, Andover, MA USA.
 RP Barbon, CM, Dana Farber Canc Inst, 44 Binney St, Boston, MA 02115 USA.
 EM ChristineM_Barbon@DFCI.harvard.edu
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 NR 73
 TC 0
 PU ACADEMIC PRESS INC ELSEVIER SCIENCE
 PI SAN DIEGO
 PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
 SN 0008-8749
 J9 CELL IMMUNOL
 JI Cell. Immunol.
 PY 2010
 VL 262
 IS 2
 BP 150
 EP 161
 DI 10.1016/j.cellimm.2010.02.007
 PG 12
 SC Cell Biology; Immunology
 GA 582LO
 UT ISI:000276599100012
 ER
 
 PT J
 AU Shen, FJ
    Zhang, C
    Zheng, HY
    Xiong, YH
    Wang, X
    Liao, WB
    Du, XJ
    Yang, SX
    Wang, LL
 AF Shen, Fujin
    Zhang, Ci
    Zheng, Hongyun
    Xiong, Yunhe
    Wang, Xi
    Liao, Wenbiao
    Du, Xianjin
    Yang, Sixing
    Wang, Linglong
 TI Long-Term Culture and Transplantation of Spermatogonial Stem Cells from
    BALB/c Mice
 SO CELLS TISSUES ORGANS
 LA English
 DT Article
 DE Spermatogonial stem cells; Cell culture; Transplantation mouse
 ID IN-VITRO; SELF-RENEWAL; MOUSE TESTES; LINE; PLURIPOTENCY; SOX2
 AB Development of a culture system that supports self-renewal and
    proliferation of spermatogonial stem cells (SSCs) is enormously
    valuable for experimental research and potential treatment for male
    infertility. Although several research groups had reported their
    successes in SSC isolation and culture, the two current accepted
    culture systems are different in cell enrichment methods, serum and
    growth factors. Previous researches also indicated SSCs from different
    mouse strains required different culture conditions. Here we report for
    the first time that SSCs from BALB/c mice could be cultured in an
    improved culture system for 3 months. The modified culture system
    consisted of an improved enzymatic procedure, the enrichment of
    undifferentiated spermatogonia by differential adherence selection of
    isolated SSCs, mouse embryonic fibroblast feeder cells, StemPro-34 SFM
    medium supplemented with glial cell line-derived neurotrophic factor
    (GDNF), basic fibroblast growth factor and GDNF-family receptor alpha 1
    (GFR alpha 1). The improved digestion method increased the viability
    and enrichment efficiency of isolated testis cells. Furthermore, basal
    culture medium with 10% fetal bovine serum as selected medium could
    increase the number of germ cell colonies in the initiation stage of
    culture. Cultured SSCs were characterized morphologically and formed
    typical colonies. Immunocytochemical staining and RT-PCR showed that
    cultured SSCs expressed Oct-4, GFR alpha 1, Sox2 and several other
    special genes resembling undifferentiated spermatogonia. Spermatogonia
    transplantation further confirmed that cultured SSCs were functionally
    normal and could restore complete spermatogenesis. The culture methods
    described here could serve as a paradigm to establish conditions for
    the culture of SSCs from other species, allowing identification of
    universal factors necessary for proliferation of SSCs. Copyright (c)
    2010 S. Karger AG, Basel
 C1 [Shen, Fujin; Zhang, Ci; Xiong, Yunhe; Liao, Wenbiao; Du, Xianjin; Yang, Sixing; Wang, Linglong] Wuhan Univ, Dept Urol, Renmin Hosp, Wuhan 430060, Peoples R China.
    [Zheng, Hongyun] Huazhong Univ Sci & Technol, Dept Pathophysiol, Tongji Med Coll, Wuhan 430074, Peoples R China.
    [Wang, Xi] Wuhan Univ, Dept Cardiol, Renmin Hosp, Wuhan 430072, Peoples R China.
 RP Zhang, C, Wuhan Univ, Dept Urol, Renmin Hosp, 238 Jiefang Rd, Wuhan
    430060, Peoples R China.
 EM urology@163.com
 FU National Natural Science Foundation of China [30400160]
 FX This work was supported by the National Natural Science Foundation of
    China (Grant No. 30400160). We thank Min Peng, Ping Hu (Renmin Hospital
    of Wuhan University, Wuhan, China), Lu Wang and Pu Yang (Tongji Medical
    College, Huazhong University of Science and Technology, Wuhan, China)
    for great assistance.
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 NR 25
 TC 1
 PU KARGER
 PI BASEL
 PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND
 SN 1422-6405
 J9 CELLS TISSUES ORGANS
 JI Cells Tissues Organs
 PY 2010
 VL 191
 IS 5
 BP 372
 EP 381
 DI 10.1159/000276586
 PG 10
 SC Anatomy & Morphology; Cell Biology; Developmental Biology
 GA 584JT
 UT ISI:000276748700004
 ER
 
 PT J
 AU Zhang, JH
    Yang, Y
    Wu, JR
 AF Zhang, Jianhua
    Yang, Ying
    Wu, Jiarui
 TI Palmitate impairs cytokinesis associated with RhoA inhibition
 SO CELL RESEARCH
 LA English
 DT Letter
 ID CLEAVAGE; ZONE
 C1 [Zhang, Jianhua; Yang, Ying; Wu, Jiarui] Chinese Acad Sci, Shanghai Inst Biol Sci, Key Lab Syst Biol, State Key Lab Mol Biol,Inst Biochem & Cell Biol, Shanghai 200031, Peoples R China.
    [Wu, Jiarui] Univ Sci & Technol China, Hefei Natl Lab Phys Sci Microscale, Hefei 230027, Anhui, Peoples R China.
    [Wu, Jiarui] Univ Sci & Technol China, Sch Life Sci, Hefei 230027, Anhui, Peoples R China.
 RP Wu, JR, Chinese Acad Sci, Shanghai Inst Biol Sci, Key Lab Syst Biol,
    State Key Lab Mol Biol,Inst Biochem & Cell Biol, 320 Yue Yang Rd,
    Shanghai 200031, Peoples R China.
 EM wujr@sibs.ac.cn
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 NR 10
 TC 0
 PU INST BIOCHEMISTRY & CELL BIOLOGY
 PI SHANGHAI
 PA SIBS, CAS, 319 YUEYAND ROAD, SHANGHAI, 200031, PEOPLES R CHINA
 SN 1001-0602
 J9 CELL RES
 JI Cell Res.
 PD APR
 PY 2010
 VL 20
 IS 4
 BP 492
 EP 494
 DI 10.1038/cr.2010.33
 PG 3
 SC Cell Biology
 GA 585PG
 UT ISI:000276838100012
 ER
 
 PT J
 AU Wang, YJ
    Huang, CX
    Yang, SN
    Jin, LJ
    Hu, XJ
    Wu, G
    Xie, Q
 AF Wang Yujing
    Huang Congxin
    Yang Shaning
    Jin Lijun
    Hu Xiaojun
    Wu Gang
    Xie Qiang
 TI Digitalis Does not Improve Left Atrial Mechanical Dysfunction After
    Successful Electrical Cardioversion of Chronic Atrial Fibrillation
 SO CELL BIOCHEMISTRY AND BIOPHYSICS
 LA English
 DT Article
 DE Digitalis; Atrial fibrillation; Cardioversion; Myocardial stunning
 ID APPENDAGE FUNCTION; TRANSESOPHAGEAL ECHOCARDIOGRAPHY; CONTRACTILE
    DYSFUNCTION; THROMBOEMBOLIC EVENTS; TIME-COURSE; PREDICTORS;
    PERSISTENT; DOFETILIDE; FLUTTER; FLOW
 AB This study was designed to investigate whether administration of
    digitalis could improve mechanical function of left atrial appendage
    (LAA) and left atrium prospectively in patients with atrial stunning.
    Fifty-four consecutive patients in whom atrial stunning was observed
    immediately after cardioversion of chronic atrial fibrillation (AF)
    were randomized into digitalis or control group for 1 week following
    cardioversion. Transthoracic echocardiography (TTE) and transesophageal
    echocardiography (TEE) were performed prior to, immediately following,
    1 day after and 1 week after cardioversion to measure transmitral flow
    velocity and LAA flow velocity. Electrical cardioversion of AF elicited
    significantly slower left atrial appendage peak emptying velocity
    (LAA-PEV) and peak filling velocity (LAA-PFV) immediately following
    cardioversion in both groups. 1 day post cardioversion, there were no
    significant differences in transmitral E wave, A wave, E/A ratio,
    LAA-PEV, LAA-PFV or left atrial appendage ejection fraction (LAA-EF)
    between digitalis and control groups. 1 week post cardioversion, no
    significant differences were found in transmitral E wave, A wave, E/A
    ratio, LAA-PEV, LAA-PFV or LAA-EF between the two groups. The
    occurrence rates of spontaneous echo contrast were not significantly
    different between digitalis and control groups one day and one week
    post cardioversion. In conclusion, digitalis did not improve left
    atrial and appendage mechanical dysfunction following cardioversion of
    chronic AF. Digitalis did not prevent the development of spontaneous
    echo contrast in left atrial chamber and appendage. This may be due to
    the fact that digitalis aggravates intracellular calcium overload
    induced by chronic AF and has a negative effect on ventricular rate.
 C1 [Yang Shaning; Jin Lijun] Changjiang Univ, Affiliated Hosp 1, Peoples Hosp Jingzhou 1, Cardiovasc Dept, Jinzhou 434000, Hubei Province, Peoples R China.
    [Wang Yujing; Huang Congxin; Hu Xiaojun; Wu Gang; Xie Qiang] Wuhan Univ, Renmins Hosp, Div Cardiol, Wuhan 430060, Hubei Province, Peoples R China.
 RP Yang, SN, Changjiang Univ, Affiliated Hosp 1, Peoples Hosp Jingzhou 1,
    Cardiovasc Dept, Hangkong Rd 8, Jinzhou 434000, Hubei Province, Peoples
    R China.
 EM yang_sn130@sina.com
 FU Department of Education of Hubei Province, China [Q20081208]
 FX This study was supported in part by Grant Q20081208 from the Department
    of Education of Hubei Province, China. We are indebted to the
    participants in the Ultrasound Department in First People's Hospital of
    Jingzhou for their outstanding commitment and cooperation.
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 NR 38
 TC 0
 PU HUMANA PRESS INC
 PI TOTOWA
 PA 999 RIVERVIEW DRIVE SUITE 208, TOTOWA, NJ 07512 USA
 SN 1085-9195
 J9 CELL BIOCHEM BIOPHYS
 JI Cell Biochem. Biophys.
 PD MAY
 PY 2010
 VL 57
 IS 1
 BP 27
 EP 34
 DI 10.1007/s12013-010-9080-5
 PG 8
 SC Biochemistry & Molecular Biology; Biophysics; Cell Biology
 GA 584GT
 UT ISI:000276740100004
 ER
 
 PT J
 AU Gong, GC
    Roach, ML
    Jiang, L
    Yang, XZ
    Tian, XC
 AF Gong, Guochun
    Roach, Marsha L.
    Jiang, Le
    Yang, Xiangzhong
    Tian, Xiuchun Cindy
 TI Culture Conditions and Enzymatic Passaging of Bovine ESC-Like Cells
 SO CELLULAR REPROGRAMMING
 LA English
 DT Article
 ID EMBRYONIC STEM-CELLS; LEUKEMIA INHIBITORY FACTOR; IN-VITRO; NUCLEAR
    TRANSFER; FACTOR LIF; BLASTOCYSTS; LINES; ESTABLISHMENT; MASS;
    DIFFERENTIATION
 AB The goals of the current study were to (1) improve culture conditions
    and (2) chemical passaging of bovine embryonic stem cell-like
    (bESC-like) cells. Specifically, the effects of human leukemia
    inhibitory factor (hLIF), two types of feeders, mouse embryonic
    fibroblast (MEF) and bovine embryonic fibroblast (BEF), as well as
    three different enzymatic treatments including Trypsin-EDTA, TrypLE,
    and Liberase Blendzymes 3 were investigated. The addition of hLIF at
    1000 U/mL to the culture medium (41.2 and 36.9%), and the use of either
    MEF or BEF feeders (40.3 and 38.1%) had no significant effect on the
    ability of inner cell masses (ICMs) to form primary cell colonies
    compared to controls. All bESC-like cells were first dissociated
    mechanically for three passages followed by enzymatic dissociation. The
    ability to maintain ESC morphology to passage 10 was compared among the
    three enzymes above. More bESC-like cell lines survived beyond passage
    10 when treated with TrypLE compared to Trypson-EDTA (28.8 and 12.6%; p
    < 0.05), and bESC-like cells differentiated quickly when treated with
    Liberase Blendzyme 3. The bESC-like cells generated in our study
    displayed typical stem cell morphology and expressed specific markers
    such as SSEA-1, AP, OCT-4, and Nanog. When removed from feeders, these
    bESC-like cells formed embryoid bodies (EBs) in a suspension culture.
    When EBs were cultured on tissue culture plates, they differentiated
    into various cell types. In summary, we were able to culture bESC-like
    cells more than 10 passages by enzymatic dissociation, which is
    important in gene targeting, maintenance, and banking of bESC lines.
 C1 [Gong, Guochun; Jiang, Le; Yang, Xiangzhong; Tian, Xiuchun Cindy] Univ Connecticut, Dept Anim Sci, Storrs, CT 06269 USA.
    [Gong, Guochun; Jiang, Le; Yang, Xiangzhong; Tian, Xiuchun Cindy] Univ Connecticut, Ctr Regenerat Biol, Storrs, CT 06269 USA.
    [Roach, Marsha L.] Zenith Biotech LLC, Guilford, CT USA.
 RP Tian, XC, Univ Connecticut, Dept Anim Sci, 1392 Storrs Rd, Storrs, CT
    06269 USA.
 EM xiuchun.tian@uconn.edu
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 NR 43
 TC 0
 PU MARY ANN LIEBERT INC
 PI NEW ROCHELLE
 PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
 SN 2152-4971
 J9 CELL REPROGRAMM
 JI Cell. Reprogramm.
 PY 2010
 VL 12
 IS 2
 BP 151
 EP 160
 DI 10.1089/cell.2009.0049
 PG 10
 SC Cell & Tissue Engineering; Biotechnology & Applied Microbiology;
    Genetics & Heredity
 GA 584DL
 UT ISI:000276730400005
 ER
 
 PT J
 AU Sung, LY
    Chang, CC
    Amano, T
    Lin, CJ
    Amano, M
    Treaster, SB
    Xu, J
    Chang, WF
    Nagy, ZP
    Yang, XZ
    Tian, XC
 AF Sung, Li-Ying
    Chang, Ching-Chien
    Amano, Tomokazu
    Lin, Chih-Jen
    Amano, Misa
    Treaster, Stephen B.
    Xu, Jie
    Chang, Wei-Fang
    Nagy, Zsolt Peter
    Yang, Xiangzhong
    Tian, X. Cindy
 TI Efficient Derivation of Embryonic Stem Cells from Nuclear Transfer and
    Parthenogenetic Embryos Derived from Cryopreserved Oocytes
 SO CELLULAR REPROGRAMMING
 LA English
 DT Article
 ID IN-VITRO; THERAPEUTIC CLONING; SOMATIC-CELLS; MOUSE OOCYTES;
    PARKINSONIAN MICE; ES CELLS; 1,2-PROPANEDIOL; VITRIFICATION; PREGNANCY;
    DISEASE
 AB Deriving histocompatible embryonic stem (ES) cells by somatic cell
    nuclear transfer (SCNT) and parthenogenetic activation (PA) requires
    fresh oocytes, which prevents their applications in humans. Here, we
    evaluated the efficiency of deriving ES cells from mature metaphase II
    (MII) and immature metaphase I (MI) vitrified oocytes, by PA or SCNT,
    in a mouse model. We successfully generated ES cell lines from PA (MII
    and MI) and SCNT (MII and MI) blastocysts. These cell lines expressed
    genes and antigens characteristic of pluripotent ES cells and produced
    full-term pups upon tetraploid embryo complementation. This study
    established an animal model for efficient generation of
    patient-specific ES cell lines using cryopreserved oocytes. This is a
    major step forward in the application of therapeutic cloning and
    parthenogenetic technology in human regenerative medicine and will
    serve as an important alternative to the iPS cell technology in
    countries/regions where these technologies are permitted.
 C1 [Tian, X. Cindy] Univ Connecticut, Dept Anim Sci, Ctr Regenerat Biol, Storrs, CT 06269 USA.
    [Sung, Li-Ying; Chang, Wei-Fang] Natl Taiwan Univ, Inst Biotechnol, Taipei 106, Taiwan.
    [Chang, Ching-Chien; Nagy, Zsolt Peter] Reprod Biol Associates, Atlanta, GA USA.
    [Xu, Jie] Evergen Biotechnol Inc, Storrs, CT USA.
 RP Tian, XC, Univ Connecticut, Dept Anim Sci, Ctr Regenerat Biol, 1392
    Storrs Rd,U 4243, Storrs, CT 06269 USA.
 EM xiuchun.tian@uconn.edu
 FU National Taiwan University ; National Science Council [NSC
    96-2321-B002-033]
 FX We appreciate the technical assistance provide by Tuz-An Lin. This
    research was supported by funds from USDA-ARS to X.C.T. and X.Y. and to
    L.Y.S. from National Taiwan University and National Science Council
    (NSC 96-2321-B002-033).
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 NR 50
 TC 3
 PU MARY ANN LIEBERT INC
 PI NEW ROCHELLE
 PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
 SN 2152-4971
 J9 CELL REPROGRAMM
 JI Cell. Reprogramm.
 PY 2010
 VL 12
 IS 2
 BP 203
 EP 211
 DI 10.1089/cell.2009.0072
 PG 9
 SC Cell & Tissue Engineering; Biotechnology & Applied Microbiology;
    Genetics & Heredity
 GA 584DL
 UT ISI:000276730400010
 ER
 
 PT J
 AU Wei, YC
    Zhu, J
    Huan, YJ
    Liu, ZF
    Yang, CR
    Zhang, XM
    Mu, YS
    Xia, P
    Liu, ZH
 AF Wei, Yanchang
    Zhu, Jiang
    Huan, Yanjun
    Liu, Zhongfeng
    Yang, Cairong
    Zhang, Xinmiao
    Mu, Yanshuang
    Xia, Ping
    Liu, Zhouhua
 TI Aberrant Expression and Methylation Status of Putatively Imprinted
    Genes in Placenta of Cloned Piglets
 SO CELLULAR REPROGRAMMING
 LA English
 DT Article
 ID EMBRYONIC STEM-CELLS; NUCLEAR TRANSFER; FETAL-DEVELOPMENT; DNA
    METHYLATION; PREIMPLANTATION EMBRYOS; BOVINE CLONES; MOUSE EMBRYOS;
    BLASTOCYSTS; REGIONS; CALVES
 AB Unlike embryos derived from fertilization, most cloned embryos die
    during postimplantation development, and those that survive to term are
    frequently defective. Many of the observed defects involve placenta.
    Abnormal placentation has been described in several cloned species.
    Imprinted genes are important regulators of placenta growth, and may be
    subjected to faulty reprogramming during somatic cell nuclear transfer.
    We aimed to determine the expression levels and methylation patterns of
    imprinted genes in placentas of live cloned piglets and dead ones.
    Quantitative real-time reverse transcriptase-polymerase chain reaction
    (RT-PCR) analysis showed that the expression of all four imprinted
    genes (IGF2, H19, PEG3, and GRB10) was significantly reduced in
    placentas of dead clones compared with placentas of live cloned piglets
    and controls (p < 0.05). In contrast, both live and dead cloned piglets
    exhibited steady-state mRNA levels for these genes within the control
    range (p > 0.05). Transcript levels for these genes in live clones
    rarely differed from those of controls in both piglets and placentas.
    Examination of the methylation status of DMR2 of IGF2 and CTCF3 of H19
    genes revealed that both genes exhibited significant high methylation
    levels in placentas of dead clones compared with placentas of live
    clones and controls. In contrast, both genes showed a normal
    differential methylation pattern in live cloned piglets and their
    placentas compared with controls. Importantly, dead cloned piglets also
    showed a normal pattern. Our results suggest that abnormal expression
    of imprinted genes in placenta may contribute to the development
    failure in pig somatic cell nuclear transfer (SCNT), which may be
    caused by abnormal methylation patterns in differentially methylated
    regions (DMRs) of imprinted genes as a result of incomplete
    reprogramming during SCNT.
 C1 [Wei, Yanchang; Zhu, Jiang; Huan, Yanjun; Liu, Zhongfeng; Yang, Cairong; Zhang, Xinmiao; Mu, Yanshuang; Liu, Zhouhua] NE Agr Univ, Coll Life Sci, Harbin, Heilongjiang, Peoples R China.
    [Xia, Ping] NE Agr Univ, Dept Obstet & Gynecol, Harbin, Heilongjiang, Peoples R China.
 RP Liu, ZH, NE Agr Univ, Coll Life Sci, 59 Mucai Steet, Harbin,
    Heilongjiang, Peoples R China.
 EM liu086@yahoo.com
 FU National Natural Science Foundation of China, NSFC [30871431]; National
    High Technology Research and Development Program (863 Program) of China
    [2008AA101006]; New Century Talent Foundation of Heilongjiang Province
    [1153-NCET-007]
 FX The authors are thankful to Dr. Yongjun Shu for his generous
    consultation on statistical analysis. The authors are also thankful to
    colleagues in the "Lab of Embryo Biotechnology'' for their helpful
    discussions. This work was supported by National Natural Science
    Foundation of China, NSFC (30871431), the National High Technology
    Research and Development Program (863 Program) of China (2008AA101006),
    and the New Century Talent Foundation of Heilongjiang Province
    (1153-NCET-007).
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 NR 42
 TC 3
 PU MARY ANN LIEBERT INC
 PI NEW ROCHELLE
 PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
 SN 2152-4971
 J9 CELL REPROGRAMM
 JI Cell. Reprogramm.
 PY 2010
 VL 12
 IS 2
 BP 213
 EP 222
 DI 10.1089/cell.2009.0090
 PG 10
 SC Cell & Tissue Engineering; Biotechnology & Applied Microbiology;
    Genetics & Heredity
 GA 584DL
 UT ISI:000276730400011
 ER
 
 PT J
 AU Delaloy, C
    Liu, L
    Lee, JA
    Su, H
    Shen, FX
    Yang, GY
    Young, WL
    Ivey, KN
    Gao, FB
 AF Delaloy, Celine
    Liu, Lei
    Lee, Jin-A
    Su, Hua
    Shen, Fanxia
    Yang, Guo-Yuan
    Young, William L.
    Ivey, Kathy N.
    Gao, Fen-Biao
 TI MicroRNA-9 Coordinates Proliferation and Migration of Human Embryonic
    Stem Cell-Derived Neural Progenitors
 SO CELL STEM CELL
 LA English
 DT Article
 ID IN-VITRO DIFFERENTIATION; POSTTRANSCRIPTIONAL REGULATION; TRANSCRIPTION
    FACTORS; ADULT NEUROGENESIS; EXPRESSION; STATHMIN; MECHANISMS;
    PRECURSORS; IDENTIFICATION; REPRESSION
 AB Human pluripotent stem cells offer promise for use in cell-based
    therapies for brain injury and diseases. However, their cellular
    behavior is poorly understood. Here we show that the expression of the
    brain-specific microRNA-9 (miR-9) is turned on in human neural
    progenitor cells (hNPCs) derived from human embryonic stem cells. Loss
    of miR-9 suppressed proliferation but promoted migration of hNPCs
    cultured in vitro. hNPCs without miR-9 activity also showed enhanced
    migration when transplanted into mouse embryonic brains or adult brains
    of a mouse model of stroke. These effects were not due to precocious
    differentiation of hNPCs. One of the key targets directly regulated by
    miR-9 encodes stathmin, which increases microtubule instability and
    whose expression in hNPCs correlates inversely with that of miR-9.
    Partial inhibition of stathmin activity suppressed the effects of miR-9
    loss on proliferation and migration of human or embryonic rat neural
    progenitors. These results identify miR-9 as a novel regulator that
    coordinates the proliferation and migration of hNPCs.
 C1 [Delaloy, Celine; Liu, Lei; Lee, Jin-A; Gao, Fen-Biao] Univ Calif San Francisco, Gladstone Inst Neurol Dis, San Francisco, CA 94158 USA.
    [Delaloy, Celine; Liu, Lei; Lee, Jin-A; Gao, Fen-Biao] Univ Calif San Francisco, Dept Neurol, San Francisco, CA 94158 USA.
    [Su, Hua; Shen, Fanxia; Yang, Guo-Yuan; Young, William L.] Univ Calif San Francisco, Cerebrovasc Res Ctr, Dept Anesthesia, San Francisco, CA 94110 USA.
    [Su, Hua; Shen, Fanxia; Yang, Guo-Yuan; Young, William L.] Univ Calif San Francisco, Cerebrovasc Res Ctr, Dept Perioperat Care, San Francisco, CA 94110 USA.
    [Su, Hua; Shen, Fanxia; Yang, Guo-Yuan; Young, William L.] Univ Calif San Francisco, Cerebrovasc Res Ctr, Dept Neurol & Neurosurg, San Francisco, CA 94110 USA.
    [Ivey, Kathy N.] Gladstone Inst Cardiovasc Dis, San Francisco, CA 94158 USA.
    [Gao, Fen-Biao] Univ Massachusetts, Sch Med, Dept Neurol, Worcester, MA 01605 USA.
    [Gao, Fen-Biao] Univ Massachusetts, Sch Med, Dept Neurobiol, Worcester, MA 01605 USA.
 RP Gao, FB, Univ Calif San Francisco, Gladstone Inst Neurol Dis, San
    Francisco, CA 94158 USA.
 FU California Institute for Regenerative Medicine (CIRM) ; NIH 
 FX We thank J Rubenstein, D Srivastava. and our lab members for
    discussions and comments, G Howard and S Ordway for editorial
    assistance, and S Mitchell for administrative assistance C D would like
    to thank Bettencourt Schueller Foundation for help with relocation to
    San Francisco C D and J -A L are supported by fellowships from the
    California Institute for Regenerative Medicine (CIRM) This work is
    supported by grants from the CIRM (F -B G) and the NIH (F -B G and W L
    Y)
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 NR 44
 TC 13
 PU CELL PRESS
 PI CAMBRIDGE
 PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
 SN 1934-5909
 J9 CELL STEM CELL
 JI Cell Stem Cell
 PD APR 2
 PY 2010
 VL 6
 IS 4
 BP 323
 EP 335
 DI 10.1016/j.stem.2010.02.015
 PG 13
 SC Cell & Tissue Engineering; Cell Biology
 GA 585KD
 UT ISI:000276823300011
 ER
 
 PT J
 AU Be'er, A
    Ariel, G
    Kalisman, O
    Helman, Y
    Sirota-Madi, A
    Zhang, HP
    Florin, EL
    Payne, SM
    Ben-Jacob, E
    Swinney, HL
 AF Be'er, Avraham
    Ariel, Gil
    Kalisman, Oren
    Helman, Yael
    Sirota-Madi, Alexandra
    Zhang, H. P.
    Florin, E. -L.
    Payne, Shelley M.
    Ben-Jacob, Eshel
    Swinney, Harry L.
 TI Lethal protein produced in response to competition between sibling
    bacterial colonies
 SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
    AMERICA
 LA English
 DT Article
 DE bacterial competition; bacterial growth inhibition; growth regulation;
    Paenibacillus dendritiformis; subtilisin
 ID COOPERATIVE ORGANIZATION; SELF-ORGANIZATION; BACILLUS-SUBTILIS;
    CANNIBALISM; FRATRICIDE; MECHANISMS; IMMUNITY; GROWTH
 AB Sibling Paenibacillus dendritiformis bacterial colonies grown on
    low-nutrient agar medium mutually inhibit growth through secretion of a
    lethal factor. Analysis of secretions reveals the presence of
    subtilisin (a protease) and a 12 kDa protein, termed sibling lethal
    factor (Slf). Purified subtilisin promotes the growth and expansion of
    P. dendritiformis colonies, whereas Slf is lethal and lyses P.
    dendritiformis cells in culture. Slf is encoded by a gene belonging to
    a large family of bacterial genes of unknown function, and the gene is
    predicted to encode a protein of approximately 20 kDa, termed
    dendritiformis sibling bacteriocin. The 20 kDa recombinant protein was
    produced and found to be inactive, but exposure to subtilisin resulted
    in cleavage to the active, 12 kDa form. The experimental results,
    combined with mathematical modeling, show that subtilisin serves to
    regulate growth of the colony. Below a threshold concentration,
    subtilisin promotes colony growth and expansion. However, once it
    exceeds a threshold, as occurs at the interface between competing
    colonies, Slf is then secreted into the medium to rapidly reduce cell
    density by lysis of the bacterial cells. The presence of genes encoding
    homologs of dendritiformis sibling bacteriocin in other bacterial
    species suggests that this mechanism for self-regulation of colony
    growth might not be limited to P. dendritiformis.
 C1 [Be'er, Avraham; Zhang, H. P.; Florin, E. -L.; Swinney, Harry L.] Univ Texas Austin, Ctr Nonlinear Dynam, Austin, TX 78712 USA.
    [Be'er, Avraham; Zhang, H. P.; Florin, E. -L.; Swinney, Harry L.] Univ Texas Austin, Dept Phys, Austin, TX 78712 USA.
    [Ariel, Gil] Univ Texas Austin, Dept Math, Austin, TX 78712 USA.
    [Kalisman, Oren; Helman, Yael; Sirota-Madi, Alexandra; Ben-Jacob, Eshel] Tel Aviv Univ, Raymond & Beverly Sackler Fac Exact Sci, Sch Phys & Astron, IL-69978 Tel Aviv, Israel.
    [Helman, Yael; Sirota-Madi, Alexandra] Tel Aviv Univ, Sackler Sch Med, IL-69978 Tel Aviv, Israel.
    [Payne, Shelley M.] Univ Texas Austin, Sect Mol Genet & Microbiol, Austin, TX 78712 USA.
    [Ben-Jacob, Eshel] Univ Calif San Diego, Ctr Theoret & Biol Phys, La Jolla, CA 92093 USA.
 RP Be'er, A, Univ Texas Austin, Ctr Nonlinear Dynam, Austin, TX 78712 USA.
 EM beerav@gmail.com
    eshelbj@gmail.com
    swinney@chaos.utexas.edu
 FU Welch Foundation [F-1573]; National Institutes of Health [AI50669];
    National Science Foundation-sponsored Center for Theoretical Biological
    Physics [PHY-0216576, 0225630]; University of California at San Diego ;
    Sid W. Richardson Foundation 
 FX We thank I. Brainis (Tel Aviv University) for providing the bacterial
    strain and the growth protocol; S. A. Craig and E. R. Murphy
    (University of Texas, Austin) for helping us with electrophoresis
    gel-runs and protein precipitation; K.D. Linse (University of Texas,
    Austin) for advice and for help with Edman protein sequence and HPLC;
    and B. Engquist and R. Tsai (University of Texas, Austin) for valuable
    suggestions on modeling and numerical algorithms. The sequencing effort
    was supported by the Tauber Family Foundation and was conducted under
    the Tauber Initiative (Tel Aviv University) in collaboration with
    GeneBee group at Moscow State University and the Genome center at the
    Weizmann Institute and DYN-GS Israel. This work was supported by R.A.
    Welch Foundation Grant F-1573 (E.L.F.), National Institutes of Health
    Grant AI50669 (S.M.P.), National Science Foundation-sponsored Center
    for Theoretical Biological Physics Grants PHY-0216576 and 0225630
    (E.B.J.), the University of California at San Diego (E.B.J.), and the
    Sid W. Richardson Foundation (H.L.S.).
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 TC 0
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 PI WASHINGTON
 PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA
 SN 0027-8424
 J9 PROC NAT ACAD SCI USA
 JI Proc. Natl. Acad. Sci. U. S. A.
 PD APR 6
 PY 2010
 VL 107
 IS 14
 BP 6258
 EP 6263
 DI 10.1073/pnas.1001062107
 PG 6
 SC Multidisciplinary Sciences
 GA 579MH
 UT ISI:000276374400026
 ER
 
 PT J
 AU Yang, J
    Wray, NR
    Visscher, PM
 AF Yang, Jian
    Wray, Naomi R.
    Visscher, Peter M.
 TI Comparing Apples and Oranges: Equating the Power of Case-Control and
    Quantitative Trait Association Studies
 SO GENETIC EPIDEMIOLOGY
 LA English
 DT Article
 DE association; case-control study; quantitative trait
 ID GENOME-WIDE ASSOCIATION; COMPLEX TRAITS; SCHIZOPHRENIA; LINKAGE
 AB Genome-wide association studies have achieved unprecedented success in
    the identification of novel genes and pathways implicated in complex
    traits. Typically, studies for disease use a case-control (CC) design
    and studies for quantitative traits (QT) are population based. The
    question that we address is what is the equivalence between CC and QT
    association studies in terms of detection power and sample size? We
    compare the binary and continuous traits by assuming a threshold model
    for disease and assuming that the effect size on disease liability has
    similar feature as on QT. We derive the approximate ratio of the
    non-centrality parameter (NCP) between CC and QT association studies,
    which is determined by sample size, disease prevalence (K) and the
    proportion of cases (v) in the CC study. For disease with prevalence
    <0.1, CC association study with equal numbers of cases and controls (v
    = 0.5) needs smaller sample size than QT association study to achieve
    equivalent power, e.g. a CC association study of schizophrenia (K =
    0.01) needs only similar to 55% sample size required for association
    study of height. So a planned meta-analysis for height on 120,000
    individuals has power equivalent to a CC study on 33,100 schizophrenia
    cases and 33,100 controls, a size not yet achievable for this disease.
    With equal sample size, when v = K, the power of CC association study
    is much less than that of QT association study because of the
    information lost by transforming a quantitative continuous trait to a
    binary trait. Genet. Epidemiol. 34:254-257, 2010. (C) 2009 Wiley-Liss,
    Inc.
 C1 [Yang, Jian; Wray, Naomi R.; Visscher, Peter M.] Queensland Inst Med Res, Brisbane, Qld 4029, Australia.
 RP Yang, J, Queensland Inst Med Res, 300 Herston Rd, Brisbane, Qld 4029,
    Australia.
 EM jian.yang@qimr.edu.au
 FU Australian National and Medical Research Council [496688, 389892];
    Australian Research Council [DP0770096]
 FX Contract grant sponsor: Australian National and Medical Research
    Council; Contract grant numbers: 496688; 389892; Contract grant
    sponsor: Australian Research Council; Contract grant number: DP0770096.
 CR BURTON PR, 2007, NATURE, V447, P661
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 NR 13
 TC 1
 PU WILEY-LISS
 PI HOBOKEN
 PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA
 SN 0741-0395
 J9 GENET EPIDEMIOL
 JI Genet. Epidemiol.
 PD APR
 PY 2010
 VL 34
 IS 3
 BP 254
 EP 257
 DI 10.1002/gepi.20456
 PG 4
 SC Genetics & Heredity; Public, Environmental & Occupational Health
 GA 580KW
 UT ISI:000276448100007
 ER
 
 PT J
 AU Lu, Y
    Zhang, HY
    Hou, J
    Wang, HQ
    Hu, XB
    Ma, YJ
    Ge, XY
    Huang, L
    Yang, YA
    Cao, RY
    Fan, H
    Liu, JJ
    Wu, J
 AF Lu Yong
    Zhang Huiyong
    Hou Jing
    Wang Huaqian
    Hu Xiangbing
    Ma Yanjun
    Ge Xiaoyu
    Huang Li
    Yang Yanan
    Cao Rongyue
    Fan Hao
    Liu Jingjing
    Wu Jie
 TI Vaccination with a potent DNA vaccine targeting B-cell epitopes of hGRP
    induces prophylactic and therapeutic antitumor activity in vivo
 SO GENE THERAPY
 LA English
 DT Article
 DE gastrin-releasing peptide; immunotherapy; prostate carcinoma;
    neutralizing antibody
 ID GASTRIN-RELEASING-PEPTIDE; RECEPTOR ANTAGONISTS INHIBIT; ENHANCE
    IMMUNOGENICITY; TANDEM REPEATS; CANCER CELLS; LUNG-CANCER; BOMBESIN;
    MICE; PROTEINS; KINASE
 AB Gastrin-releasing peptide (GRP), a bombesin-like peptide, is an
    autocrine or paracrine growth factor that can stimulate the growth of
    various cancer cells, making it an ideal target antigen to develop
    vaccines against cancer. In this study, we developed a novel DNA
    vaccine that encodes six tandem repeats of B-cell epitope GRP(18-27)
    (GRP6) flanked by HSP65 as carrier and four tandem repeats of
    mycobacterial HSP70(407-426) (M4) as helper T-cell epitopes for
    enhancement of immunogenicity. When intramuscularly immunized to mice,
    this anti-GRP DNA vaccine-induced GRP-specific antibody ( Ab) responses
    that were at least 10-fold higher in magnitude compared with HSP65-GRP6
    protein vaccine. Both prophylactic and therapeutic antitumor immunities
    induced by vaccination significantly suppressed the growth of
    GRP-dependent prostate carcinoma RM-1 in vivo and prolonged the
    survival of tumor-inoculated mice. Out results also showed that the
    immune sera with high titer of GRP-specific Abs effectively inhibited
    the growth of tumor in mice and dose dependently inhibited
    proliferation of cultured RM-1 cells in vitro, suggesting that the GRP
    neutralizing Ab is responsible for the protective and therapeutic
    antitumor activity of vaccination. These findings may be of great
    importance in the further exploration of the applications of growth
    factors identified in human in cancer therapy. Gene Therapy (2010) 17,
    459-468; doi: 10.1038/gt.2009.165; published online 4 February 2010
 C1 [Lu Yong; Zhang Huiyong; Hou Jing; Wang Huaqian; Hu Xiangbing; Ma Yanjun; Ge Xiaoyu; Huang Li; Yang Yanan; Cao Rongyue; Liu Jingjing; Wu Jie] China Pharmaceut Univ, Minigene Pharm Lab, Biopharmaceut Coll, Nanjing 210009, Peoples R China.
    [Zhang Huiyong] Xinxiang Med Univ, Dept Life Sci & Technol, Xinxiang, Peoples R China.
    [Lu Yong; Fan Hao] Shanghai Yijiu Biomed Cooperat Ltd, Shanghai, Peoples R China.
 RP Wu, J, China Pharmaceut Univ, Minigene Pharm Lab, Biopharmaceut Coll,
    24 TongjiaXiang, Nanjing 210009, Peoples R China.
 EM Minigene@21cn.com
 FU China National Natural Science Fund Committee [30500458, 30701023,
    30672464, 30572272, 30872393, 30772570]; Natural Science Foundation of
    Jiangsu Province [BK 2007170, BK2007169]
 FX This work was supported by the China National Natural Science Fund
    Committee (grant nos. 30500458, 30701023, 30672464, 30572272, 30872393
    and 30772570); the Natural Science Foundation of Jiangsu Province (no.
    BK 2007170 and BK2007169).
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 NR 25
 TC 0
 PU NATURE PUBLISHING GROUP
 PI LONDON
 PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
 SN 0969-7128
 J9 GENE THERAPY
 JI Gene Ther.
 PD APR
 PY 2010
 VL 17
 IS 4
 BP 459
 EP 468
 DI 10.1038/gt.2009.165
 PG 10
 SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology;
    Genetics & Heredity; Medicine, Research & Experimental
 GA 580CZ
 UT ISI:000276425800003
 ER
 
 PT J
 AU Yang, N
    Nijhuis, ER
    Volders, HH
    Eijsink, JJH
    Lendvai, A
    Zhang, B
    Hollema, H
    Schuuring, E
    Wisman, GBA
    van der Zee, AGJ
 AF Yang, Nan
    Nijhuis, Esther R.
    Volders, Haukeline H.
    Eijsink, Jasper J. H.
    Lendvai, Agnes
    Zhang, Bo
    Hollema, Harry
    Schuuring, Ed
    Wisman, G. Bea A.
    van der Zee, Ate G. J.
 TI Gene promoter methylation patterns throughout the process of cervical
    carcinogenesis
 SO CELLULAR ONCOLOGY
 LA English
 DT Article
 DE Methylation; cervical (intraepithelial) neoplasia; DAPK; CCNA1; CADM1
 ID ABERRANT DNA METHYLATION; HUMAN-PAPILLOMAVIRUS DNA; SQUAMOUS-CELL
    CARCINOMA; UTERINE CERVIX; CANCER; HYPERMETHYLATION; NEOPLASIA; PCR;
    PREVALENCE; EXPRESSION
 AB Objectives: To determine methylation status of nine genes, previously
    described to be frequently methylated in cervical cancer, in squamous
    intraepithelial lesions (SIL).
    Methods: QMSP was performed in normal cervix, low-grade ( L) SIL,
    high-grade (H) SIL, adenocarcinomas and squamous cell cervical cancers,
    and in corresponding cervical scrapings.
    Results: Only CCNA1 was never methylated in normal cervices and rarely
    in LSILs. All other genes showed methylation in normal cervices, with
    CALCA, SPARC and RAR-beta(2) at high levels. Methylation frequency of 6
    genes (DAPK, APC, TFPI2, SPARC, CCNA1 and CADM1) increased with
    severity of the underlying cervical lesion. DAPK showed the highest
    increase in methylation frequency between LSIL and HSIL (10% vs. 40%, p
    < 0.05), while CCNA1 and TFPI2 were most prominently methylated in
    cervical cancers compared to HSILs (25% vs. 52%, p < 0.05, 30% vs. 58%,
    p < 0.05). CADM1 methylation in cervical cancers was related to depth
    of invasion ( p < 0.05) and lymph vascular space involvement ( p <
    0.01), suggesting a role in invasive potential of cervical cancers.
    Methylation ratios in scrapings reflected methylation status of the
    underlying lesions ( p < 0.05).
    Conclusion: Methylation of previously reported cervical cancer specific
    genes frequently occurs in normal epithelium. However, frequency of
    methylation increases during cervical carcinogenesis, with CCNA1 and
    DAPK as the best markers to distinguish normal/LSIL from HSIL/cancer
    lesions.
 C1 [Yang, Nan; Nijhuis, Esther R.; Volders, Haukeline H.; Eijsink, Jasper J. H.; Lendvai, Agnes; Wisman, G. Bea A.; van der Zee, Ate G. J.] Univ Groningen, Dept Gynecol Oncol, Univ Med Ctr Groningen, NL-9700 RB Groningen, Netherlands.
    [Yang, Nan; Zhang, Bo] Peking Univ, Dept Pathol, Sch Basic Med Sci, Hlth Sci Ctr, Beijing 100871, Peoples R China.
    [Hollema, Harry; Schuuring, Ed] Univ Groningen, Dept Pathol, Univ Med Ctr Groningen, NL-9700 RB Groningen, Netherlands.
 RP Wisman, GBA, Univ Groningen, Dept Gynecol Oncol, Univ Med Ctr
    Groningen, POB 30-001, NL-9700 RB Groningen, Netherlands.
 EM g.b.a.wisman@og.umcg.nl
 FU Dutch Cancer Society (NKB) [RUG 2004-3161]
 FX This study was supported by OncoMethylome Sciences S. A., Liege,
    Belgium and by the Dutch Cancer Society (NKB) (project-number RUG
    2004-3161). Nan Yang is a recipient of Bernoulli Bursary.
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 NR 41
 TC 2
 PU IOS PRESS
 PI AMSTERDAM
 PA NIEUWE HEMWEG 6B, 1013 BG AMSTERDAM, NETHERLANDS
 SN 1570-5870
 J9 CELL ONCOL
 JI Cell. Oncol.
 PY 2010
 VL 32
 IS 1-2
 BP 131
 EP 143
 DI 10.3233/CLO-2009-0510
 PG 13
 SC Oncology; Cell Biology; Pathology
 GA 580PQ
 UT ISI:000276461800012
 ER
 
 PT J
 AU Yang, H
    Qian, XH
    Cong, R
    Li, JW
    Yao, Q
    Jiao, XY
    Ju, G
    You, SW
 AF Yang, Hao
    Qian, Xin-Hong
    Cong, Rui
    Li, Jing-wen
    Yao, Qin
    Jiao, Xi-Ying
    Ju, Gong
    You, Si-Wei
 TI Evidence for Heterogeneity of Astrocyte De-Differentiation in vitro:
    Astrocytes Transform into Intermediate Precursor Cells Following
    Induction of ACM from Scratch-Insulted Astrocytes
 SO CELLULAR AND MOLECULAR NEUROBIOLOGY
 LA English
 DT Article
 DE Astrocytes; De-differentiation; Intermediate precursor cell; A2B5; NG2;
    Neural stem cell; Cell culture
 ID CENTRAL-NERVOUS-SYSTEM; NEURAL STEM-CELLS; RAT SPINAL-CORD;
    NG2-EXPRESSING CELLS; NG2-POSITIVE CELLS; NG2 PROTEOGLYCAN; PROGENITOR
    CELLS; OLIGODENDROGLIAL PROGENITORS; SUBVENTRICULAR ZONE; DEMYELINATION
 AB Our previous study definitely demonstrated that the mature astrocytes
    could undergo a de-differentiation process and further transform into
    pluripotential neural stem cells (NSCs), which might well arise from
    the effect of diffusible factors released from scratch-insulted
    astrocytes. However, these neurospheres passaged from one
    neurosphere-derived from de-differentiated astrocytes possessed a
    completely distinct characteristic in the differentiation behavior,
    namely heterogeneity of differentiation. The heterogeneity in cell
    differentiation has become a crucial but elusive issue. In this study,
    we show that purified astrocytes could de-differentiate into
    intermediate precursor cells (IPCs) with addition of scratch-insulted
    astrocyte-conditioned medium (ACM) to the culture, which can express
    NG2 and A2B5, the IPCs markers. Apart from the number of NG2(+) and
    A2B5(+) cells, the percentage of proliferative cells as labeled with
    BrdU progressively increased with prolonged culture period ranging from
    1 to 10 days. Meanwhile, the protein level of A2B5 in cells also
    increased significantly. These results revealed that not all astrocytes
    could de-differentiate fully into NSCs directly when induced by ACM,
    rather they generated intermediate or more restricted precursor cells
    that might undergo progressive de-differentiation to generate NSCs.
 C1 [Yang, Hao; Li, Jing-wen; Yao, Qin; Jiao, Xi-Ying; Ju, Gong; You, Si-Wei] Fourth Mil Med Univ, Inst Neurosci, Xian 710032, Peoples R China.
    [Qian, Xin-Hong] Fourth Mil Med Univ, Xijing Hosp, Dept Pediat, Xian 710032, Peoples R China.
    [Cong, Rui] Fourth Mil Med Univ, Xijing Hosp, Dept Inst Orthopaed, Xian 710032, Peoples R China.
 RP Ju, G, Fourth Mil Med Univ, Inst Neurosci, 17 W Chang Le Rd, Xian
    710032, Peoples R China.
 EM yanghao71_99@yahoo.com
    jugong@fmmu.edu.cn
    yonsiwei@fmmu.edu.cn
 FU Natural Science Foundation of China [30973088, 30872829, 30571998];
    Chinese PLA [06G089, 08Z028]
 FX This work was supported by the Natural Science Foundation of China
    (Grant Nos. 30973088, 30872829, and 30571998), Chinese PLA national
    scientific technological project (06G089), and the 11th Five-year
    Special-purpose Programme for PLA (08Z028).
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 NR 32
 TC 1
 PU SPRINGER/PLENUM PUBLISHERS
 PI NEW YORK
 PA 233 SPRING ST, NEW YORK, NY 10013 USA
 SN 0272-4340
 J9 CELL MOL NEUROBIOL
 JI Cell. Mol. Neurobiol.
 PD APR
 PY 2010
 VL 30
 IS 3
 BP 483
 EP 491
 DI 10.1007/s10571-009-9474-3
 PG 9
 SC Cell Biology; Neurosciences
 GA 580XQ
 UT ISI:000276484500018
 ER
 
 PT J
 AU Gan, L
    Liu, P
    Lu, H
    Chen, S
    Yang, J
    McCarthy, JB
    Knudsen, KE
    Huang, H
 AF Gan, L.
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 TI Cyclin D1 promotes anchorage-independent cell survival by inhibiting
    FOXO-mediated anoikis (vol 16, pg 1408, 2009)
 SO CELL DEATH AND DIFFERENTIATION
 LA English
 DT Correction
 CR GAN L, 2009, CELL DEATH DIFFER, V16, P1408, DOI 10.1038/cdd.2009.86
 NR 1
 TC 0
 PU NATURE PUBLISHING GROUP
 PI LONDON
 PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
 SN 1350-9047
 J9 CELL DEATH DIFFERENTIATION
 JI Cell Death Differ.
 PD MAY
 PY 2010
 VL 17
 IS 5
 BP 900
 EP 900
 DI 10.1038/cdd.2010.15
 PG 1
 SC Biochemistry & Molecular Biology; Cell Biology
 GA 581HU
 UT ISI:000276513600018
 ER
 
 PT J
 AU Yang, J
    Darley, RL
    Hallett, M
    Evans, WH
 AF Yang, Jian
    Darley, Richard L.
    Hallett, Maurice
    Evans, W. Howard
 TI Low Connexin Channel-Dependent Intercellular Communication in Human
    Adult Hematopoietic Progenitor/Stem Cells: Probing Mechanisms of
    Autologous Stem Cell Therapy
 SO CELL COMMUNICATION AND ADHESION
 LA English
 DT Article
 ID GAP JUNCTIONAL COMMUNICATION; MESENCHYMAL STROMAL CELLS;
    MYOCARDIAL-INFARCTION; EXPRESSION; TRANSPLANTATION; CARDIOMYOCYTES;
    HEMICHANNELS; REPAIR; HEART; MOUSE
 AB Human bone marrow is a clinical source of autologous progenitor stem
    cells showing promise for cardiac repair following ischemic insult.
    Functional improvements following delivery of adult bone marrow
    CD34<SU+</SU cells into heart tissue may require metabolic/electrical
    communication between participating cells. Since connexin43 (Cx43)
    channels are implicated in cardiogenesis and provide intercellular
    connectivity in the heart, the authors analyzed the expression of 20
    connexins (Cx) in CD34<SU+</SU cells and in monocytes and granulocytes
    in bone marrow and spinal cord. Reverse transcriptase-polymerase chain
    reaction (RT-PCR) detected only low expression of Cx43 and Cx37. Very
    low level dye coupling was detected by flow cytometry between
    CD34<SU+</SU cells and other Cx43 expressing cells, including HL-1
    cardiac cells, and was not inhibited by specific gap junction
    inhibitors. The results indicate that CD34<SU+</SU cells are unlikely
    to communicate via gap junctions and the authors conclude that use of
    CD34<SU+</SU cells to repair damaged hearts is unlikely to involve gap
    junctions. The results concur with the hypothesis that bone marrow
    cells elicit improved cardiac function through release of undefined
    paracrine mediators.
 C1 [Evans, W. Howard] Cardiff Univ, Sch Med, Wales Heart Res Inst, Cardiff CF14 4XN, S Glam, Wales.
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    [Hallett, Maurice] Cardiff Univ, Sch Med, Dept Surg, Cardiff CF14 4XN, S Glam, Wales.
    [Yang, Jian; Evans, W. Howard] Cardiff Univ, Sch Med, Dept Med Biochem & Immunol, Cardiff CF14 4XN, S Glam, Wales.
 RP Evans, WH, Cardiff Univ, Sch Med, Wales Heart Res Inst, Cardiff CF14
    4XN, S Glam, Wales.
 EM whewmb@cardiff.ac.uk
 FU British Heart Foundation [PG/05/051]
 FX This work was supported by grant PG/05/051 from the British Heart
    Foundation.
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 TC 0
 PU INFORMA HEALTHCARE
 PI LONDON
 PA TELEPHONE HOUSE, 69-77 PAUL STREET, LONDON EC2A 4LQ, ENGLAND
 SN 1541-9061
 J9 CELL COMMUN ADHES
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 PD DEC
 PY 2009
 VL 16
 IS 5-6
 BP 138
 EP 145
 DI 10.3109/15419061003653763
 PG 8
 SC Biochemistry & Molecular Biology; Cell Biology
 GA 581VZ
 UT ISI:000276554700003
 ER
 
 PT J
 AU Lee, MW
    Chanda, D
    Yang, JQ
    Oh, H
    Kim, SS
    Yoon, YS
    Hong, S
    Park, KG
    Lee, IK
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    Hanson, RW
    Choi, HS
    Koo, SH
 AF Lee, Min-Woo
    Chanda, Dipanjan
    Yang, Jianqi
    Oh, Hyunhee
    Kim, Su Sung
    Yoon, Young-Sil
    Hong, Sungpyo
    Park, Keun-Gyu
    Lee, In-Kyu
    Choi, Cheol Soo
    Hanson, Richard W.
    Choi, Hueng-Sik
    Koo, Seung-Hoi
 TI Regulation of Hepatic Gluconeogenesis by an ER-Bound Transcription
    Factor, CREBH
 SO CELL METABOLISM
 LA English
 DT Article
 ID ENDOPLASMIC-RETICULUM STRESS; INSULIN-RESISTANCE; INTRAMEMBRANE
    PROTEOLYSIS; COACTIVATOR PGC-1; CREB/ATF-FAMILY; LIVER; ATF6; CLEAVAGE;
    METABOLISM; PROTEIN
 AB Endoplasmic reticulum (ER)-bound transcription factor families are
    shown to be involved in the control of various metabolic pathways.
    Here, we report a critical function of ER-bound transcription factor,
    CREBH, in the regulation of hepatic gluconeogenesis. Expression of
    CREBH is markedly induced by fasting or in the insulin-resistant state
    in rodents in a dexamethasone- and PGC-1 alpha-dependent manner, which
    results in the accumulation of active nuclear form of CREBH (CREBH-N).
    Overexpression of constitutively active CREBH activates transcription
    of PEPCK-C or G6Pase by binding to its enhancer site that is distinct
    from the well-characterized CREB/CRTC2 regulatory sequences in vivo. Of
    interest, knockdown of CREBH in liver significantly reduces blood
    glucose levels without altering expression of genes involved in the ER
    stress signaling cascades in mice. These data suggest a crucial role
    for CREBH in the regulation of hepatic glucose metabolism in mammals.
 C1 [Chanda, Dipanjan; Choi, Hueng-Sik] Chonnam Natl Univ, Sch Biol Sci & Technol, Hormone Res Ctr, Kwangju 500757, South Korea.
    [Lee, Min-Woo; Yoon, Young-Sil; Hong, Sungpyo; Koo, Seung-Hoi] Sungkyunkwan Univ, Sch Med, Dept Mol Cell Biol, Suwon 440746, Gyeonggi Do, South Korea.
    [Choi, Hueng-Sik] Chonnam Natl Univ, Sch Med, Dept Biomed Sci, Res Inst Med Sci, Kwangju 501746, South Korea.
    [Yang, Jianqi; Hanson, Richard W.] Case Western Reserve Univ, Sch Med, Dept Biochem, Cleveland, OH 44106 USA.
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    [Choi, Cheol Soo] Gachon Univ Med & Sci, Gil Med Ctr, Div Endocrinol, Inchon 405760, South Korea.
    [Lee, In-Kyu] Kyungpook Natl Univ, Sch Med, Res Inst Aging & Metab, Dept Internal Med, Taegu 700422, South Korea.
    [Lee, In-Kyu] Kyungpook Natl Univ, Sch Med, Res Inst Aging & Metab, Dept Biochem, Taegu 700422, South Korea.
    [Lee, In-Kyu] Kyungpook Natl Univ, Sch Med, Res Inst Aging & Metab, World Class Univ Program, Taegu 700422, South Korea.
    [Park, Keun-Gyu] Keimyung Univ, Sch Med, Dept Internal Med, Taegu, South Korea.
 RP Choi, HS, Chonnam Natl Univ, Sch Biol Sci & Technol, Hormone Res Ctr,
    Kwangju 500757, South Korea.
 EM hsc@chonnam.ac.kr
    shkoo@med.skku.ac.kr
 FU Ministry for Health, Welfare, and Family Affairs, Republic of Korea
    [A080150]; NRF [NRL-ROA-2005-000-10047-0]
 FX We would like to thank Sun Myung Park and Yo-Na Kim for technical
    assistance. We would also like to thank Dr. Seok-Yong Choi for critical
    reading. This work was supported by a grant of the Korea Healthcare
    technology R&D Project, Ministry for Health, Welfare, and Family
    Affairs, Republic of Korea (A080150) (S.-H.K.) and by the NRF through
    the National Research Laboratory program (NRL-ROA-2005-000-10047-0)
    (H.-S.C.).
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 NR 29
 TC 6
 PU CELL PRESS
 PI CAMBRIDGE
 PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
 SN 1550-4131
 J9 CELL METAB
 JI Cell Metab.
 PD APR 7
 PY 2010
 VL 11
 IS 4
 BP 331
 EP 339
 DI 10.1016/j.cmet.2010.02.016
 PG 9
 SC Cell Biology; Endocrinology & Metabolism
 GA 581TE
 UT ISI:000276546700015
 ER
 
 PT J
 AU Huang, Y
    Lin, M
    Wu, JR
    Yang, LY
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    Wu, Jiao-Ren
    Yang, Li-Ye
    Xiang, Zu
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 SO BLOOD CELLS MOLECULES AND DISEASES
 LA English
 DT Letter
 C1 [Huang, Yue; Lin, Min; Wu, Jiao-Ren; Yang, Li-Ye] Chaozhou Cent Hosp, Chaozhou 521021, Guangdong, Peoples R China.
    [Xiang, Zu] Decipher Biosci LTD, Shenzhen 518034, Guangdong, Peoples R China.
 RP Yang, LY, Chaozhou Cent Hosp, Chaozhou 521021, Guangdong, Peoples R
    China.
 EM yangleeyee@sina.com
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 NR 5
 TC 2
 PU ACADEMIC PRESS INC ELSEVIER SCIENCE
 PI SAN DIEGO
 PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
 SN 1079-9796
 J9 BLOOD CELLS MOLECULES DIS
 JI Blood Cells Mol. Dis.
 PD APR 15
 PY 2010
 VL 44
 IS 4
 BP 215
 EP 216
 DI 10.1016/j.bcmd.2010.01.003
 PG 2
 SC Hematology
 GA 581RC
 UT ISI:000276541000004
 ER
 
 PT J
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    Yang, LY
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    Lin, Min
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    Zheng, Lei
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 SO BLOOD CELLS MOLECULES AND DISEASES
 LA English
 DT Letter
 ID GLOBIN GENE; HEMOGLOBIN; VARIANTS
 C1 [Lin, Min; Zheng, Lei; Wang, Qian] So Med Univ, Nangfang Hosp, Lab Med Ctr, Guangzhou 510515, Guangdong, Peoples R China.
    [Zhang, Ling] Guangzhou Kingmed Ctr Clin Lab, Guangzhou 510330, Guangdong, Peoples R China.
    [Lin, Min; Yang, Li-Ye] Chaozhou Cent Hosp, Cent Lab, Chaozhou 521021, Guangdong, Peoples R China.
 RP Wang, Q, So Med Univ, Nangfang Hosp, Lab Med Ctr, Guangzhou 510515,
    Guangdong, Peoples R China.
 EM nflab@163.com
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 NR 5
 TC 0
 PU ACADEMIC PRESS INC ELSEVIER SCIENCE
 PI SAN DIEGO
 PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
 SN 1079-9796
 J9 BLOOD CELLS MOLECULES DIS
 JI Blood Cells Mol. Dis.
 PD APR 15
 PY 2010
 VL 44
 IS 4
 BP 217
 EP 218
 DI 10.1016/j.bcmd.2010.01.008
 PG 2
 SC Hematology
 GA 581RC
 UT ISI:000276541000005
 ER
 
 PT J
 AU Srinivasan, RS
    Geng, X
    Yang, Y
    Wang, YD
    Mukatira, S
    Studer, M
    Porto, MPR
    Lagutin, O
    Oliver, G
 AF Srinivasan, R. Sathish
    Geng, Xin
    Yang, Ying
    Wang, Yingdi
    Mukatira, Suraj
    Studer, Michele
    Porto, Marianna P. R.
    Lagutin, Oleg
    Oliver, Guillermo
 TI The nuclear hormone receptor Coup-TFII is required for the initiation
    and early maintenance of Prox1 expression in lymphatic endothelial cells
 SO GENES & DEVELOPMENT
 LA English
 DT Article
 DE Lymphatics; Prox1; Coup-TFII; mouse; endothelial cell
 ID TRANSGENIC MICE; IN-VIVO; RBP-J; VASCULATURE; FOREBRAIN;
    HAPLOINSUFFICIENCY; TRANSCRIPTION; IDENTITY; DEFECTS; SYSTEM
 AB The homeobox gene Prox1 is crucial for mammalian lymphatic vascular
    development. In the absence of Prox1, lymphatic endothelial cells
    (LECs) are not specified. The maintenance of LEC identity also requires
    the constant expression of Prox1. However, the mechanisms controlling
    the expression of this gene in LECs remain poorly understood. The
    SRY-related gene Sox18 is required to induce Prox1 expression in venous
    LEC progenitors. Although Sox18 is also expressed in embryonic
    arteries, these vessels do not express Prox1, nor do they give rise to
    LECs. This finding suggests that some venous endothelial cell-specific
    factor is required for the activation of Prox1. Here we demonstrate
    that the nuclear hormone receptor Coup-TFII is necessary for the
    activation of Prox1 in embryonic veins by directly binding a conserved
    DNA domain in the regulatory region of Prox1. In addition, we show that
    the direct interaction between nuclear hormone receptors and Prox1 is
    also necessary for the maintenance of Prox1 expression during early
    stages of LEC specification and differentiation.
 C1 [Srinivasan, R. Sathish; Geng, Xin; Yang, Ying; Wang, Yingdi; Porto, Marianna P. R.; Lagutin, Oleg; Oliver, Guillermo] St Jude Childrens Hosp, Dept Genet & Tumor Cell Biol, Memphis, TN 38105 USA.
    [Mukatira, Suraj] St Jude Childrens Hosp, Hartwell Ctr Bioinformat & Biotechnol, Memphis, TN 38105 USA.
    [Studer, Michele] Telethon Inst Genet & Med, Dev Disorders Program, I-80131 Naples, Italy.
 RP Oliver, G, St Jude Childrens Hosp, Dept Genet & Tumor Cell Biol, 332 N
    Lauderdale St, Memphis, TN 38105 USA.
 EM guillermo.oliver@stjude.org
 FU NIH [R01-HL073402]; American Lebanese Syrian Associated Charities
    (ALSAC) 
 FX We thank Drs. S. Tsai and M.-J. Tsai for providing the Coup-TFII floxed
    mouse strain; Dr. J. Westmoreland for the Prox1<SUP>+/flox</SUP>; R26R
    mouse strain; Dr. J. Johnson for the Rbpj floxed mouse strain; Dr. Y.
    Lee for help with the design of primers and probes for real-time PCR;
    Drs. J. Downing, S. Baker, and R. Endersby for providing the GFPCre
    cDNA cassette; Drs. F. Mathias and P. Koopmann for the Sox18 in situ
    probe; Dr. M. Yanagisawa for the Tie2-Cre strain; Dr. E. Dejana for the
    H5V cells; Mr. S. Connell, Dr. L. Zhao, Dr. Y. Ouyang and Dr. J.
    Peterson for help with confocal imaging; and Dr. A. McArthur for
    editing of this manuscript. We thank all of the members of our
    laboratory for their helpful suggestions and discussions. This work was
    supported by NIH grant R01-HL073402 ( to G.O) and the American Lebanese
    Syrian Associated Charities (ALSAC).
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 NR 34
 TC 11
 PU COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT
 PI WOODBURY
 PA 500 SUNNYSIDE BLVD, WOODBURY, NY 11797-2924 USA
 SN 0890-9369
 J9 GENE DEVELOP
 JI Genes Dev.
 PD APR 1
 PY 2010
 VL 24
 IS 7
 BP 696
 EP 707
 DI 10.1101/gad.1859310
 PG 12
 SC Cell Biology; Developmental Biology; Genetics & Heredity
 GA 577PD
 UT ISI:000276235400008
 ER
 
 PT J
 AU Bian, SY
    Gai, LY
    Ye, P
    Guo, ZK
    Li, QF
    Yang, YF
    Wang, H
    Wang, LS
 AF Bian Su Yan
    Gai Lu Yue
    Ye Ping
    Guo Zi Kuan
    Li Qing Fang
    Yang Yue Feng
    Wang Hua
    Wang Li-Sheng
 TI Sphingosine kinase-1 protects transplanted mesenchymal stem cells and
    improves the performance of the infarcted heart Research Article
 SO GENE THERAPY AND MOLECULAR BIOLOGY
 LA English
 DT Article
 DE infracted; myocardiocyte; hypoxia
 ID LEFT-VENTRICULAR FUNCTION; HEPATOCYTE GROWTH-FACTOR;
    MYOCARDIAL-INFARCTION; OVEREXPRESSING AKT; RAT; ACTIVATION; INJURY;
    SPHINGOSINE-1-PHOSPHATE; REPAIR; DIFFERENTIATION
 AB In this study we investigated whether sphingosine kinase-1 (SPK1)
    modification could offer cytoprotective effects on mesenchymal stem
    cells (MSCs) in vitro and in vivo in a myocardial infarction rat model.
    MSCs carrying green fluorescent protein (MSCs/GFP), SPK1 (MSCs/SPK1) or
    with firefly luciferase genes (MSCs/GFP/luc and MSCs/SPK1/luc) were
    obtained and functionally identified. The in vitro protective effects
    of SPK1 on MSCs were evaluated after exposure to serum-deprivation and
    hypoxia stimuli. Cells (1 x 106) were injected intramyocardially around
    the infarcted zone and the fate of the transplanted cells was traced by
    SPK1 and luciferase assessment in the ischemic myocardium. The survival
    of the remaining myocardiocytes was evaluated by in situ TUNEL assay
    72hours after cell transplantation. The morphological and functional
    features of the injured heart were observed with echocardiography,
    hemodynamic and histological examinations. The results showed that SPK1
    protected MSCs both in vitro and in vivo. MSCs/SPK1/luc implantation
    elevated SPK1 activities in the ischemic myocardium, which peaked on
    day 3 and reduced to the baseline on day 7. Compared with MSCs/GFP/luc,
    luciferase activity was significantly higher in MSCs/SPK1/luc-injected
    myocardium (p<0.01 on days 3 and 5 post-injection). The percentage of
    TUNEL-positive cells in the ischemic area was significantly lower in
    MSCs/SPK1 (%, 15.5 +/- 2.3 vs. MSCs/GFP 23.1 +/- 4.9, p<0.05).
    Concordantly, the parameters including fractional shortening (%, 29.33
    +/- 2.94 vs. MSCs/GFP 23.29 +/- 2.86, p<0.05), ejection fraction (%,
    60.35 +/- 4.96 vs. 51.99 +/- 5.16, p<0.05), left ventricular
    end-diastolic pressure (15.3 +/- 3.6 vs. 18.2 +/- 3.3 mmHg, p<0.05) and
    blood vessel density (number per field: 33.82 +/- 5.45 vs. 23.06 +/-
    4.01, p<0.01) were greatly improved in MSCs/SPK1, though those of the
    infarct size, collagen deposition in non-infracted area and the
    spherical indexes of the hearts were comparable between two cell
    treatment groups. In conclusion, MSCs/SPK1 improve the performance of
    the infarcted hearts by providing prosurvival signals to the
    transplanted MSCs and myocardiocytes.
 C1 [Guo Zi Kuan; Li Qing Fang; Yang Yue Feng; Wang Hua; Wang Li-Sheng] Beijing Inst Radiat Med, Dept Expt Hematol, Beijing 100850, Peoples R China.
    [Bian Su Yan; Gai Lu Yue; Ye Ping] Gen Hosp PLA, Dept Geriatr Cardiol, Beijing 100853, Peoples R China.
 RP Wang, LS, Beijing Inst Radiat Med, Dept Expt Hematol, 27 Taiping Rd,
    Beijing 100850, Peoples R China.
 EM wanghualjh@gmail.com
    wangls@nic.bmi.ac.cn
 FU Chinese National Science Foundation [30871018]; Chinese National Basic
    Research and Development [2006CB504105]; Chinese High-Tech Program
    '863' [2007AA021007, 2007AA02Z454]
 FX We thank Prof. Jia-Xi Wang for his critical reviewing on this
    manuscript. This work was supported by Chinese National Science
    Foundation (No. 30871018), Chinese National Basic Research and
    Development Grants '973' (No. 2006CB504105), and Chinese High-Tech
    Program '863' (No. 2007AA021007 and No. 2007AA02Z454).
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 NR 35
 TC 0
 PU GENE THERAPY PRESS
 PI ATHENS
 PA GREGORIOU AFXENTIOU 7, ALIMOS, ATHENS, 17455, GREECE
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 J9 GENE THER MOL BIOL
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 VL 13B
 BP 274
 EP 283
 PG 10
 SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology;
    Medicine, Research & Experimental
 GA 575QR
 UT ISI:000276083000003
 ER
 
 PT J
 AU Sun, B
    Yang, ZS
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 LA English
 DT Article
 DE Gene therapy; VEGF; radiation damage; mice
 ID ENDOTHELIAL GROWTH-FACTOR; COLON-CANCER CELLS; CELLULAR PROLIFERATION;
    FACTOR RECEPTOR; MUSCLE
 AB The study was designed to study the effect of intramuscular injections
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    preventing radiation damage in the mouse and the molecular mechanism of
    this protection. The recombinant pcDNA3.1-VEGF(165) plasmid was
    successfully constructed and intramuscular injection of this plasmid
    can remarkably decrease the mortality of mice after severe radiation
    damage, decrease the apoptosis rates of cells in the thymus and spleen,
    and improve the pathologic change of organs of the immune system. Our
    work indicates that VEGF injection can be one of the effective methods
    for preventing severe radiation injury. These studies provide the
    experimental basis for further clinical usage of VEGF.
 C1 [Yang, Z. S.; Zhou, Z. Y.] Soochow Univ, Inst Radiat Med & Publ Hlth, Coll Med, Suzhou 215123, Peoples R China.
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 RP Yang, ZS, Soochow Univ, Inst Radiat Med & Publ Hlth, Coll Med, Suzhou
    215123, Peoples R China.
 EM fd@suda.edu.cn
 FU National Natural Science Foundation of China [30570549]; National
    Defense Basic Science and Technology Foundation [A3820060138]
 FX This work was supported by the National Natural Science Foundation of
    China (No. 30570549), and the National Defense Basic Science and
    Technology Foundation (No. A3820060138).
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 TC 0
 PU GENE THERAPY PRESS
 PI ATHENS
 PA GREGORIOU AFXENTIOU 7, ALIMOS, ATHENS, 17455, GREECE
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 J9 GENE THER MOL BIOL
 JI Gene Ther. Mol. Biol.
 PY 2009
 VL 13B
 BP 308
 EP 315
 PG 8
 SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology;
    Medicine, Research & Experimental
 GA 575QR
 UT ISI:000276083000006
 ER
 
 PT J
 AU Sall, A
    Zhang, HFM
    Qiu, DX
    Liu, ZB
    Yuan, J
    Liu, Z
    Lim, T
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 AF Sall, Alhousseynou
    Zhang, Huifang M.
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    Liu, Zhongbin
    Yuan, Ji
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    Marchant, David
    McManus, Bruce
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 TI Pro-apoptotic activity of mBNIP-21 depends on its BNIP-2 and Cdc42GAP
    homology (BCH) domain and is enhanced by coxsackievirus B3 infection
 SO CELLULAR MICROBIOLOGY
 LA English
 DT Article
 ID CYTOCHROME-C RELEASE; CELL-DEATH; BCL-2 FAMILY; GENE-EXPRESSION; RHO
    GTPASES; BH3 DOMAIN; PROTEIN; MITOCHONDRIAL; ACTIVATION; PATHWAY
 AB P>Our previous study reported that mouse BNIP-21 (mBNIP-21) induces
    apoptosis through a mitochondria-dependent pathway. To map the
    functional domains of mBNIP-21, we performed mutational analyses and
    demonstrated that the BNIP-2 and Cdc42GAP homology (BCH) domain is
    required for apoptosis induction by mBNIP-21 targeting the mitochondria
    and inducing cytochrome c release. This pro-apoptotic activity was
    enhanced by coxsackievirus infection. However, deletion of the Bcl-2
    homology 3 (BH3)-like domain, a well-known cell 'death domain' in
    proapoptotic Bcl-2 family proteins, did not affect the activity of
    mBNIP-21. These data were further supported by transfection of a mouse
    Bax (mBax) mutant, whose BH3 was replaced by the mBNIP-21 BH3-like
    domain. This replacement significantly reduced the pro-apoptotic
    activity of mBax. We also found that the predicted calcium binding
    domain has no contribution to the mBNIP-21-induced apoptosis. Further
    mapping of the motifs of BCH domain demonstrated that deletion of the
    hydrophobic motif proximal to the C-terminal of the BCH significantly
    reduced its proapoptotic activity. These findings suggest that
    mBNIP-21, as a member of the BNIP subgroup of the Bcl-2-related
    proteins, functions without need of BH3 but its BCH domain is critical
    for its activity in inducing cell elongation, membrane protrusions and
    apoptotic cell death.
 C1 [Yang, Decheng] Univ British Columbia, St Pauls Hosp, Providence Heart & Lung Inst,Dept Pathol, iCapture Ctr, Vancouver, BC, Canada.
    Univ British Columbia, St Pauls Hosp, Providence Heart & Lung Inst,Lab Med, iCapture Ctr, Vancouver, BC, Canada.
 RP Yang, DC, Univ British Columbia, St Pauls Hosp, Providence Heart & Lung
    Inst,Dept Pathol, iCapture Ctr, Vancouver, BC, Canada.
 EM dyang@mrl.ubc.ca
 FU Canadian Institutes of Health Research ; Heart and Stroke Foundation ;
    IMPACT/CIHR ; Michael Smith Foundation of Health Research 
 FX We thank Dr Boon Chuan Low, The National University of Singapore for
    providing us with the human BNIP-2 antibody and Dr John C. Reed,
    Burnham Institute for Medical Research, CA, USA for the plasmid
    expressing Bax protein. We also thank Brian Wong for his assistance in
    the manuscript preparation. This work was supported by grants from the
    Canadian Institutes of Health Research and the Heart and Stroke
    Foundation of BC and Yukon. Dr Alhousseynou Sall is supported in part
    by the IMPACT/CIHR postdoctoral fellowship. Ji Yuan is supported by a
    Doctoral Research Award from the Canadian Institutes of Health Research
    and Michael Smith Foundation of Health Research. Zhen Liu is supported
    by a Doctoral Research Award from the Heart and Stroke Foundation of
    Canada.
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 NR 41
 TC 3
 PU WILEY-BLACKWELL PUBLISHING, INC
 PI MALDEN
 PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
 SN 1462-5814
 J9 CELL MICROBIOL
 JI Cell Microbiol.
 PD MAY
 PY 2010
 VL 12
 IS 5
 BP 599
 EP 614
 DI 10.1111/j.1462-5822.2009.01416.x
 PG 16
 SC Cell Biology; Microbiology
 GA 577LA
 UT ISI:000276223400004
 ER
 
 PT J
 AU Bao, XX
    Wang, B
    Zhang, JB
    Yan, T
    Yang, WP
    Jiao, FC
    Liu, J
    Wang, S
 AF Bao, Xuexiang
    Wang, Bin
    Zhang, Jinbei
    Yan, Ting
    Yang, Weiping
    Jiao, Fangchao
    Liu, Jing
    Wang, Shun
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 LA English
 DT Article
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 ID SEROTONIN-CONTAINING NEURONS; TRYPTOPHAN-HYDROXYLASE; SYSTEM; INSECTS;
    DOPAMINE; ISOFORM
 AB We previously demonstrated that tryptophan hydroxylase (TPH), the
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    5-HT-like immunoreactive neurons were also immunoreactive for TPH and
    bilaterally symmetrical; 83 neurons were found in each hemisphere of
    the brain and suboesophageal ganglion of adult Drosophila. This
    technique of colocalizing 5-HT and TPH revealed a larger number of
    serotonergic neurons in the brain and suboesophageal ganglion than that
    previous reported, thus updating our knowledge of the 5-HT neuronal
    system of Drosophila.
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 RP Bao, XX, NE Normal Univ, Sch Life Sci, Lab Insect Brain Neurobiol,
    Changchun 130024, Jilin, Peoples R China.
 EM xuexiangb@yahoo.com.cn
 FU National Natural Science Foundation of China [30470546]; Natural
    Science Foundation of Jilin Province [20030550-7]
 FX This work was supported by grants from the National Natural Science
    Foundation of China (grant no. 30470546) and the Natural Science
    Foundation of Jilin Province (grant no. 20030550-7).
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 PI NEW YORK
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 PY 2010
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 EP 59
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 PG 9
 SC Cell Biology
 GA 576QF
 UT ISI:000276160000005
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    Ferrara, N
 AF Bais, Carlos
    Wu, Xiumin
    Yao, Jenny
    Yang, Suya
    Crawford, Yongping
    McCutcheon, Krista
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    Vernes, Jean-Michel
    Eastham-Anderson, Jeffrey
    Haughney, Peter
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    Hagenbeek, Thijs
    Kasman, Ian
    Reslan, Hani Bou
    Ross, Jed
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    Carano, Richard A. D.
    Meng, Yu-Ju Gloria
    Hongo, Jo-Anne
    Stephan, Jean-Philippe
    Shibuya, Masabumi
    Ferrara, Napoleone
 TI PlGF Blockade Does Not Inhibit Angiogenesis during Primary Tumor Growth
 SO CELL
 LA English
 DT Article
 ID VEGFR1-ACTIVITY-INDEPENDENT METASTASIS FORMATION; HIGH-AFFINITY
    BINDING; FACTOR RECEPTOR-1; TYROSINE KINASE; IN-VIVO; VEGF; FLT-1;
    ANTIBODY; TARGETS; CANCER
 AB It has been recently reported that treatment with an anti-placenta
    growth factor (PlGF) antibody inhibits metastasis and primary tumor
    growth. Here we show that, although anti-PlGF treatment inhibited wound
    healing, extravasation of B16F10 cells, and growth of a tumor
    engineered to overexpress the PlGF receptor (VEGFR-1), neutralization
    of PlGF using four novel blocking antibodies had no significant effect
    on tumor angiogenesis in 15 models. Also, genetic ablation of the
    tyrosine kinase domain of VEGFR-1 in the host did not result in growth
    inhibition of the anti-VEGF-A sensitive or resistant tumors tested.
    Furthermore, combination of anti-PlGF with anti-VEGF-A antibodies did
    not result in greater antitumor efficacy than anti-VEGF-A monotherapy.
    In conclusion, our data argue against an important role of PlGF during
    primary tumor growth in most models and suggest that clinical
    evaluation of anti-PlGF antibodies may be challenging.
 C1 [Bais, Carlos; Wu, Xiumin; Yao, Jenny; Yang, Suya; Crawford, Yongping; McCutcheon, Krista; Tan, Christine; Kolumam, Ganesh; Vernes, Jean-Michel; Eastham-Anderson, Jeffrey; Haughney, Peter; Kowanetz, Marcin; Hagenbeek, Thijs; Kasman, Ian; Reslan, Hani Bou; Ross, Jed; Van Bruggen, Nick; Carano, Richard A. D.; Meng, Yu-Ju Gloria; Hongo, Jo-Anne; Stephan, Jean-Philippe; Shibuya, Masabumi; Ferrara, Napoleone] Genentech Inc, San Francisco, CA 94080 USA.
    [Shibuya, Masabumi] Tokyo Med & Dent Univ, Grad Sch Med & Dent, Dept Mol Oncol, Tokyo 1138510, Japan.
 RP Bais, C, Genentech Inc, 1 DNA Way, San Francisco, CA 94080 USA.
 EM bais@gene.com
    nf@gene.com
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 NR 49
 TC 17
 PU CELL PRESS
 PI CAMBRIDGE
 PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
 SN 0092-8674
 J9 CELL
 JI Cell
 PD APR 1
 PY 2010
 VL 141
 IS 1
 BP 166
 EP 177
 DI 10.1016/j.cell.2010.01.033
 PG 12
 SC Biochemistry & Molecular Biology; Cell Biology
 GA 577GS
 UT ISI:000276211100021
 ER
 
 PT J
 AU Zhao, JJ
    Lin, JH
    Lwin, T
    Yang, H
    Guo, JP
    Kong, W
    Dessureault, S
    Moscinski, LC
    Rezania, D
    Dalton, WS
    Sotomayor, E
    Tao, JG
    Cheng, JQ
 AF Zhao, Jian-Jun
    Lin, Jianhong
    Lwin, Tint
    Yang, Hua
    Guo, Jianping
    Kong, William
    Dessureault, Sophie
    Moscinski, Lynn C.
    Rezania, Dorna
    Dalton, William S.
    Sotomayor, Eduardo
    Tao, Jianguo
    Cheng, Jin Q.
 TI microRNA expression profile and identification of miR-29 as a
    prognostic marker and pathogenetic factor by targeting CDK6 in mantle
    cell lymphoma
 SO BLOOD
 LA English
 DT Article
 ID CHRONIC LYMPHOCYTIC-LEUKEMIA; HUMAN SOLID TUMORS; DOWN-REGULATION;
    POOR-PROGNOSIS; MESSENGER-RNA; BREAST-CANCER; LUNG-CANCER; STEM-CELLS;
    SIGNATURE; SURVIVAL
 AB Mantle cell lymphoma (MCL) is one of the most aggressive B-cell
    lymphomas. Although several protein-coding genes are altered,
    expression signature and importance of microRNA (miRNA) have not been
    well documented in this malignancy. Here, we performed miRNA-expression
    profile in 30 patients with MCL using a platform containing 515 human
    miRNAs. Eighteen miRNAs were down-regulated and 21 were up-regulated in
    MCL compared with normal B lymphocytes. The most frequently altered
    miRNAs are decrease of miR-29a/b/c, miR-142-3p/5p, and miR-150 and
    increase of miR-124a and miR-155. Notably, expression levels of miR-29
    family are associated with prognosis. The patients with significant
    downregulated miR-29 had short survival compared with those who express
    relatively high levels of miR-29. The prognostic value of miR-29 is
    comparable with the Mantle Cell Lymphoma International Prognostic
    Index. Furthermore, we demonstrate miR-29 inhibition of CDK6 protein
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    D1 overexpression is a primary event and exerts its function through
    activation of CDK4/CDK6, our results in primary MCL cells indicate that
    down-regulation of miR-29 could cooperate with cyclin D1 in MCL
    pathogenesis. Thus, our findings provide not only miRNA expression
    signature but also a novel prognostic marker and pathogenetic factor
    for this malignancy. (Blood. 2010;115(13):2630-2639)
 C1 [Zhao, Jian-Jun; Lin, Jianhong; Lwin, Tint; Yang, Hua; Guo, Jianping; Kong, William; Dessureault, Sophie; Moscinski, Lynn C.; Rezania, Dorna; Dalton, William S.; Sotomayor, Eduardo; Tao, Jianguo; Cheng, Jin Q.] Univ S Florida, Coll Med, H Lee Moffitt Canc Ctr & Res Inst, Tampa, FL 33612 USA.
 RP Tao, JG, Univ S Florida, Coll Med, H Lee Moffitt Canc Ctr & Res Inst,
    12902 Magnolia Dr, Tampa, FL 33612 USA.
 EM jianguo.tao@moffitt.org
    jin.cheng@moffitt.org
 FU National Institutes of Health [CA137041, CA107078]; Department of
    Defense [W81XWH-08-1-0444, W81XWH-08-2-0101, W81XWH-08-1-0116];
    Bankhead-Coley [09BB-05]; Leukemia Research Foundation ; Lymphoma
    Research Foundation 
 FX This work was supported by the National Institutes of Health (CA137041
    and CA107078), the Department of Defense (W81XWH-08-1-0444,
    W81XWH-08-2-0101, and W81XWH-08-1-0116), Bankhead-Coley (grant 09BB-05)
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    Foundation (S. D.).
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 NR 46
 TC 13
 PU AMER SOC HEMATOLOGY
 PI WASHINGTON
 PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
 SN 0006-4971
 J9 BLOOD
 JI Blood
 PD APR 1
 PY 2010
 VL 115
 IS 13
 BP 2630
 EP 2639
 DI 10.1182/blood-2009-09-243147
 PG 10
 SC Hematology
 GA 577DI
 UT ISI:000276201000012
 ER
 
 PT J
 AU Terhzaz, S
    Finlayson, AJ
    Stirrat, L
    Yang, JL
    Tricoire, H
    Woods, DJ
    Dow, JAT
    Davies, SA
 AF Terhzaz, Selim
    Finlayson, Andrew J.
    Stirrat, Laura
    Yang, JingLi
    Tricoire, Herve
    Woods, Debra J.
    Dow, Julian A. T.
    Davies, Shireen-A
 TI Cell-specific inositol 1,4,5 trisphosphate 3-kinase mediates epithelial
    cell apoptosis in response to oxidative stress in Drosophila
 SO CELLULAR SIGNALLING
 LA English
 DT Article
 DE H2O2; Stress; Mitochondria; Inositol phosphates; bcl-2
 ID 1,4,5-TRISPHOSPHATE 3-KINASES; REDOX REGULATION; MELANOGASTER; CALCIUM;
    MITOCHONDRIA; PATHWAY; GENE; EXPRESSION; OXIDASE; MECHANISMS
 AB Organismal stress responses to oxidative stress are relevant to ageing
    and disease and involve key cell-/tissue-specific signal transduction
    mechanisms. Using Drosophila, an established in vivo model for stress
    studies, we show that cell-specific inositol phosphate signalling
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    vertebrate kidney and liver) is a key epithelial sensor for organismal
    oxidative stress responses: precise targeting of either
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    reversibly modulates survival of stress-challenged adult flies. In
    vivo, targeted IP3K-1 directly increases H2O2 production, pro-apoptotic
    caspase-9 activity and mitochondrial membrane potential. The
    mitochondrial calcium load in tubule principal cells-assessed by
    luminescent and fluorescent genetically-encoded mitochondrial calcium
    reporters-is significantly increased by IP3K-1 under oxidative stress
    conditions, leading to apoptosis.
    The Drosophila orthologues of human apoptotic bcl-2 genes include debcl
    and buffy. Oxidative stress challenge does not modulate gene expression
    of either debcl or buffy in tubules; and altered debcl expression does
    not influence survival rates under oxidative stress challenge. Finally,
    targeted over-expression of either debcl or buffy to tubule principal
    cells does not impact on tubule caspase-9 activity. Thus, IP3K-1
    modulates epithelial cell apoptosis without involvement of bcl-2-type
    proteins. (C) 2010 Elsevier Inc. All rights reserved.
 C1 [Terhzaz, Selim; Finlayson, Andrew J.; Stirrat, Laura; Yang, JingLi; Dow, Julian A. T.; Davies, Shireen-A] Univ Glasgow, Fac Biomed & Life Sci, Glasgow G11 6NU, Lanark, Scotland.
    [Tricoire, Herve] Univ Paris 07, CNRS, Lab Genet Stress & Vieillissement, F-75205 Paris 13, France.
    [Woods, Debra J.] Pfizer Anim Hlth, Vet Med Res & Dev, Kalamazoo, MI USA.
 RP Davies, SA, Univ Glasgow, Fac Biomed & Life Sci, Glasgow G11 6NU,
    Lanark, Scotland.
 EM s.a.davies@bio.gla.ac.uk
 FU UK Biotechnology and Biological Sciences Research Council (BBSRC) ;
    Pfizer, Inc. USA 
 FX This work was funded by grants from the UK Biotechnology and Biological
    Sciences Research Council (BBSRC) and Pfizer, Inc. USA, to JATD and SD.
    We are very grateful to Dr L Quinn, Melbourne for UAS-debcl and -buffy
    lines; and we thank P. Cabrero and V. R. Chintapalli (Glasgow), for
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 NR 57
 TC 0
 PU ELSEVIER SCIENCE INC
 PI NEW YORK
 PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
 SN 0898-6568
 J9 CELL SIGNAL
 JI Cell. Signal.
 PD MAY
 PY 2010
 VL 22
 IS 5
 BP 737
 EP 748
 DI 10.1016/j.cellsig.2009.12.009
 PG 12
 SC Cell Biology
 GA 574JG
 UT ISI:000275984600004
 ER
 
 PT J
 AU Zhao, Y
    Shen, HY
    Chen, XY
    Xiong, RP
    Li, P
    Liu, P
    Yang, N
    Zhou, YG
 AF Zhao, Yan
    Shen, Hai-Ying
    Chen, Xing-Yun
    Xiong, Ren-Ping
    Li, Ping
    Liu, Ping
    Yang, Nan
    Zhou, Yuan-Guo
 TI Genetic Variations of Heat Shock Protein 84 in Mice Mediate Cellular
    Glucocorticoid Response
 SO CELLULAR PHYSIOLOGY AND BIOCHEMISTRY
 LA English
 DT Article
 DE Heat shock protein 90; Glucocorticoid receptor; Heat stress;
    Dexamethasone; Geldanamycin
 ID HSP90/HSP70-BASED CHAPERONE MACHINERY; ACUTE LYMPHOBLASTIC-LEUKEMIA;
    MOLECULAR-MECHANISMS; ATPASE ACTIVITY; RECEPTOR ISOFORMS; HUMAN HSP90;
    RESISTANCE; BINDING; HEAT-SHOCK-PROTEIN-90; EXPRESSION
 AB Heat shock protein 90 (Hsp90), encoded by hsp84 and hsp86 in mice, has
    been confirmed to modulate glucocorticoid receptor (GR) function;
    however, the contribution of Hsp90 in glucocorticoid (GC)
    sensibility/resistance has received less attention. Previously, we
    found that genetic variations of Hsp84 are related to differences in
    the in vivo GC-GR responses between BALB/c and C57BL/6 mice suffering
    from traumatic injury. To evaluate the modulation of Hsp84
    polymorphisms on the GC response, we used a cellular heat-stress injury
    (HSI) model combined with a transgene-plasmid infection approach and
    assessed HSI-induced cellular damage and GR nuclear translocation, with
    or without dexamethasone pretreatment. We demonstrated that after HSI,
    fibroblasts from the C57BL/6 line exhibit higher cellular survival,
    higher nuclear GR levels and lower lactate dehydrogenase activity
    compared to those from the BALB/c line. We showed that
    dexamethasone-rescued HSI-induced damage is accompanied by increasing
    nuclear GR levels in both lines. Importantly, this protection against
    HSI was greater in C57BL/6 fibroblasts and was resistant to
    geldanamycin, a selective inhibitor of Hsp90. Importantly, transfection
    of the hsp84-transgene from C57BL/6 mice increased the nuclear GR
    levels and lessened HSI-induced damage in BALB/c fibroblasts. Our data
    thereby demonstrate that Hsp84 from C57BL/6 mice modulates higher
    cellular GC-GR responsiveness. Copyright (C) 2010 S. Karger AG, Basel
 C1 [Zhao, Yan; Shen, Hai-Ying; Chen, Xing-Yun; Xiong, Ren-Ping; Li, Ping; Liu, Ping; Yang, Nan; Zhou, Yuan-Guo] Third Mil Med Univ, Ctr Mol Biol, State Key Lab Trauma Burn & Combined Injury, Inst Surg Res, Chongqing 400042, Peoples R China.
    [Zhao, Yan; Shen, Hai-Ying; Chen, Xing-Yun; Xiong, Ren-Ping; Li, Ping; Liu, Ping; Yang, Nan; Zhou, Yuan-Guo] Third Mil Med Univ, Daping Hosp, Chongqing 400042, Peoples R China.
 RP Zhou, YG, Third Mil Med Univ, Ctr Mol Biol, State Key Lab Trauma Burn &
    Combined Injury, Inst Surg Res, Chongqing 400042, Peoples R China.
 EM ygzhou@cta.cq.cn
 FU National Basic Research Program of China [2005CB522602]; National
    Natural Science Foundation of China [30470988, 30871170]
 FX This work was supported by the National Basic Research Program of China
    (No. 2005CB522602) and the National Natural Science Foundation of China
    (No. 30470988 and No. 30871170)
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 NR 40
 TC 0
 PU KARGER
 PI BASEL
 PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND
 SN 1015-8987
 J9 CELL PHYSIOL BIOCHEM
 JI Cell. Physiol. Biochem.
 PY 2010
 VL 25
 IS 4-5
 BP 359
 EP 366
 DI 10.1159/000303039
 PG 8
 SC Cell Biology; Physiology
 GA 574DK
 UT ISI:000275968600001
 ER
 
 PT J
 AU Huo, R
    Li, Z
    Lu, CC
    Xie, Y
    Wang, B
    Tu, YJ
    Hu, JT
    Xu, CQ
    Yang, BF
    Dong, DL
 AF Huo, Rong
    Li, Zhe
    Lu, Cui-Cui
    Xie, Yan
    Wang, Bin
    Tu, Yu-Jie
    Hu, Jun-Tao
    Xu, Chang-Qing
    Yang, Bao-Feng
    Dong, De-Li
 TI Inhibition of 2-Aminoethoxydiphenyl Borate-induced Rat Atrial Ectopic
    Activity by Anti-arrhythmic Drugs
 SO CELLULAR PHYSIOLOGY AND BIOCHEMISTRY
 LA English
 DT Article
 DE 2-aminoethoxydiphenyl borate; Anti-arrhythmic drugs; Ectopic activity;
    Atria
 ID CALCIUM-ENTRY CHANNELS; OPERATED CA2+ ENTRY; VENTRICULAR MYOCYTES;
    RECEPTOR FUNCTION; PACEMAKER CELLS; K+ CURRENTS; RELEASE; 2-APB; MOUSE;
    STIMULATION
 AB Background/Aims: 2-aminoethoxydiphenyl borate (2-APB) provokes
    spontaneous mechanical activity in isolated rat left atria. The present
    study is to characterize 2-APB-induced ectopic activity in rat atria
    and to investigate the inhibition of 2-APB-induced ectopic activity by
    anti-arrhythmic drugs. Methods: 2-APB-induced ectopic activity was
    measured through an isometric force transducer connected to a
    multichannel acquisition and analysis system. Intracellular [Ca2+](i)
    was measured with fluorescence laser scanning confocal microscopy.
    Voltage-dependent L-type Ca2+ currents were recorded by using
    patch-clamp technique. Results: 2-APB dose-dependently increased the
    ectopic activity of left atria at 1, 5, 10, 20, 50 mu M.
    Anti-arrhythmic drugs, quinidine (10 mu M), lidocaine (10 mu M),
    verapamil (5 mu M), and amiodarone (50 mu M, 100 mu M) inhibited
    2-APB-induced ectopic activity. 2-APB-induced ectopic activity was
    inhibited by Ca2+-free bath, Na+/Ca2+ exchanger blockers, 3',
    4'-dichlorobenzamil hydrochloride (DHC) and Ni2+, not by non-selective
    cation channel blocker Gd3+. 2-APB also induced ectopic contractions in
    ventricular tissue straps and the ectopic contractions were inhibited
    by quinidine, verapamil and DHC. Lidocaine, verapamil and DHC inhibited
    2-APB-induced increase of intracellular Ca2+ concentration in
    cardiomyocytes. Low molecular weight heparin inhibited phenylephrine
    (PE)-induced but not 2-APB - induced atria ectopic activity, and the
    pattern of 2-APB-induced ectopic activity was continuous, distinct from
    the discontinuous activity induced by PE. Conclusion: 2-APB-induced
    atria ectopic activity was inhibited by classic anti-arrhythmic drugs
    quinidine, lidocaine, verapamil, amiodarone, and Na+/Ca2+ exchanger
    blockers. It can be used for testing agents able to affect any of Na+,
    Ca2+ channel, Na+/Ca2+ exchanger without selectivity. Copyright (C)
    2010 S. Karger AG, Basel
 C1 [Huo, Rong; Li, Zhe; Lu, Cui-Cui; Xie, Yan; Wang, Bin; Tu, Yu-Jie; Hu, Jun-Tao; Yang, Bao-Feng; Dong, De-Li] Harbin Med Coll, Dept Pharmacol, Harbin 150081, Peoples R China.
    [Xu, Chang-Qing] Harbin Med Coll, Dept Pathophysiol, Harbin 150081, Peoples R China.
    Biopharmaceut Key Lab Heilongjiang Prov, Harbin, Peoples R China.
 RP Dong, DL, Harbin Med Coll, Dept Pharmacol, Baojian Rd 157, Harbin
    150081, Peoples R China.
 EM delidong2004@yahoo.com.cn
 FU National Natural Science Foundation of China [30873064]; National
    Excellent Doctoral Dissertation of PR China [2007B72]; Program for New
    Century Excellent Talents in University 
 FX This work was supported by National Natural Science Foundation of China
    (30873064), A Foundation for the Author of National Excellent Doctoral
    Dissertation of PR China (2007B72), and Program for New Century
    Excellent Talents in University.
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 NR 39
 TC 0
 PU KARGER
 PI BASEL
 PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND
 SN 1015-8987
 J9 CELL PHYSIOL BIOCHEM
 JI Cell. Physiol. Biochem.
 PY 2010
 VL 25
 IS 4-5
 BP 425
 EP 432
 DI 10.1159/000303047
 PG 8
 SC Cell Biology; Physiology
 GA 574DK
 UT ISI:000275968600008
 ER
 
 PT J
 AU Du, J
    Zhang, LJ
    Yang, Y
    Li, WX
    Chen, L
    Ge, YB
    Sun, CQ
    Zhu, YC
    Gu, L
 AF Du, Jun
    Zhang, Lijia
    Yang, Yu
    Li, Weixing
    Chen, Ling
    Ge, Yingbin
    Sun, Chongqi
    Zhu, Yichao
    Gu, Luo
 TI ATP Depletion-induced Actin Rearrangement Reduces Cell Adhesion via p38
    MAPK-HSP27 Signaling in Renal Proximal Tubule Cells
 SO CELLULAR PHYSIOLOGY AND BIOCHEMISTRY
 LA English
 DT Article
 DE Actin cytoskeleton; ATP depletion; Cell adhesion; Tubular epithelial
    cells; p38MAPK; HSP27
 ID EPITHELIAL-CELLS; PROTEIN-KINASE; ISCHEMIA; CYTOSKELETON; ACTIVATION;
    INJURY; FAILURE; HSP27; DEATH; PHOSPHORYLATION
 AB Ischemia causes desquamation of proximal tubular epithelial cells
    leading to acute renal failure. However, the molecular mechanisms
    underlying the detachment of proximal tubule cells remain unknown. In
    this study, we reported that ATP depletion resulted in actin
    polymerization, a shift of filamentous actin from weblike structure to
    fragmented parallel stress fibers, followed by a reduction of cellular
    adhesion ability. The pre-treatment with Jasplakinolide, an actin
    stabilizer, prevented ATP depletion-induced actin polymerization and
    reduction of cell adhesion, indicating that the cytoskeleton
    reorganization decreased the cellular adhesion ability. Furthermore,
    the ATP depletion markedly increased the levels of p38MAPK and HSP27
    phosphorylation with enhanced translocation of phosphorylated HSP27
    from cytoskeleton to cytoplasm. The inhibition of p38MAPK by SB203580
    blocked the ATP depletion to induce HSP27 phosphorylation and actin
    polymerization. These findings suggest that ischemia remodels
    filamentous actin leading to desquamation of proximal tubular
    epithelial cells through p38 MAPK-HSP27 signaling. Copyright (C) 2010
    S. Karger AG, Basel
 C1 [Zhu, Yichao; Gu, Luo] Nanjing Med Univ, Ctr Canc, Nanjing 210029, Peoples R China.
    [Du, Jun; Zhang, Lijia; Yang, Yu; Chen, Ling; Ge, Yingbin] Nanjing Med Univ, Dept Physiol, Nanjing 210029, Peoples R China.
    [Li, Weixing] Taizhou Polytech Coll, Dept Med, Taizhou, Peoples R China.
    [Sun, Chongqi] Nanjing Med Univ, Kangda Coll, Nanjing 210029, Peoples R China.
 RP Gu, L, Nanjing Med Univ, Ctr Canc, 140 HanZhong Rd, Nanjing 210029,
    Peoples R China.
 EM lgu@njmu.edu.cn
 FU National Natural Science Foundation of China [30872926]; China Ministry
    of Health [WKJ2005-2-02]
 FX This work was supported by grants from the National Natural Science
    Foundation of China (No 30872926) and from China Ministry of Health
    Grant (WKJ2005-2-02) to Dr. L Gu. J Du and L. J. Zhang contributed
    equally to this work.
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 NR 39
 TC 1
 PU KARGER
 PI BASEL
 PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND
 SN 1015-8987
 J9 CELL PHYSIOL BIOCHEM
 JI Cell. Physiol. Biochem.
 PY 2010
 VL 25
 IS 4-5
 BP 501
 EP 510
 DI 10.1159/000303055
 PG 10
 SC Cell Biology; Physiology
 GA 574DK
 UT ISI:000275968600016
 ER
 
 PT J
 AU Yang, Z
    Jiang, J
    Stewart, DM
    Qi, SK
    Yamane, K
    Li, JW
    Zhang, Y
    Wong, JM
 AF Yang, Ze
    Jiang, Jun
    Stewart, David M.
    Qi, Shankang
    Yamane, Kenichi
    Li, Jiwen
    Zhang, Yi
    Wong, Jiemin
 TI AOF1 is a histone H3K4 demethylase possessing demethylase
    activity-independent repression function
 SO CELL RESEARCH
 LA English
 DT Article
 DE AOF1; histone H3K4 demethylase; chromatin; repression; Zf-CW
 ID DOMAIN-CONTAINING PROTEINS; NONHISTONE PROTEINS; ANDROGEN-RECEPTOR;
    CRYSTAL-STRUCTURE; XENOPUS-OOCYTES; LSD1; METHYLATION; TRANSCRIPTION;
    DEACETYLASE; INTERPLAY
 AB LSD1 (KDM1 under the new nomenclature) was the first identified
    lysine-specific histone demethylase belonging to the flavin-dependent
    amine oxidase family. Here, we report that AOF1 (KDM1B under the new
    nomenclature), a mammalian protein related to LSD1, also possesses
    histone demethylase activity with specificity for H3K4me1 and H3K4me2.
    Like LSD1, the highly conserved SWIRM domain is required for its
    enzymatic activity. However, AOF1 differs from LSD1 in several aspects.
    First, AOF1 does not appear to form stable protein complexes containing
    histone deacetylases. Second, AOF1 is found to localize to chromosomes
    during the mitotic phase of the cell cycle, whereas LSD1 does not.
    Third, AOF1 represses transcription when tethered to DNA and this
    repression activity is independent of its demethylase activity.
    Structural and functional analyses identified its unique N-terminal
    Zf-CW domain as essential for the demethylase activity-independent
    repression function. Collectively, our study identifies AOF1 as the
    second histone demethylase in the family of flavin-dependent amine
    oxidases and reveals a demethylase-independent repression function of
    AOF1.
 C1 [Yang, Ze; Qi, Shankang; Li, Jiwen; Wong, Jiemin] E China Normal Univ, Inst Biomed Sci, Shanghai 200241, Peoples R China.
    [Yang, Ze; Qi, Shankang; Li, Jiwen; Wong, Jiemin] E China Normal Univ, Sch Life Sci, Shanghai 200241, Peoples R China.
    [Jiang, Jun] Third Mil Med Univ, Daping Hosp, Inst Surg Res, Dept Urol, Chongqing 400042, Peoples R China.
    [Stewart, David M.] Univ Texas MD Anderson Canc Ctr, Dept Genet, Houston, TX 77030 USA.
    [Yamane, Kenichi; Zhang, Yi] Howard Hughes Med Inst, Chapel Hill, NC 27599 USA.
    [Yamane, Kenichi; Zhang, Yi] Univ N Carolina, Chapel Hill, NC 27599 USA.
 RP Wong, JM, E China Normal Univ, Inst Biomed Sci, Shanghai 200241,
    Peoples R China.
 EM jmweng@bio.ecnu.edu.cn
 FU National Natural Science Foundation of China [90919025, 30871381];
    Ministry of Science and Technology of China [2009CB918402,
    2009CB825601]; Research Platform for Cell Signaling Networks from the
    Science and Technology Commission of Shanghai Municipality [06DZ22923]
 FX We thank Dr Ramin Shiekhattar (Wistar Institute, USA) for the
    baculoviruses expressing Flag-LSD1 and Drs Jianguo Song and Degui Chen
    (Shanghai Institute of Biochemistry and Cell Biology, China) for
    anti-HDAC1 antibody and H3K36me2 antibody, respectively. This study was
    partially supported by grants from the National Natural Science
    Foundation of China (90919025, 30871381), the Ministry of Science and
    Technology of China (2009CB918402, 2009CB825601) and the Research
    Platform for Cell Signaling Networks from the Science and Technology
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 J9 CELL RES
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 PD MAR
 PY 2010
 VL 20
 IS 3
 BP 276
 EP 287
 DI 10.1038/cr.2010.12
 PG 12
 SC Cell Biology
 GA 572GS
 UT ISI:000275816300005
 ER
 
 PT J
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    Liu, Bei
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    Shen, Yuankai
    Zuniga-Pflucker, Juan Carlos
    Aguila, Hector L.
    Goldschneider, Irving
    Li, Zihai
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 SO BLOOD
 LA English
 DT Article
 ID TRANSCRIPTION FACTOR XBP-1; UNFOLDED PROTEIN RESPONSE; PLASMA-CELL
    DIFFERENTIATION; BONE-MARROW; LYMPHOID PROGENITOR; ALPHA-4 INTEGRINS;
    STEM-CELLS; MICE; EXPRESSION; PRECURSOR
 AB Integrins contribute to lymphopoiesis, whereas Toll-like receptors
    (TLRs) facilitate the myeloid replenishment during inflammation. The
    combined role of TLRs and integrin on hematopoiesis remains unclear.
    gp96 (grp94, HSP90b1) is an endoplasmic reticulum master chaperone for
    multiple TLRs. We report herein that gp96 is also essential for
    expression of 14 hematopoietic system-specific integrins. Genetic
    deletion of gp96 thus enables us to determine the collective roles of
    gp96, integrins, and TLRs in hematopoiesis. We found that gp96-null
    hematopoietic stem cells could support long-term myelopoiesis. B-and
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 C1 [Staron, Matthew; Yang, Yi; Liu, Bei; Li, Janet; Shen, Yuankai; Aguila, Hector L.; Goldschneider, Irving; Li, Zihai] Univ Connecticut, Sch Med, Dept Immunol, Farmington, CT 06030 USA.
    [Zuniga-Pflucker, Juan Carlos] Univ Toronto, Dept Immunol, Sunnybrook Res Inst, Toronto, ON, Canada.
 RP Li, ZH, Univ Connecticut, Sch Med, Dept Immunol, MC 1601,263 Farmington
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 EM zihai@uchc.edu
 FU National Institutes of Health [AI070603, AI077283, 5T32AI007080];
    [RC1HL100556]
 FX This work was supported by the National Institutes of Health (grants
    AI070603, AI077283, and RC1HL100556; Z.L.). M.S. is supported in part
    by the National Institutes of Health (training grant 5T32AI007080).
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 NR 56
 TC 4
 PU AMER SOC HEMATOLOGY
 PI WASHINGTON
 PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
 SN 0006-4971
 J9 BLOOD
 JI Blood
 PD MAR 25
 PY 2010
 VL 115
 IS 12
 BP 2380
 EP 2390
 DI 10.1182/blood-2009-07-233031
 PG 11
 SC Hematology
 GA 574IF
 UT ISI:000275981900011
 ER
 
 PT J
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 SO BLOOD
 LA English
 DT Article
 ID COLORECTAL-CANCER; DOWN-REGULATION; CELLS; PROMOTER; TUMORIGENESIS;
    ACTIVATION; MECHANISMS; EXPRESSION; GENOME; TUMORS
 AB Eph receptors and their ephrin ligands are involved in normal
    hematopoietic development and tumorigenesis. Using methylated CpG
    island amplification/DNA promoter microarray, we identified several EPH
    receptor and EPHRIN genes as potential hypermethylation targets in
    acute lymphoblastic leukemia (ALL). We subsequently studied the DNA
    methylation status of the Eph/ephrin family by bisulfite
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    EPHB1, -B2, -B3, -B4, EFNA1, -A3, -A5, and EFNB1 and -B2 genes was
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    Expression analysis of EPHB4, EFNB2, and EFNA5 genes demonstrated that
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    promoter region of EPHB4 and demonstrated that promoter
    hypermethylation can result in EPHB4 transcriptional silencing.
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 C1 [Kuang, Shao-Qing; Fang, Zhi-Hong; Yang, Hui; Tong, Weigang; Garcia-Manero, Guillermo] Univ Texas MD Anderson Canc Ctr, Dept Leukemia, Houston, TX 77030 USA.
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 RP Garcia-Manero, G, Univ Texas MD Anderson Canc Ctr, Dept Leukemia, Box
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 EM ggarciam@mdanderson.org
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    Cancer Center Physician-Scientist Award ; Commonwealth Cancer
    Foundation for Research 
 FX This work was supported by a Leukemia SPORE (P50 CA100632) Career
    Development Award to S.-Q.K. and by National Cancer Institute grants
    CA100067 and CA105771, the Leukemia & Lymphoma Society of America, and
    an M. D. Anderson Cancer Center Physician-Scientist Award from the
    Commonwealth Cancer Foundation for Research (all to G.G.-M.).
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 NR 29
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 PI WASHINGTON
 PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
 SN 0006-4971
 J9 BLOOD
 JI Blood
 PD MAR 25
 PY 2010
 VL 115
 IS 12
 BP 2412
 EP 2419
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 PG 8
 SC Hematology
 GA 574IF
 UT ISI:000275981900015
 ER
 
 PT J
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 AF Yang, Chia-Ping Huang
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 LA English
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 DE taxol; epothilone B; CENP-E; BubR1; drug resistance; kinetochore;
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 ID MICROTUBULE-STABILIZING AGENTS; BETA-TUBULIN; KINETOCHORE LOCALIZATION;
    SPINDLE CHECKPOINT; TAXOL; PACLITAXEL; ANEUPLOIDY; DYNAMICS;
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 AB Centromere associated protein-E (CENP-E), a mitotic checkpoint protein,
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    spindle-assembly checkpoint have occurred in EpoB40 cells during the
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 C1 [Yang, Chia-Ping Huang; Liu, Lingling; Ikui, Amy E.; Horwitz, Susan Band] Albert Einstein Coll Med, Dept Mol Pharmacol, Bronx, NY 10467 USA.
 RP Yang, CPH, Albert Einstein Coll Med, Dept Mol Pharmacol, Bronx, NY
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 EM chia-ping.h.yang@einstein.yu.edu
 FU NIH [CA077263, CA124898]; National Foundation for Cancer Research ;
    Breast Cancer Research Foundation ; Department of Defense
    [W81XWH-04-1-0754]
 FX This work was supported by NIH CA077263, CA124898, the National
    Foundation for Cancer Research, the Breast Cancer Research Foundation
    (S. B. H.) and Department of Defense W81XWH-04-1-0754 (C. P. H. Y.).
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    Takeda, Kazuyoshi
    Hagiwara, Yoshiaki
    Maeda, Masahiro
    Segawa, Tatsuya
    Suyama, Masafumi
    Watanabe, Sumio
    Hino, Okio
 TI Antitumor activity of anti-C-ERC/mesothelin monoclonal antibody in vivo
 SO CANCER SCIENCE
 LA English
 DT Article
 ID ASBESTOS-RELATED MESOTHELIOMA; EXPRESSING TUMOR XENOGRAFTS;
    PANCREATIC-CANCER; N-ERC/MESOTHELIN; OVARIAN-CANCER; MOLECULAR-CLONING;
    IMMUNOTOXIN SS1P; EKER RAT; T-CELLS; MARKER
 AB Mesothelioma is an aggressive cancer often caused by chronic asbestos
    exposure, and its prognosis is very poor despite the therapies
    currently used. Due to the long latency period between asbestos
    exposure and tumor development, the worldwide incidence will increase
    substantially in the next decades. Thus, novel effective therapies are
    warranted to improve the prognosis. The ERC/mesothelin gene (MSLN) is
    expressed in wide variety of human cancers, including mesotheliomas,
    and encodes a precursor protein cleaved by proteases to generate
    C-ERC/mesothelin and N-ERC/mesothelin. In this study, we investigated
    the antitumor activity of C-ERC/mesothelin-specific mouse monoclonal
    antibody, 22A31, against tumors derived from a human mesothelioma cell
    line, ACC-MESO-4, in a xenograft experimental model using female BALB/c
    athymic nude mice. Treatment with 22A31 did not inhibit cell
    proliferation of ACC-MESO-4 in vitro; however, therapeutic treatment
    with 22A31 drastically inhibited tumor growth in vivo. 22A31 induced
    antibody-dependent cell-mediated cytotoxicity by natural killer (NK)
    cells, but not macrophages, in vitro. Consistently, the F(ab')(2)
    fragment of 22A31 did not inhibit tumor growth in vivo, nor did it
    induce antibody-dependent cell mediated cytotoxicity (ADCC) in vitro.
    Moreover, NK cell depletion diminished the antitumor effect of 22A31.
    Thus, 22A31 induced NK cell-mediated ADCC and exerted antitumor
    activity in vivo. 22A31 could have potential as a therapeutic tool to
    treat C-ERC/mesothelin-expressing cancers including mesothelioma.
    (Cancer Sci 2010; 101: 969-974)
 C1 [Inami, Koichi; Abe, Masaaki; Hagiwara, Yoshiaki; Hino, Okio] Juntendo Univ, Sch Med, Dept Pathol & Oncol, Tokyo 113, Japan.
    [Inami, Koichi; Suyama, Masafumi; Watanabe, Sumio] Juntendo Univ, Sch Med, Dept Gastroenterol, Tokyo 113, Japan.
    [Takeda, Kazuyoshi] Juntendo Univ, Sch Med, Dept Immunol, Tokyo 113, Japan.
    [Hagiwara, Yoshiaki; Maeda, Masahiro; Segawa, Tatsuya] Immunobiol Labs Co Ltd, Gunma, Japan.
 RP Hino, O, Juntendo Univ, Sch Med, Dept Pathol & Oncol, Tokyo 113, Japan.
 EM ohino@juntendo.ac.jp
 FU Ministry of Education, Culture, Sport, and Science and Technology,
    Government of Japan 
 FX We would like to thank Masumi Maruo, Hidehiro Okura, Sun Guo Dong, Wang
    Lu, Piao Xiang Hua, Kazu Shiomi, Danqing Zhang, Shuji Matsuoka,
    Toshiyuki Kobayashi, and members of the Department of Gastroenterology,
    Juntendo Hospital, for their help in the preparation of this study.
    This work was supported by a Grant-in-Aid for Cancer Research and
    Grants-in-Aid for Scientific Research from the Ministry of Education,
    Culture, Sports and Science and Technology of Japan and the Ministry of
    Health, Labor and Welfare of Japan. This study was partially supported
    by a consignment expense for the molecular imaging program on 'Research
    Base for PET Diagnosis' from the Ministry of Education, Culture, Sport,
    and Science and Technology, Government of Japan.
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 NR 49
 TC 1
 PU WILEY-BLACKWELL PUBLISHING, INC
 PI MALDEN
 PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
 SN 1347-9032
 J9 CANCER SCI
 JI Cancer Sci.
 PD APR
 PY 2010
 VL 101
 IS 4
 BP 969
 EP 974
 DI 10.1111/j.1349-7006.2009.01463.x
 PG 6
 SC Oncology
 GA 571CK
 UT ISI:000275728200021
 ER
 
 PT J
 AU Paudyal, P
    Paudyal, B
    Hanaoka, H
    Oriuchi, N
    Iida, Y
    Yoshioka, H
    Tominaga, H
    Watanabe, S
    Watanabe, S
    Ishioka, NS
    Endo, K
 AF Paudyal, Pramila
    Paudyal, Bishnuhari
    Hanaoka, Hirofumi
    Oriuchi, Noboru
    Iida, Yashuhiko
    Yoshioka, Hiroki
    Tominaga, Hideyuki
    Watanabe, Satoshi
    Watanabe, Shigeki
    Ishioka, Noriko S.
    Endo, Keigo
 TI Imaging and biodistribution of Her2/neu expression in non-small cell
    lung cancer xenografts with 64Cu-labeled trastuzumab PET
 SO CANCER SCIENCE
 LA English
 DT Article
 ID METASTATIC BREAST-CANCER; IN-SITU HYBRIDIZATION; PHASE-II TRIAL;
    MONOCLONAL-ANTIBODY; HER-2/NEU; LINES; IMMUNOHISTOCHEMISTRY;
    GEMCITABINE; CARCINOMAS; CYCLOTRON
 AB Non-small cell lung carcinomas (NSCLC) overexpress the Her2/neu gene in
    approximately 59% of cases. Trastuzumab, a humanized monoclonal
    antibody, interferes with Her2 signaling and is approved for the
    treatment of Her2/neu overexpressing breast cancer. However, its
    therapeutic use in Her2/neu overexpressing NSCLC remains obscure. The
    present study aimed to determine the role of 64 Cu-labeled trastuzumab
    positron emission tomography (PET) for non-invasive imaging of Her2/neu
    expression in NSCLC. Trastuzumab was conjugated with the bifunctional
    chelator 1, 4, 7, 10-tetraazacyclododecane-1, 4, 7, 10-tetraacetic acid
    (DOTA) and radiolabeled with Cu-64. The molecular specificity of
    DOTA-trastuzumab was determined in NSCLC cell lines with Her2/neu
    overexpression (NCI-H2170) and negative expression (NCI-H520). Imaging
    of Her2/neu expression was performed in NCI-H2170 tumor-bearing mice
    with 64 Cu-DOTA-trastuzumab PET and 64 Cu-DOTA-IgG. In vitro studies
    revealed specific binding of DOTA-trastuzumab in the Her2/neu positive
    NCI-H2170 cells, while no binding was seen in the Her2/neu negative
    NCI-H520 cell line. Biodistribution and PET studies revealed a
    significantly high accumulation of 64 CuDOTA-trastuzumab in the
    Her2/neu overexpressing NCI-H2170 tumor at 24 and 48 h post-injection
    (21.4 +/- 1.4% and 23.2 +/- 5.1% injection dose/gram (% ID/g),
    respectively). PET imaging of Her2/neu negative NCI-H520 tumors showed
    much less uptake of 64 CuDOTA- trastuzumab (4.0% ID/g). The NCI-H2170
    tumor uptake of 64 Cu-DOTA-trastuzumab was significantly higher than
    that of 64 Cu-DOTA-IgG (P < 0.0001). 64 Cu-DOTA-trastuzumab showed a
    very clear image of a Her2/neu positive tumor and appeared to be
    effective as a PET tracer for imaging of Her2/neu gene expression in
    NSCLC, suggesting its potential clinical use for identifying patients
    that might benefit from trastuzumab-based therapy. (Cancer Sci 2010;
    101: 1045-1050)
 C1 [Paudyal, Pramila; Paudyal, Bishnuhari; Oriuchi, Noboru; Yoshioka, Hiroki; Tominaga, Hideyuki; Endo, Keigo] Gunma Univ, Grad Sch Med, Dept Diagnost Radiol, Maebashi, Gunma, Japan.
    [Paudyal, Pramila; Paudyal, Bishnuhari; Oriuchi, Noboru; Yoshioka, Hiroki; Tominaga, Hideyuki; Endo, Keigo] Gunma Univ, Grad Sch Med, Dept Nucl Med, Maebashi, Gunma, Japan.
    [Watanabe, Satoshi; Watanabe, Shigeki; Ishioka, Noriko S.] Japan Atom Energy Agcy, Quantum Beam Sci Directorate, Takasaki, Gumma, Japan.
 RP Paudyal, P, Gunma Univ, Grad Sch Med, Dept Diagnost Radiol, Maebashi,
    Gunma, Japan.
 EM pramila@med.gunma-u.ac.jp
 FU Ministry of Education, Culture, Sports, Science and Technology of Japan 
 FX This work was supported by the 21st century COE program from the
    Ministry of Education, Culture, Sports, Science and Technology of Japan.
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 NR 35
 TC 3
 PU WILEY-BLACKWELL PUBLISHING, INC
 PI MALDEN
 PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
 SN 1347-9032
 J9 CANCER SCI
 JI Cancer Sci.
 PD APR
 PY 2010
 VL 101
 IS 4
 BP 1045
 EP 1050
 PG 6
 SC Oncology
 GA 571CK
 UT ISI:000275728200031
 ER
 
 PT J
 AU Tamaki, K
    Sasano, H
    Maruo, Y
    Takahashi, Y
    Miyashita, M
    Moriya, T
    Sato, Y
    Hirakawa, H
    Tamaki, N
    Watanabe, M
    Ishida, T
    Ohuchi, N
 AF Tamaki, Kentaro
    Sasano, Hironobu
    Maruo, Yohei
    Takahashi, Yayoi
    Miyashita, Minoru
    Moriya, Takuya
    Sato, Yasufumi
    Hirakawa, Hisashi
    Tamaki, Nobumitsu
    Watanabe, Mika
    Ishida, Takanori
    Ohuchi, Noriaki
 TI Vasohibin-1 as a potential predictor of aggressive behavior of ductal
    carcinoma in situ of the breast
 SO CANCER SCIENCE
 LA English
 DT Article
 ID NEGATIVE FEEDBACK REGULATOR; ANGIOGENESIS INHIBITOR; TUMOR
    ANGIOGENESIS; ENDOTHELIAL-CELLS; GROWTH-FACTOR; CANCER; EXPRESSION;
    BEVACIZUMAB; PATTERNS; GRADE
 AB Vasohibin-1 is a recently identified negative feedback regulator of
    angiogenesis induced by VEGF-A and bFGF. In this study, we first
    evaluated mRNA expression of vasohibin-1 and CD31 in 39 Japanese female
    breast carcinoma specimens including 22 invasive ductal carcinoma (IDC)
    and 17 ductal carcinoma in situ (DCIS) using a real-time quantitative
    RT-PCR (QRT-PCR) with LightCycler system. In addition, we also
    immunolocalized vasohibin-1 and CD31 and compared their
    immunoreactivity to nuclear grades and histological grades of 100
    carcinoma cases (50 IDC and 50 DCIS). There were no statistically
    significant differences of CD31 mRNA expression and the number of CD31
    positive vessels between DCIS and IDC (P = 0.250 and P = 0.191,
    respectively), whereas there was a statistically significant difference
    in vasohibin-1 mRNA expression and the number of vasohibin-1 positive
    vessels in DCIS and IDC (P = 0.022 and P <= 0.001, respectively). There
    was a significant positive correlation between vasohibin-1 mRNA level
    and Ki-67 labeling index in DCIS (r(2) = 0.293, P <= 0.001). In
    addition, vasohibin-1 mRNA expression was correlated with high nuclear
    and histological grades in DCIS cases and a significant positive
    correlation was detected between the number of vasohibin-1 positive
    vessels and Ki-67 labeling index or nuclear grade or Van Nuys
    classification of carcinoma cells (P <= 0.001, respectively). These
    results all indicate the possible correlation between aggressive
    biological features in DCIS including increased tumor cell
    proliferation and the status of neovascularization determined by
    vasohibin-1 immunoreactivity. (Cancer Sci 2010; 101: 1051-1058) (Cancer
    Sci 2010; 101: 1051-1058).
 C1 [Moriya, Takuya] Kawasaki Med Univ, Dept Pathol 2, Okayama, Japan.
    [Tamaki, Nobumitsu] Dept Breast Surg, Nahanishi Clin, Okinawa, Japan.
    [Tamaki, Kentaro; Miyashita, Minoru; Ishida, Takanori; Ohuchi, Noriaki] Tohoku Univ, Grad Sch Med, Dept Surg Oncol, Sendai, Miyagi 980, Japan.
    [Sasano, Hironobu; Maruo, Yohei; Takahashi, Yayoi; Miyashita, Minoru; Watanabe, Mika] Tohoku Univ Hosp, Dept Pathol, Tohoku, Miyagi, Japan.
    [Moriya, Takuya] Kawasaki Med Univ, Dept Pathol 2, Okayama, Japan.
    [Sato, Yasufumi] Tohoku Univ, Inst Dev Aging & Canc, Dept Vasc Biol, Sendai, Miyagi 980, Japan.
    [Hirakawa, Hisashi] Tohoku Kosai Hosp, Dept Surg, Tohoku, Miyagi, Japan.
    [Tamaki, Nobumitsu] Nahanishi Clin, Dept Breast Surg, Okinawa, Japan.
 RP Tamaki, K, Tohoku Univ, Grad Sch Med, Dept Surg Oncol, Sendai, Miyagi
    980, Japan.
 EM nahanisikenta@yahoo.co.jp
 FU Japanese Ministry of Health, Labour and Welfare for Researches on
    Intractable Diseases ; Risk Analysis Research on Food and
    Pharmaceuticals ; Development of Multidisciplinary Treatment Algorithm
    with Biomarkers and Modeling of the Decision-making Process with
    Artificial Intelligence for Primary Breast Cancer ; Japanese Ministry
    of Education, Culture, Sports, Science and Technology [18390109];
    Yasuda Medical Foundation 
 FX We appreciate Katsuhiko Ono, MT, for his excellent technical
    assistance. This work was partly supported by the grants from the
    Japanese Ministry of Health, Labour and Welfare for Researches on
    Intractable Diseases, Risk Analysis Research on Food and
    Pharmaceuticals, and Development of Multidisciplinary Treatment
    Algorithm with Biomarkers and Modeling of the Decision-making Process
    with Artificial Intelligence for Primary Breast Cancer. This work was
    also partly supported by Grant-in-Aid for Scientific Research
    (18390109) from the Japanese Ministry of Education, Culture, Sports,
    Science and Technology, and the Yasuda Medical Foundation.
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 NR 42
 TC 2
 PU WILEY-BLACKWELL PUBLISHING, INC
 PI MALDEN
 PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
 SN 1347-9032
 J9 CANCER SCI
 JI Cancer Sci.
 PD APR
 PY 2010
 VL 101
 IS 4
 BP 1051
 EP 1058
 PG 8
 SC Oncology
 GA 571CK
 UT ISI:000275728200032
 ER
 
 PT J
 AU Zhao, JX
    Ji, WQ
    Wu, J
    Chen, XH
    Cheng, XN
    Wang, JW
    Pang, YH
    Liu, SH
    Yang, QH
 AF Zhao, Ji-Xin
    Ji, Wan-Quan
    Wu, Jun
    Chen, Xin-Hong
    Cheng, Xue-Ni
    Wang, Jian-Wei
    Pang, Yu-Hui
    Liu, Shu-Hui
    Yang, Qun-Hui
 TI Development and identification of a wheat-Psathyrostachys huashanica
    addition line carrying HMW-GS, LMW-GS and gliadin genes
 SO GENETIC RESOURCES AND CROP EVOLUTION
 LA English
 DT Article
 DE Disomic addition line; GISH; PAGE; Psathyrostachys huashanica; Triticum
    aestivum
 ID GLUTENIN SUBUNIT GENES; STORAGE PROTEINS; CHROMOSOMAL LOCATION; ALLELIC
    VARIATION; AGROPYRON-ELONGATUM; TRITICUM-AESTIVUM; COMMON WHEAT; BREAD
    WHEAT; STRIPE-RUST; SDS-PAGE
 AB Psathyrostachys huashanica Keng, in the family Poaceae, subtribe
    Triticeae is an endangered and endemic species of China. It is
    characterized as Shaanxi, drought tolerant and fungus and disease
    resistant. In this paper, a wheat (Triticum aestivum L.)-P. huashanica
    disomic addition line "H9021-28-5" was developed using cytogenetics
    methods including SDS-PAGE, A-PAGE, and GISH. These investigations
    revealed that the chromosome number and configuration of "H9021-28-5"
    were 2n = 44 = 22 II. The mitotic and meiotic GISH analysis indicated
    that "H9021-28-5" contained 42 wheat chromosomes and a pair of P.
    huashanica chromosomes. The SDS-PAGE and A-PAGE analysis showed that
    "H9021-28-5" carried the HMW-GS, LMW-GS and gliadin genes of P.
    huashanica. The results suggest that these storage protein genes of P.
    huashanica had been transferred into common wheat. Development of this
    new germplasm is significant for enriching and improving wheat
    resources of storage proteins genes, and for continuing to exploit the
    advantageous genes of P. huashanica.
 C1 [Zhao, Ji-Xin; Ji, Wan-Quan; Wu, Jun; Chen, Xin-Hong; Wang, Jian-Wei; Pang, Yu-Hui; Liu, Shu-Hui; Yang, Qun-Hui] NW A & F Univ, Coll Agron, Yangling 712100, Shaanxi, Peoples R China.
    [Cheng, Xue-Ni] NW A & F Univ, Coll Life Sci, Yangling 712100, Shaanxi, Peoples R China.
 RP Chen, XH, NW A & F Univ, Coll Agron, Yangling 712100, Shaanxi, Peoples
    R China.
 EM cxh2089@126.com
 FU National Natural Science Foundation of China ; Ministry of Education
    [NCET-06-0862]; Major Innovation Project for Science and Technology of
    Shaanxi Province [2008ZDKG-07, 2008ZDGC-02]
 FX The authors thank Prof. Song Wei-ning and Dr. Zhang Xiao-ke at
    Northwest A & F University for critically reviewing the manuscript.
    This research was supported by the National Natural Science Foundation
    of China (No. 30771345), 'New Century Talents Support Scheme' project
    from Ministry of Education (No. NCET-06-0862), and '13115' Major
    Innovation Project for Science and Technology of Shaanxi Province (No.
    2008ZDKG-07, 2008ZDGC-02).
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 NR 44
 TC 0
 PU SPRINGER
 PI DORDRECHT
 PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
 SN 0925-9864
 J9 GENET RESOUR CROP EVOLUTION
 JI Genet. Resour. Crop Evol.
 PD MAR
 PY 2010
 VL 57
 IS 3
 BP 387
 EP 394
 DI 10.1007/s10722-009-9477-4
 PG 8
 SC Agronomy; Plant Sciences
 GA 567QC
 UT ISI:000275460700010
 ER
 
 PT J
 AU Zhang, C
    Wang, YS
    Wu, H
    Zhang, ZX
    Cai, Y
    Hou, HY
    Zhao, W
    Yang, XM
    Ma, JX
 AF Zhang, C.
    Wang, Y-S
    Wu, H.
    Zhang, Z-X
    Cai, Y.
    Hou, H-Y
    Zhao, W.
    Yang, X-M
    Ma, J-X
 TI Inhibitory efficacy of hypoxia-inducible factor 1 alpha short hairpin
    RNA plasmid DNA-loaded poly (D, L-lactide-co-glycolide) nanoparticles
    on choroidal neovascularization in a laser-induced rat model
 SO GENE THERAPY
 LA English
 DT Article
 DE poly (D, L-lactic/glycolic acid) nanoparticles; plasmid DNA; RNA
    interference; hypoxia-inducible factor 1 alpha
 ID RETINAL-PIGMENT EPITHELIUM; ENDOTHELIAL GROWTH-FACTOR;
    SHORT-INTERFERING RNAS; HUMAN RPE CELLS; MACULAR DEGENERATION;
    MAMMALIAN-CELLS; GENE DELIVERY; TARGETING HIF-1-ALPHA; DRUG-DELIVERY;
    BLOOD-FLOW
 AB The aim of this study was to evaluate the possibility of poly (D,
    L-lactide-co-glycolide) nanoparticle (NPs) as a gene vector for
    functional plasmid DNA (pDNA) and to investigate its inhibitory
    efficacy on experimental choroidal neovascularization (CNV). We
    developed intravitreal administered, hypoxia-inducible factor 1 alpha
    (HIF-1 alpha) short hairpin RNA and green fluorescent protein (GFP)
    co-expressed pDNA-loaded NPs (pshHIF-1 alpha NPs). CNV was induced by
    laser photocoagulation in 112 rats. The rats were then randomly
    assigned to be injected intravitreally with phosphate-buffered saline
    (PBS), blank NPs, naked pDNA, control pDNA NPs and pshHIF-1 alpha NPs,
    respectively, and non-injection group was set as the control.
    Immunofluorescence staining, fluorescein fundus angiography and
    histologic analysis were performed to evaluate the inhibitory efficacy
    on CNV. The results showed that the expression of GFP preferentially
    localized in the retinal pigment epithelium cell layer and lasted for 4
    weeks. The fluorescein leakage areas of CNV were significantly larger
    in the PBS, blank NPs, control pDNA NPs, non-injection group and naked
    pDNA group than in pshHIF-1 alpha NPs group (P<0.01). The mean
    thickness of the CNV lesions in the intravitreally pshHIF-1 alpha
    NPs-treated group was significantly smaller than other groups (P<0.01).
    No signs of functional or ultrastructural destruction in retina were
    detected. Therefore, pshHIF-1a NPs may act as a novel therapeutic
    option to transfer specific pDNA and inhibit the formation of
    experimental CNV. Gene Therapy (2010) 17, 338-351;
    doi:10.1038/gt.2009.158; published online 24 December 2009
 C1 [Zhang, C.; Wang, Y-S; Wu, H.; Zhang, Z-X; Cai, Y.; Hou, H-Y; Zhao, W.; Yang, X-M; Ma, J-X] Fourth Mil Med Univ, Xijing Hosp, Inst Ophthalmol Chinese PLA, Dept Ophthalmol, Xian 710032, Peoples R China.
 RP Wang, YS, Fourth Mil Med Univ, Xijing Hosp, Inst Ophthalmol Chinese
    PLA, Dept Ophthalmol, Xian 710032, Peoples R China.
 EM wangys@fmmu.edu.cn
    wuhxa@yahoo.com.cn
 FU National Natural Science Foundation of China [30371516, 30672291];
    Scientific Research Foundation for the Returned Overseas Chinese
    Scholars, State Education Ministry, China ; Alexander Von Humboldt
    Foundation in Germany [V8151/02085]
 FX This work was supported by grants from the National Natural Science
    Foundation of China (No. 30371516, No. 30672291) and the Scientific
    Research Foundation for the Returned Overseas Chinese Scholars, State
    Education Ministry, China (2004). The project was sponsored partly by
    the equipment donation from the Alexander Von Humboldt Foundation in
    Germany (to YSW, V8151/02085).
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 NR 79
 TC 0
 PU NATURE PUBLISHING GROUP
 PI LONDON
 PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
 SN 0969-7128
 J9 GENE THERAPY
 JI Gene Ther.
 PD MAR
 PY 2010
 VL 17
 IS 3
 BP 338
 EP 351
 DI 10.1038/gt.2009.158
 PG 14
 SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology;
    Genetics & Heredity; Medicine, Research & Experimental
 GA 566SE
 UT ISI:000275392600005
 ER
 
 PT J
 AU Krykbaev, R
    Fitz, LJ
    Reddy, PS
    Winkler, A
    Xuan, DJ
    Yang, XK
    Fleming, M
    Wolf, SF
 AF Krykbaev, Rustem
    Fitz, Lori J.
    Reddy, Padmalatha S.
    Winkler, Aaron
    Xuan, Dejun
    Yang, Xiaoke
    Fleming, Margaret
    Wolf, Stanley F.
 TI Evolutionary and biochemical differences between human and monkey
    acidic mammalian chitinases
 SO GENE
 LA English
 DT Article
 DE Acidic Mammalian Chitinase; Ortholog; Pseudoortholog; Pseudogene;
    Macaca gene; Enzyme
 ID GLYCOSYL HYDROLASES; MOLECULAR-CLONING; CRYSTAL-STRUCTURE;
    CHITOTRIOSIDASE; INSIGHTS; FAMILY; SITE; RESIDUES; PROTEIN; ASTHMA
 AB Acidic mammalian chitinase (AMCase), an enzyme implicated in the
    pathology of asthma, is capable of chitin cleavage at a low pH optimum.
    The corresponding gene (CHIA) can be found in genome databases of a
    variety of mammals, but the enzyme properties of only the human and
    mouse proteins were extensively studied. We wanted to compare enzymes
    of closely related species, such as humans and macaques. In our attempt
    to study macaque AMCase, we searched for CHIA-like genes in human and
    macaque genomes. We found that both genomes contain several additional
    CHIA-like sequences. In humans, CHIA-L1 (hCHIA-L1) is an apparent
    pseudogene and has the highest homology to CHIA. To determine which of
    the two genes is functional in monkeys, we assessed their tissue
    expression levels. In our experiments, CHIA-L1 expression was not
    detected in human stomach tissue, while CHIA was expressed at high
    levels. However in the, cynomolgus macaque stomach tissue, the
    expression pattern of these two genes was reversed: CHIA-L1 was
    expressed at high levels and CHIA was undetectable. We hypothesized
    that in macaques CHIA-L1 (mCHIAL1), and not CHIA, is a gene encoding an
    acidic chitinase, and cloned it, using the sequence of human CHIA-Ll as
    a guide for the primer design. We named the new enzyme MACase (Macaca
    Acidic Chitinase) to emphasize its differences from AMCase. MACase
    shares a similar tissue expression pattern and pH optimum with human
    AMCase, but is 50 times more active in our enzymatic activity assay.
    DNA sequence of the mCHIA-L1 has higher percentage identity to the
    human pseudogene hCHIA-L1 (91.7%) than to hCHIA (84%). Our results
    suggest alternate evolutionary paths for human and monkey acidic
    chitinases. (C) 2009 Elsevier B.V. All rights reserved.
 C1 [Krykbaev, Rustem; Fitz, Lori J.; Winkler, Aaron; Xuan, Dejun; Yang, Xiaoke; Fleming, Margaret; Wolf, Stanley F.] Pfizer Biotherapeut Res & Dev, Dept Inflammat & Immunol, Cambridge, MA 02140 USA.
    [Reddy, Padmalatha S.] Pfizer Biotherapeut Res & Dev, Dept Global Biotherapeut Technol, Cambridge, MA 02140 USA.
 RP Krykbaev, R, Pfizer Biotherapeut Res & Dev, Dept Inflammat & Immunol,
    200 CambridgePk Dr, Cambridge, MA 02140 USA.
 EM rkrykbaev@wyeth.com
    lfitz@wyeth.com
    preddy@wyeth.com
    awinkler@wyeth.com
    dxuan@wyeth.com
    xyang@wyeth.com
    mfleming@wyeth.com
    swolf@wyeth.com
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 NR 31
 TC 1
 PU ELSEVIER SCIENCE BV
 PI AMSTERDAM
 PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
 SN 0378-1119
 J9 GENE
 JI Gene
 PD MAR 1
 PY 2010
 VL 452
 IS 2
 BP 63
 EP 71
 DI 10.1016/j.gene.2009.12.005
 PG 9
 SC Genetics & Heredity
 GA 566GY
 UT ISI:000275359300003
 ER
 
 PT J
 AU Wang, ZT
    Li, XY
    Li, ZY
    Yang, L
    Sasaki, Y
    Wang, S
    Zhou, LM
    Araki, S
    Mezawa, M
    Takai, H
    Ogata, Y
 AF Wang, Zhitao
    Li, Xinyue
    Li, Zhengyang
    Yang, Li
    Sasaki, Yoko
    Wang, Shuang
    Zhou, Liming
    Araki, Shouta
    Mezawa, Masaru
    Takai, Hideki
    Ogata, Yorimasa
 TI Effects of inorganic polyphosphate on bone sialoprotein gene expression
 SO GENE
 LA English
 DT Article
 DE Bone sialoprotein; Inorganic polyphosphate; Osteoblasts; Transcription
 ID RAT BSP GENE; CELL-FREE SYSTEM; RESPONSE ELEMENT; PHOSPHATIDYLINOSITOL
    3-KINASE; OSTEOBLAST DIFFERENTIATION; PROXIMAL PROMOTER;
    GROWTH-FACTORS; MESSENGER-RNA; HUMAN BREAST; IN-VITRO
 AB Inorganic polyphosphate (poly(P)) is a biopolymer existing in almost
    all cells and tissues. The biological functions of poly(P) in
    micro-organisms have been extensively investigated in studies of
    poly(P) in eukaryotic cells, especially osteoblasts, and are
    increasing. Bone sialoprotein (BSP) is thought to function in bone
    mineralization, and is selectively expressed by differentiated
    osteoblasts. In this study, application of sodium phosphate glass type
    25 (SPG25, 12.5 and 125 mu M) increased BSP mRNA levels at 12 h in
    osteoblast-like ROS 17/2.8 cells. In transient transfection assay, 12.5
    and 125 mu M SPG25 increased luciferase activities of the constructs
    pLUC3 (-116 to +60), pLUC4 (-425 to +60), pLUC5 (-801 to +60) and pLUC6
    (-938 to +60). Introduction of 2 bp mutations to the luciferase
    constructs showed that the effects of SPG25 were mediated by a FGF2
    response element (FRE) and a homeodomain protein binding site (HOX).
    Luciferase activities induced by SPG25 were blocked by tyrosine kinase
    inhibitor herbimycine A. MAP kinase kinase inhibitor U0126,
    PI3-kinase/Akt inhibitor LY249002 and inorganic phosphate transport
    inhibitor foscarnet. Gel shift analyses showed that both 12.5 and 125
    mu M SPG25 increased nuclear protein binding to FRE and HOX elements.
    These studies demonstrate that SPG25 stimulates BSP transcription by
    targeting FRE and HOX elements in the proximal promoter of the rat BSP
    gene. (C) 2010 Elsevier B.V. All rights reserved.
 C1 [Wang, Zhitao; Li, Xinyue; Li, Zhengyang; Yang, Li; Sasaki, Yoko; Wang, Shuang; Zhou, Liming; Araki, Shouta; Mezawa, Masaru; Takai, Hideki; Ogata, Yorimasa] Nihon Univ, Sch Dent Matsudo, Dept Periodontol, Chiba 2718587, Japan.
    [Wang, Zhitao; Li, Xinyue; Li, Zhengyang; Yang, Li] Tianjin Stomatol Hosp, Tianjin, Peoples R China.
    [Wang, Shuang] Tianjin Med Univ, Stomatol Coll, Tianjin, Peoples R China.
    [Takai, Hideki; Ogata, Yorimasa] Nihon Univ, Sch Dent Matsudo, Res Inst Oral Sci, Chiba 2718587, Japan.
 RP Ogata, Y, Nihon Univ, Sch Dent Matsudo, Dept Periodontol, Chiba
    2718587, Japan.
 EM ogata.yorimasa@nihon-u.ac.jp
 FU Ministry of Education, Culture, Sports, Science, and Technology (MEXT)
    [20082012]; Nihon University Multidisciplinary Research [2009-2010]
 FX This work was supported in part by a Grant from the Supporting Project
    for Strategic Research in Private Universities by the Ministry of
    Education, Culture, Sports, Science, and Technology (MEXT), 20082012,
    and Nihon University Multidisciplinary Research Grant for 2009-2010.
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 NR 60
 TC 1
 PU ELSEVIER SCIENCE BV
 PI AMSTERDAM
 PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
 SN 0378-1119
 J9 GENE
 JI Gene
 PD MAR 1
 PY 2010
 VL 452
 IS 2
 BP 79
 EP 86
 DI 10.1016/j.gene.2009.12.010
 PG 8
 SC Genetics & Heredity
 GA 566GY
 UT ISI:000275359300005
 ER
 
 PT J
 AU Shen, L
    Liu, XW
    Hou, WG
    Yang, GD
    Wu, YS
    Zhang, R
    Li, X
    Che, HL
    Lu, ZF
    Zhang, YQ
    Liu, XP
    Yao, LB
 AF Shen, Lan
    Liu, Xuewu
    Hou, Wugang
    Yang, Guodong
    Wu, Yousheng
    Zhang, Rui
    Li, Xia
    Che, Honglei
    Lu, Zifan
    Zhang, Yuanqiang
    Liu, Xinping
    Yao, Libo
 TI NDRG2 is highly expressed in pancreatic beta cells and involved in
    protection against lipotoxicity
 SO CELLULAR AND MOLECULAR LIFE SCIENCES
 LA English
 DT Article
 DE NDRG2; Pancreatic beta cell; Protein kinase Akt; Free fatty acid;
    Apoptosis
 ID ENDOPLASMIC-RETICULUM STRESS; DOWNSTREAM-REGULATED GENE-2; NITRIC-OXIDE
    SYNTHASE; FREE FATTY-ACIDS; INDUCED APOPTOSIS; ER STRESS; PROTEIN; AKT;
    TISSUES; CANCER
 AB The N-myc downstream-regulated gene 2 (NDRG2) is involved in cell
    differentiation and apoptosis, but its function in the pancreas remains
    to be established. Herein we examine the expression and function of
    NDRG2 in the endocrine pancreas. NDRG2 immunoreactivity was localized
    mainly in the cytoplasm of pancreatic beta cells. When beta-TC3 cells
    were exposed chronically to high levels of free fatty acid (FFA), cell
    viability was impaired, and Akt and NDRG2 phosphorylation were reduced.
    NDRG2 is a potential substrate of protein kinase Akt. Overexpression of
    constitutively active Akt enhanced NDRG2 phosphorylation and abolished
    the apoptosis induced by FFA in beta-TC3 cells, whereas NDRG2
    knock-down attenuated Akt-mediated protection of beta cells against
    fatty acid-triggered apoptosis. Collectively, these data indicate that
    NDRG2 acts as a key molecule in pancreatic beta cells and is involved
    in the Akt-mediated protection of beta cells against lipotoxicity.
 C1 [Shen, Lan; Liu, Xuewu; Yang, Guodong; Wu, Yousheng; Zhang, Rui; Li, Xia; Che, Honglei; Lu, Zifan; Liu, Xinping; Yao, Libo] Fourth Mil Med Univ, State Key Lab Canc Biol, Dept Biochem & Mol Biol, Xian 710032, Peoples R China.
    [Hou, Wugang; Zhang, Yuanqiang] Fourth Mil Med Univ, Dept Histol & Embryol, Xian 710032, Peoples R China.
    [Hou, Wugang] Fourth Mil Med Univ, Xijing Hosp, Dept Anesthesiol, Xian 710032, Peoples R China.
 RP Yao, LB, Fourth Mil Med Univ, State Key Lab Canc Biol, Dept Biochem &
    Mol Biol, 17 Chang Le W Rd, Xian 710032, Peoples R China.
 EM lanshen@fmmu.edu.cn
    bioyao@fmmu.edu.cn
 FU National Natural Science Foundation of China [30600314, 30670303,
    30830054, 30801309, 30170465]
 FX This work was supported by grants from the National Natural Science
    Foundation of China (nos. 30600314, 30670303, 30830054, 30801309 and
    30170465). We thank members of our laboratory for helpful discussions.
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 NR 38
 TC 0
 PU BIRKHAUSER VERLAG AG
 PI BASEL
 PA VIADUKSTRASSE 40-44, PO BOX 133, CH-4010 BASEL, SWITZERLAND
 SN 1420-682X
 J9 CELL MOL LIFE SCI
 JI Cell. Mol. Life Sci.
 PD APR
 PY 2010
 VL 67
 IS 8
 BP 1371
 EP 1381
 DI 10.1007/s00018-010-0258-1
 PG 11
 SC Biochemistry & Molecular Biology; Cell Biology
 GA 569VZ
 UT ISI:000275632100013
 ER
 
 PT J
 AU Yang, PH
    Xing, L
    Tang, C
    Jia, WH
    Zhao, ZP
    Liu, K
    Gao, X
    Wang, XL
 AF Yang, Penghui
    Xing, Li
    Tang, Chong
    Jia, Weihong
    Zhao, Zhongpeng
    Liu, Kun
    Gao, Xiao
    Wang, Xiliang
 TI Response of BALB/c mice to a monovalent influenza A (H1N1) 2009 split
    vaccine
 SO CELLULAR & MOLECULAR IMMUNOLOGY
 LA English
 DT Article
 DE BALB/c mice; influenza; influenza A (H1N1); split vaccine
 ID ANIMAL-MODELS; A/H5N1 VACCINE; VIRUS-VACCINE; H5N1 VACCINE;
    IMMUNOGENICITY; SAFETY; ANTIGENS; ANTIBODY; IMMUNITY; FERRETS
 AB The novel influenza A (H1N1) 2009 virus has emerged to cause the first
    pandemic of the twenty-first century. Disease outbreaks caused by the
    influenza A (H1N1) virus have prompted concerns about the potential for
    a pandemic and have driven the development of vaccines against this
    subtype of influenza A. In this study, we developed a monovalent
    influenza A (H1N1) split vaccine and evaluated its effects in BALB/c
    mice. Mice were immunized subcutaneously with 2 doses of the vaccine
    containing hemagglutinin (HA) alone or HA plus an aluminum hydroxide
    (Al(OH)(3)) adjuvant. Immunization with varying doses of HA (3.75, 7.5,
    15, 30, 45 or 60 mu g) was performed to induce the production of
    neutralizing antibodies. The vaccine elicited strong hemagglutination
    inhibition (HI) and microneutralization, and addition of the adjuvant
    augmented the antibody response. A preliminary safety evaluation showed
    that the vaccine was not toxic at large doses (0.5 ml containing 60 mu
    g HA+600 pg Al(OH)(3) or 60 mu g HA). Moreover, the vaccine was found
    to be safe at a dose of 120 mu g HA+ 1200 pg Al(OH)(3) or 120 mu g HA
    in 1.0 ml in rats. In conclusion;, the present study provides support
    for the clinical evaluation of influenza A (H1N1) vaccination as a
    public health intervention to mitigate a possible pandemic.
    Additionally, our findings support the further evaluation of the
    vaccine used in this study in primates or humans. Cellular & Molecular
    Immunology (2010) 7, 116-122; doi: 10.1038/cmi.2009.116; published
    online 1 February 2010
 C1 [Wang, Xiliang] Beijing Inst Microbiol & Epidemiol, Dept Immunol, State Key Lab Pathogen & Biosecur, Beijing 100071, Peoples R China.
 RP Wang, XL, Beijing Inst Microbiol & Epidemiol, Dept Immunol, State Key
    Lab Pathogen & Biosecur, 20 Dongdajie St, Beijing 100071, Peoples R
    China.
 EM xiliangw@yahoo.com
 FU National Scientific and Technical Supporting Program of China
    [2009CB522102]; National Programs for High Technology Research and
    Development of China [2006AA02Z450]
 FX We thank Hualan Vaccine Inc. (Xinxiang, Henan, China) for providing the
    influenza A (H1N1) split vaccine. We are grateful to Dr H. Fen-Tian for
    his critical reading of the manuscript. This work was carried out in
    part with funding from the National Scientific and Technical Supporting
    Program of China (2009CB522102) and National Programs for High
    Technology Research and Development of China (2006AA02Z450). No other
    potential conflict of interest relevant to this article exists.
 CR *WHO, 2009, SIT UPD INFL H1N1
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 NR 34
 TC 2
 PU NATURE PUBLISHING GROUP
 PI NEW YORK
 PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
 SN 1672-7681
 J9 CELL MOL IMMUNOL
 JI Cell. Mol. Immunol.
 PD MAR
 PY 2010
 VL 7
 IS 2
 BP 116
 EP 122
 DI 10.1038/cmi.2009.116
 PG 7
 SC Immunology
 GA 567AK
 UT ISI:000275414400007
 ER
 
 PT J
 AU Gao, LR
    Xu, RY
    Zhang, NK
    Chen, Y
    Wang, ZG
    Zhu, ZM
    Fei, YX
    Cao, Y
    Xu, HT
    Yang, Y
 AF Gao, Lian Ru
    Xu, Ru Yi
    Zhang, Ning Kun
    Chen, Yu
    Wang, Zhi Guo
    Zhu, Zhi Ming
    Fei, Yu Xing
    Cao, Yi
    Xu, Hong Tao
    Yang, Ye
 TI Increased Apelin Following Bone Marrow Mononuclear Cell Transplantation
    Contributes to the Improvement of Cardiac Function in Patients With
    Severe Heart Failure
 SO CELL TRANSPLANTATION
 LA English
 DT Article
 DE Cell transplantation; Apelin; Heart failure; Paracrine
 ID MESENCHYMAL STEM-CELLS; ORPHAN RECEPTOR APJ; MYOCARDIAL-INFARCTION;
    PROGENITOR CELLS; LIGAND; TRANSDIFFERENTIATION; CARDIOMYOCYTES;
    REGENERATION; SECRETION; TRIAL
 AB We previously reported that intracoronary implantation of bone marrow
    mononuclear cells (BMMC) into ischemic hearts improved cardiac function
    after myocardial infarction. However, the mechanisms have not been
    elucidated. The present study investigates whether apelin, a newly
    described inotropic peptide with important cardiovascular regulatory
    properties, contributes to the functional improvement in patients with
    severe heart failure after cell transplantation. Forty consecutive
    patients with severe heart failure secondary to myocardial infarction
    were assigned to the BMMC therapy group or the standard medication
    group according to each patient's decision on a signed consent
    document. In 20 patients intracoronary cell infusion was performed, and
    another 20 patients were matched to receive standard medication as
    therapeutic Controls. An additional 20 healthy subjects were designated
    as normal controls. Clinical manifestations, echocardiograms, and
    biochemical assays were recorded. Plasma apelin and brain natriuretic
    protein (BNP) levels were determined by enzyme immunoassay. Baseline
    levels of plasma apelin were significantly lower in all heart failure
    patients compared to normal Subjects. In patients who underwent cell
    transplantation, apelin increased significantly front 3 to 21 days
    after operation, followed by significant improvement in cardiac
    function. In parallel, BNP varied inversely with the increase of
    apelin. In patients receiving standard medical treatment, apelin
    remained at a lower level. Our findings indicated that increased apelin
    levels following cell therapy may act as a paracrine mediator produced
    front BMMCs and play an important role in the treatment of heart
    failure through autocrine and paracrine mechanisms.
 C1 [Gao, Lian Ru; Zhang, Ning Kun; Chen, Yu; Wang, Zhi Guo; Zhu, Zhi Ming; Fei, Yu Xing; Cao, Yi; Xu, Hong Tao; Yang, Ye] Navy Gen Hosp, Dept Cardiol, Beijing 100037, Peoples R China.
    [Xu, Ru Yi] Chinese Peoples Liberat Army Gen Hosp, Dept Geriatr Cardiol, Beijing, Peoples R China.
 RP Gao, LR, Navy Gen Hosp, Dept Cardiol, 6 Fucheng Rd, Beijing 100037,
    Peoples R China.
 EM lianru@yahoo.com.cn
 FU National Advanced Technology Development the Plan of China
    [2006AA02Z469]
 FX This study was supported by a grant of the National Advanced Technology
    Development the Plan of China (863 plan) (2006AA02Z469). We thank Dr.
    Joel S. Karliner, Professor of Medicine, University of California San
    Francisco, and Associate Chief of Medicine for Research, Department of
    Veterans Affairs Medical Center, University of California San
    Francisco, USA for valuable comments and helpful suggestions in writing
    and revising this manuscript.
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 NR 29
 TC 4
 PU COGNIZANT COMMUNICATION CORP
 PI ELMSFORD
 PA 3 HARTSDALE ROAD, ELMSFORD, NY 10523-3701 USA
 SN 0963-6897
 J9 CELL TRANSPLANT
 JI Cell Transplant.
 PY 2009
 VL 18
 IS 12
 BP 1311
 EP 1318
 DI 10.3727/096368909X474843
 PG 8
 SC Cell & Tissue Engineering; Medicine, Research & Experimental;
    Transplantation
 GA 563PY
 UT ISI:000275146400005
 ER
 
 PT J
 AU Goldberg, AD
    Banaszynski, LA
    Noh, KM
    Lewis, PW
    Elsaesser, SJ
    Stadler, S
    Dewell, S
    Law, M
    Guo, XY
    Li, X
    Wen, DC
    Chapgier, A
    DeKelver, RC
    Miller, JC
    Lee, YL
    Boydston, EA
    Holmes, MC
    Gregory, PD
    Greally, JM
    Rafii, S
    Yang, CW
    Scambler, PJ
    Garrick, D
    Gibbons, RJ
    Higgs, DR
    Cristea, IM
    Urnov, FD
    Zheng, DY
    Allis, CD
 AF Goldberg, Aaron D.
    Banaszynski, Laura A.
    Noh, Kyung-Min
    Lewis, Peter W.
    Elsaesser, Simon J.
    Stadler, Sonja
    Dewell, Scott
    Law, Martin
    Guo, Xingyi
    Li, Xuan
    Wen, Duancheng
    Chapgier, Ariane
    DeKelver, Russell C.
    Miller, Jeffrey C.
    Lee, Ya-Li
    Boydston, Elizabeth A.
    Holmes, Michael C.
    Gregory, Philip D.
    Greally, John M.
    Rafii, Shahin
    Yang, Chingwen
    Scambler, Peter J.
    Garrick, David
    Gibbons, Richard J.
    Higgs, Douglas R.
    Cristea, Ileana M.
    Urnov, Fyodor D.
    Zheng, Deyou
    Allis, C. David
 TI Distinct Factors Control Histone Variant H3.3 Localization at Specific
    Genomic Regions
 SO CELL
 LA English
 DT Article
 ID ZINC-FINGER NUCLEASES; EMBRYONIC STEM-CELLS; REPEAT-CONTAINING RNA;
    ATR-X SYNDROME; MAMMALIAN TELOMERES; SYNDROME PROTEIN; GENE-EXPRESSION;
    POLYMERASE-II; DNA-SYNTHESIS; ES CELLS
 AB The incorporation of histone H3 variants has been implicated in the
    epigenetic memory of cellular state. Using genome editing with
    zinc-finger nucleases to tag endogenous H3.3, we report genome-wide
    profiles of H3 variants in mammalian embryonic stem cells and neuronal
    precursor cells. Genome-wide patterns of H3.3 are dependent on amino
    acid sequence and change with cellular differentiation at
    developmentally regulated loci. The H3.3 chaperone Hira is required for
    H3.3 enrichment at active and repressed genes. Strikingly, Hira is not
    essential for localization of H3.3 at telomeres and many transcription
    factor binding sites. Immunoaffinity purification and mass spectrometry
    reveal that the proteins Atrx and Daxx associate with H3.3 in a
    Hira-independent manner. Atrx is required for Hira-independent
    localization of H3.3 at telomeres and for the repression of telomeric
    RNA. Our data demonstrate that multiple and distinct factors are
    responsible for H3.3 localization at specific genomic locations in
    mammalian cells.
 C1 [Guo, Xingyi; Zheng, Deyou] Albert Einstein Coll Med, Dept Neurol, Bronx, NY 10461 USA.
    [Greally, John M.] Albert Einstein Coll Med, Dept Med, Bronx, NY 10461 USA.
    [Greally, John M.; Zheng, Deyou] Albert Einstein Coll Med, Dept Genet, Bronx, NY 10461 USA.
    [Zheng, Deyou] Albert Einstein Coll Med, Dept Neurosci, Bronx, NY 10461 USA.
    [Goldberg, Aaron D.; Banaszynski, Laura A.; Noh, Kyung-Min; Lewis, Peter W.; Elsaesser, Simon J.; Stadler, Sonja; Allis, C. David] Rockefeller Univ, Lab Chromatin Biol & Epigenet, New York, NY 10065 USA.
    [Dewell, Scott] Rockefeller Univ, Genom Resource Ctr, New York, NY 10065 USA.
    [Li, Xuan; Yang, Chingwen] Rockefeller Univ, Gene Targeting Resource Ctr, New York, NY 10065 USA.
    [Law, Martin; Garrick, David; Gibbons, Richard J.; Higgs, Douglas R.] John Radcliffe Hosp, Weatherall Inst Mol Med, MRC Mol Haematol Unit, Oxford OX3 9DS, England.
    [Wen, Duancheng; Rafii, Shahin] Weill Cornell Med Coll, Howard Hughes Med Inst, New York, NY 10065 USA.
    [Wen, Duancheng; Rafii, Shahin] Weill Cornell Med Coll, Ansary Stem Cell Inst, New York, NY 10065 USA.
    [Wen, Duancheng; Rafii, Shahin] Weill Cornell Med Coll, Dept Med Genet, New York, NY 10065 USA.
    [Chapgier, Ariane; Scambler, Peter J.] Inst Child Hlth, Mol Med Unit, London WC1N 1EH, England.
    [DeKelver, Russell C.; Miller, Jeffrey C.; Lee, Ya-Li; Boydston, Elizabeth A.; Holmes, Michael C.; Gregory, Philip D.; Urnov, Fyodor D.] Sangamo BioSci, Point Richmond Tech Ctr, Richmond, CA 94804 USA.
    [Cristea, Ileana M.] Princeton Univ, Dept Mol Biol, Princeton, NJ 08544 USA.
 RP Zheng, DY, Albert Einstein Coll Med, Dept Neurol, Bronx, NY 10461 USA.
 EM deyou.zheng@einstein.yu.edu
    alliscd@rockefeller.edu
 FU National Institutes of Health (NIH) [GM07739, RR00862, RR022220,
    DP1DA026192, GM53122, GM53512]; Damon Runyon Cancer Research Foundation
    ; Rockefeller University ; Starr Foundation ; New York State Department
    of Health [C023046]; Howard Hughes Medical Institute ; Biotechnology
    and Biological Sciences Research Council UK ; British Heart Foundation
    ; Albert Einstein College of Medicine of Yeshiva University 
 FX We thank L. Baker, E.M. Duncan, G.G. Wang for critical reading of the
    manuscript, P. Wu, A. Sfeir, and T. de Lange for telomere reagents and
    helpful discussion, P.D. Adams for Hira antibodies, R. Jaenisch for F1
    hybrid male 129SVJae x M. m. castaneus ESCs, G. Almouzni for H3.1 and
    H3.3-FLAG-HA HeLa cells, K. Zhao for sharing his native ChIP-seq
    protocol, E. Moehle for drawing the gene editing schemes, N. Jina of
    the University College London Genomics Core, K.R. Molloy for assistance
    with mass spectrometric analysis, and S. Mazel and A. North of the
    Rockefeller University Flow Cytometry and Bio-Imaging Resource Centers.
    A. D. G. is supported by National Institutes of Health (NIH) Medical
    Scientist Training Program grant GM07739. L. A. B. is a Damon Runyon
    Cancer Research Foundation fellow. This work was funded by
    institutional support from The Rockefeller University and grants from
    the Tri-Institutional Stem Cell Initiative (funded by the Starr
    Foundation), Empire State Stem Cell fund through New York State
    Department of Health contract #C023046, the Howard Hughes Medical
    Institute (S.R.), Biotechnology and Biological Sciences Research
    Council UK and the British Heart Foundation (P.J.S.), startup funds
    from the Albert Einstein College of Medicine of Yeshiva University
    (D.Z.), and NIH grants RR00862, RR022220, DP1DA026192 (I.M.C.),
    GM53122, and GM53512 (C.D.A.). J.C.M., M.C.H., Y.L.L., P.D.G., and
    F.D.U. are full-time employees of Sangamo BioSciences, Inc.
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 NR 69
 TC 57
 PU CELL PRESS
 PI CAMBRIDGE
 PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
 SN 0092-8674
 J9 CELL
 JI Cell
 PD MAR 5
 PY 2010
 VL 140
 IS 5
 BP 678
 EP 691
 DI 10.1016/j.cell.2010.01.003
 PG 14
 SC Biochemistry & Molecular Biology; Cell Biology
 GA 564EZ
 UT ISI:000275197400017
 ER
 
 PT J
 AU Yang, XY
    Lu, X
    Lombes, M
    Rha, GB
    Chi, YI
    Guerin, TM
    Smart, EJ
    Liu, J
 AF Yang, Xingyuan
    Lu, Xin
    Lombes, Marc
    Rha, Geun Bae
    Chi, Young-In
    Guerin, Theresa M.
    Smart, Eric J.
    Liu, Jun
 TI The G(0)/G(1) Switch Gene 2 Regulates Adipose Lipolysis through
    Association with Adipose Triglyceride Lipase
 SO CELL METABOLISM
 LA English
 DT Article
 ID HORMONE-SENSITIVE LIPASE; CHANARIN-DORFMAN-SYNDROME; EPITHELIUM-DERIVED
    FACTOR; LIPID STORAGE DISEASE; INSULIN-RESISTANCE; TRIACYLGLYCEROL
    LIPASE; STIMULATED LIPOLYSIS; ENERGY-METABOLISM; CRYSTAL-STRUCTURE;
    PERILIPIN-A
 AB Adipose triglyceride lipase (ATGL) is the rate-limiting enzyme for
    triacylglycerol (TAG) hydrolysis in adipocytes. The precise mechanisms
    whereby ATGL is regulated remain uncertain. Here, we demonstrate that a
    protein encoded by G(0)/G(1) switch gene 2 (G0S2) is a selective
    regulator of ATGL. G0S2 is highly expressed in adipose tissue and
    differentiated adipocytes. When overexpressed in HeLa cells, G0S2
    localizes to lipid droplets and prevents their degradation mediated by
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    hydrophobic domain of G0S2 and the patatin-like domain of ATGL. More
    importantly, interaction with G0S2 inhibits ATGL TAG hydrolase
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    lipolysis in adipocytes, whereas overexpression of G0S2 diminishes the
    rate of lipolysis in both adipocytes and adipose tissue explants. Thus
    G0S2 functions to attenuate ATGL action both in vitro and in vivo and
    by this mechanism regulates TAG hydrolysis.
 C1 [Yang, Xingyuan; Lu, Xin; Guerin, Theresa M.; Smart, Eric J.; Liu, Jun] Univ Kentucky, Dept Pediat, Lexington, KY 40536 USA.
    [Yang, Xingyuan; Lu, Xin; Guerin, Theresa M.; Smart, Eric J.; Liu, Jun] Univ Kentucky, Kentucky Pediat Res Inst, Lexington, KY USA.
    [Rha, Geun Bae; Chi, Young-In] Univ Kentucky, Dept Mol & Cellular Biochem, Lexington, KY USA.
    [Rha, Geun Bae; Chi, Young-In] Univ Kentucky, Struct Biol Ctr, Lexington, KY USA.
    [Lombes, Marc] Fac Med Paris Sud, INSERM, U693, Le Kremlin Bicetre, France.
 RP Liu, J, Univ Kentucky, Dept Pediat, Lexington, KY 40536 USA.
 EM jun.liu@uky.edu
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 NR 43
 TC 16
 PU CELL PRESS
 PI CAMBRIDGE
 PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
 SN 1550-4131
 J9 CELL METAB
 JI Cell Metab.
 PD MAR 3
 PY 2010
 VL 11
 IS 3
 BP 194
 EP 205
 DI 10.1016/j.cmet.2010.02.003
 PG 12
 SC Cell Biology; Endocrinology & Metabolism
 GA 565WE
 UT ISI:000275325400006
 ER
 
 PT J
 AU Lorenzo, VF
    Yang, Y
    Simonson, TS
    Nussenzveig, R
    Jorde, LB
    Prchal, JT
    Ge, RL
 AF Lorenzo, V. F.
    Yang, Y.
    Simonson, T. S.
    Nussenzveig, R.
    Jorde, L. B.
    Prchal, J. T.
    Ge, R. L.
 TI Genetic adaptation to extreme hypoxia: Study of high-altitude pulmonary
    edema in a three-generation Han Chinese family (vol 43, pg 221, 2009)
 SO BLOOD CELLS MOLECULES AND DISEASES
 LA English
 DT Correction
 C1 [Lorenzo, V. F.; Yang, Y.; Simonson, T. S.; Nussenzveig, R.; Jorde, L. B.; Prchal, J. T.; Ge, R. L.] Univ Utah, Salt Lake City, UT 84132 USA.
 RP Prchal, JT, Univ Utah, SOM 5C210,30 N 1900 E, Salt Lake City, UT 84132
    USA.
 EM josef.prchal@hsc.utah.edu
 CR LORENZO VF, 2009, BLOOD CELL MOL DIS, V43, P221, DOI
    10.1016/j.bcmd.2009.04.006
 NR 1
 TC 0
 PU ACADEMIC PRESS INC ELSEVIER SCIENCE
 PI SAN DIEGO
 PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
 SN 1079-9796
 J9 BLOOD CELLS MOLECULES DIS
 JI Blood Cells Mol. Dis.
 PD MAR 15
 PY 2010
 VL 44
 IS 3
 BP 198
 EP 198
 DI 10.1016/j.bcmd.2009.12.008
 PG 1
 SC Hematology
 GA 564MC
 UT ISI:000275217800014
 ER
 
 PT J
 AU Huang, JG
    Yang, M
    Liu, P
    Yang, GD
    Wu, CA
    Zheng, CC
 AF Huang, Jin-Guang
    Yang, Mei
    Liu, Pei
    Yang, Guo-Dong
    Wu, Chang-Ai
    Zheng, Cheng-Chao
 TI Genome-wide profiling of developmental, hormonal or environmental
    responsiveness of the nucleocytoplasmic transport receptors in
    Arabidopsis
 SO GENE
 LA English
 DT Article
 DE Importin; Exportin; Nuclear pore complex; Signaling pathway; Abiotic
    stress
 ID NUCLEAR-LOCALIZATION SEQUENCES; PORE-TARGETING COMPLEX; IMPORTIN-ALPHA;
    SIGNAL-TRANSDUCTION; BETA; EXPRESSION; PROTEIN; PLANTS; EXPORT; LIGHT
 AB Being poilkilothermic and sessile organisms, plants have to respond
    quickly to changing environmental cues, and a higher order of gene
    regulation is required The significance of nucleocytoplasmic transport
    via importin alpha and importin beta (alpha/beta) has been exhibited in
    a wide spectrum of biological processes However, most of these
    receptors have not been characterized as to which cellular or
    development processes are required and how their expression is
    regulated by environmental stimuli Here we pursued a phylogenetic
    analysis and investigated the expression patterns of all 8 IMP alpha s
    and 18 IMP beta s in Arabidopsis The IMP alpha isoforms could be
    tracked back to a common ancestor, while the IMP beta s derived from
    different ones The majority of transport receptor genes were
    constitutively expressed Intriguingly, AtIMP alpha 5, 7, 8 and AtIMP
    beta 5 were specifically expressed in different tissues AtIMP beta 3
    was the sole receptor that was obviously modulated by exogenous
    phytohormones, whereas three IMP alpha s and five IMP beta s exhibited
    responses to environmental stimuli Furthermore, our RT-PCR data
    provided direct evidence that AtIMP alpha 5, 8 and AtIMP beta 5 are not
    pseudogenes and we also corrected the open reading frame annotation of
    AtIMP alpha 8 These genome-wide profilin g results not only widen our
    understanding of these transport receptors, but also provide strong
    evidence supporting the role of transport receptors in multiple
    signaling pathways and give us an insight into the further analysis of
    nucleocytoplasmic trafficking in Arabidopsis (C) 2009 Elsevier B V All
    rights reserved
 C1 [Huang, Jin-Guang; Yang, Mei; Liu, Pei; Yang, Guo-Dong; Wu, Chang-Ai; Zheng, Cheng-Chao] Shandong Agr Univ, State Key Lab Crop Biol, Coll Life Sci, Tai An 271018, Shandong, Peoples R China.
    [Liu, Pei] Zhejiang Univ, Coll Biosyst Engn & Food Sci, Hangzhou 310028, Zhejiang, Peoples R China.
 RP Zheng, CC, Shandong Agr Univ, State Key Lab Crop Biol, Coll Life Sci,
    Tai An 271018, Shandong, Peoples R China.
 FU National Basic Research Program [2006CB1001006]; Changjiang Scholars
    and Innovative Research Team in University [IRT0635]; National Special
    Program for Research and Industrialization of Transgenic Plants in
    China [2009ZX08009-092B]
 FX This work was supported by the National Basic Research Program (Grant
    No. 2006CB1001006), the Program for Changjiang Scholars and Innovative
    Research Team in University (Grant No. IRT0635) and the National
    Special Program for Research and Industrialization of Transgenic Plants
    (Grant No. 2009ZX08009-092B) in China.
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 NR 44
 TC 0
 PU ELSEVIER SCIENCE BV
 PI AMSTERDAM
 PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
 SN 0378-1119
 J9 GENE
 JI Gene
 PD FEB 1
 PY 2010
 VL 451
 IS 1-2
 BP 38
 EP 44
 DI 10.1016/j.gene.2009.11.009
 PG 7
 SC Genetics & Heredity
 GA 561YA
 UT ISI:000275014800006
 ER
 
 PT J
 AU Huang, Y
    Yang, X
    Wu, Y
    Jing, W
    Cai, X
    Tang, W
    Liu, L
    Liu, Y
    Grottkau, BE
    Lin, Y
 AF Huang, Y.
    Yang, X.
    Wu, Y.
    Jing, W.
    Cai, X.
    Tang, W.
    Liu, L.
    Liu, Y.
    Grottkau, B. E.
    Lin, Y.
 TI gamma-secretase inhibitor induces adipogenesis of adipose-derived stem
    cells by regulation of Notch and PPAR-gamma
 SO CELL PROLIFERATION
 LA English
 DT Article
 ID ACTIVATED-RECEPTOR-GAMMA; SIGNALING PATHWAY; TRANSCRIPTION FACTOR;
    DIFFERENTIATION; EXPRESSION; PREF-1; PROLIFERATION; PREADIPOCYTES;
    SPECIFICATION; TARGET
 AB Objective:
    To determine the inhibitory effect and mechanism of Notch signalling on
    adipogenesis of mouse adipose-derived stem cells (mASCs).
    Materials and methods:
    Varied concentrations of
    N-[N-(3,5-difluorophenacetyl)-l-alanyl]-S-phenylglycine t-butylester
    (DAPT) were added to mASCs 3 days before adipogenic induction with
    insulin-containing differentiation medium. The process of adipogenesis
    and ability of lipid droplet accumulation were analysed using oil red-O
    staining. The Notch signalling pathway (Notch-1, -2, -3, -4, Hes-1 and
    Hey-1) and adipogenesis-related factors (PPAR-gamma, DLK-1/Pref-1 and
    Acrp) were tested using real-time PCR, Western blot analysis and
    immunofluorescence staining assays.
    Results:
    We demonstrated that Notch-2-Hes-1 signalling pathway was inhibited
    dose-dependently by DAPT in mASCs. In addition, transcription of
    PPAR-gamma was promoted by DAPT before adipogenic induction, while
    inhibitor of adipogenesis DLK-1/Pref-1 was further depressed. At early
    stages of differentiation (2-4 days), adipogenesis in mASCs was
    advanced and significantly enhanced in 5 and 10 mu m DAPT pre-treated
    cases. On day 4, in differentiated mASCs cases with DAPT pre-treatment,
    we also found promotion of activation of de-PPAR-gamma and depression
    of HES-1, DLK-1/Pref-1 mRNA and protein expression.
    Conclusions:
    We conclude that blocking Notch signalling with DAPT enhances
    adipogenesis of differentiated mASCs at an early stage. It may be due
    to depression of DLK-1/Pref-1 and promotion of de-PPAR-gamma
    activation, which work through inhibition of Notch-2-Hes-1 pathway by
    DAPT.
 C1 [Grottkau, B. E.; Lin, Y.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Orthopaed Surg,Children & Pediat Orthopaed L, Boston, MA USA.
    [Huang, Y.; Yang, X.; Wu, Y.; Jing, W.; Cai, X.; Tang, W.; Liu, L.; Liu, Y.; Lin, Y.] Sichuan Univ, State Key Lab Oral Dis, W China Coll Stomatol, Chengdu 610064, Peoples R China.
    [Huang, Y.] Capital Med Univ, Beijing Friendship Hosp, Dept Oral & Maxillofacial Surg, Beijing, Peoples R China.
 RP Grottkau, BE, Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept
    Orthopaed,Children & Pediat Orthopaed Lab Ti, Boston, MA 02115 USA.
 EM bgrottkau@partners.org
    yunfenglin@scu.edu.cn
 FU National Natural Science Foundation of China [30801304]; Anthony and
    Constance Franchi Fund for Pediatric Orthopaedics at the MassGeneral
    Hospital for Children ; Specialized Research Fund for the Doctoral
    Program of Higher Education [20070610062]; State Key Laboratory of Oral
    Diseases, Sichuan University [SKLOD011]; Applied Fundamental Project of
    Sichuan Province [2008JY0028-2]
 FX This study was funded by the National Natural Science Foundation of
    China (30801304), the Anthony and Constance Franchi Fund for Pediatric
    Orthopaedics at the MassGeneral Hospital for Children, Specialized
    Research Fund for the Doctoral Program of Higher Education
    (20070610062), Opening Funding of the State Key Laboratory of Oral
    Diseases, Sichuan University (SKLOD011) and Applied Fundamental Project
    of Sichuan Province (2008JY0028-2).
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 NR 49
 TC 1
 PU WILEY-BLACKWELL PUBLISHING, INC
 PI MALDEN
 PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
 SN 0960-7722
 J9 CELL PROLIFERATION
 JI Cell Prolif.
 PD APR
 PY 2010
 VL 43
 IS 2
 BP 147
 EP 156
 DI 10.1111/j.1365-2184.2009.00661.x
 PG 10
 SC Cell Biology
 GA 560VR
 UT ISI:000274932500006
 ER
 
 PT J
 AU Shimizu, S
    Hong, P
    Arumugam, B
    Pokomo, L
    Boyer, J
    Koizumi, N
    Kittipongdaja, P
    Chen, A
    Bristol, G
    Galic, Z
    Zack, JA
    Yang, O
    Chen, ISY
    Lee, B
    An, DS
 AF Shimizu, Saki
    Hong, Patrick
    Arumugam, Balamurugan
    Pokomo, Lauren
    Boyer, Joshua
    Koizumi, Naoya
    Kittipongdaja, Panyamol
    Chen, Angela
    Bristol, Greg
    Galic, Zoran
    Zack, Jerome A.
    Yang, Otto
    Chen, Irvin S. Y.
    Lee, Benhur
    An, Dong Sung
 TI A highly efficient short hairpin RNA potently down-regulates CCR5
    expression in systemic lymphoid organs in the hu-BLT mouse model
 SO BLOOD
 LA English
 DT Article
 ID SHORT-INTERFERING RNAS; HUMAN IMMUNE-SYSTEM; HIV-1 INFECTION; T-CELLS;
    DISEASE PROGRESSION; LENTIVIRAL VECTOR; HUMANIZED MICE;
    MAMMALIAN-CELLS; CO-RECEPTORS; REV SIRNA
 AB Inhibiting the expression of the HIV-1 coreceptor CCR5 holds great
    promise for controlling HIV-1 infection in patients. Here we report
    stable knockdown of human CCR5 by a short hairpin RNA(shRNA) in a
    humanized bone marrow/liver/thymus (BLT) mouse model. We delivered a
    potent shRNA against CCR5 into human fetal liver-derived CD34(+)
    hematopoietic progenitor/stem cells (HPSCs) by lentiviral vector
    transduction. We transplanted vector-transduced HPSCs solidified with
    Matrigel and a thymus segment under the mouse kidney capsule.
    Vector-transduced autologous CD34(+) cells were subsequently injected
    in the irradiated mouse, intended to create systemic reconstitution.
    CCR5 expression was down-regulated in human T cells and
    monocytes/macrophages in systemic lymphoid tissues, including
    gut-associated lymphoid tissue, the major site of HIV-1 replication.
    The shRNA-mediated CCR5 knockdown had no apparent adverse effects on
    T-cell development as assessed by polyclonal T-cell receptor V beta
    family development and naive/memory T-cell differentiation. CCR5
    knockdown in the secondary transplanted mice suggested the potential of
    long-term hematopoietic reconstitution by the shRNA-transduced HPSCs.
    CCR5 tropic HIV-1 infection was effectively inhibited in mouse-derived
    human splenocytes ex vivo. These results demonstrate that lentiviral
    vector delivery of shRNA into human HPSCs could stably down-regulate
    CCR5 in systemic lymphoid organs in vivo. (Blood. 2010;115:1534-1544)
 C1 [An, Dong Sung] Univ Calif Los Angeles, David Geffen Sch Med, Div Hematol Oncol, AIDS Inst, Los Angeles, CA 90095 USA.
    [Shimizu, Saki; Pokomo, Lauren; Boyer, Joshua; Koizumi, Naoya; Kittipongdaja, Panyamol; Bristol, Greg; Galic, Zoran; Zack, Jerome A.; Chen, Irvin S. Y.; An, Dong Sung] Univ Calif Los Angeles, David Geffen Sch Med, Dept Med, Div Hematol Oncol, Los Angeles, CA 90095 USA.
    [Hong, Patrick; Arumugam, Balamurugan; Zack, Jerome A.; Yang, Otto; Chen, Irvin S. Y.; Lee, Benhur] Univ Calif Los Angeles, David Geffen Sch Med, Dept Microbiol, Los Angeles, CA 90095 USA.
    [Hong, Patrick; Arumugam, Balamurugan; Zack, Jerome A.; Yang, Otto; Chen, Irvin S. Y.; Lee, Benhur] Univ Calif Los Angeles, David Geffen Sch Med, Dept Immunol, Los Angeles, CA 90095 USA.
    [Hong, Patrick; Arumugam, Balamurugan; Zack, Jerome A.; Yang, Otto; Chen, Irvin S. Y.; Lee, Benhur] Univ Calif Los Angeles, David Geffen Sch Med, Dept Mol Genet, Los Angeles, CA 90095 USA.
    [Chen, Angela] Univ Calif Los Angeles, David Geffen Sch Med, Dept Obstet & Gynecol, Los Angeles, CA 90095 USA.
 RP An, DS, Univ Calif Los Angeles, David Geffen Sch Med, Div Hematol
    Oncol, AIDS Inst, 188 BSRB,615 Charles E Young Dr S, Los Angeles, CA
    90095 USA.
 EM an@ucla.edu
 FU Rheumatology Fellowship Training Grant [T32 AR053463]; UCLA AIDS
    Institute ; UCLA Center for AIDS Research (CFAR) ; National Institute
    of Allergy and Infectious Diseases [AI028697]; National Heart, Lung,
    and Blood Institute [1R01HL086409]; National Cancer Institute [CA086306]
 FX The authors thank Victor Garcia for valuable information and Jennifer
    Fulcher, Alvin Welch, Ana Beatriz Ruiz, Stephanie Matyas, Min Zhou,
    Patrick Kim, Ruth Cortado, Encarnacion Montecino-Rodriguez, Eun Mi Hur,
    Sonal Patel, Parvataneni Ram, and Broad Stem Cell Research Center flow
    core facility at UCLA for their reagents and technical support.
    This work was supported by the Rheumatology Fellowship Training Grant
    T32 AR053463, UCLA AIDS Institute, UCLA Center for AIDS Research
    (CFAR), National Institute of Allergy and Infectious Diseases
    (AI028697), National Heart, Lung, and Blood Institute (1R01HL086409),
    and the National Cancer Institute (CA086306).
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 NR 46
 TC 6
 PU AMER SOC HEMATOLOGY
 PI WASHINGTON
 PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
 SN 0006-4971
 J9 BLOOD
 JI Blood
 PD FEB 25
 PY 2010
 VL 115
 IS 8
 BP 1534
 EP 1544
 DI 10.1182/blood-2009-04-215855
 PG 11
 SC Hematology
 GA 561KB
 UT ISI:000274974200011
 ER
 
 PT J
 AU Guan, CM
    Ye, C
    Yang, XM
    Gao, JG
 AF Guan, Chunmei
    Ye, Chao
    Yang, Xiaomei
    Gao, Jiangang
 TI A Review of Current Large-Scale Mouse Knockout Efforts
 SO GENESIS
 LA English
 DT Review
 DE knockout mouse; gene trapping; gene targeting; transposon; ES cells
 ID EMBRYONIC STEM-CELLS; HUMAN-GENOME-PROJECT; GENE-TRAP MUTAGENESIS;
    FUNCTIONAL GENOMICS; INSERTIONAL MUTAGENESIS; CRE RECOMBINASE;
    CHROMOSOMAL REARRANGEMENTS; HOMOLOGOUS RECOMBINATION; MULTIPURPOSE
    ALLELES; SOMATIC INTEGRATION
 AB After the successful completion of the human genome project (HGP),
    biological research in the post-genome era urgently needs an efficient
    approach for functional analysis of genes. Utilization of knockout
    mouse models has been powerful for elucidating the function of genes as
    well as finding new therapeutic interventions for human diseases. Gene
    trapping and gene targeting are two independent techniques for making
    knockout mice from embryonic stem (ES) cells. Gene trapping is
    high-throughput, random, and sequence-tagged while gene targeting
    enables the knockout of specific genes. It has been about 20 years
    since the first gene targeting and gene trapping mice were generated.
    In recent years, new tools have emerged for both gene targeting and
    gene trapping, and organizations have been formed to knock out genes in
    the mouse genome using either of the two methods. The knockout mouse
    project (KOMP) and the international gene trap consortium (IGTC) were
    initiated to create convenient resources for scientific research
    worldwide and knock out all the mouse genes. Organizers of KOMP regard
    it as important as the HGP. Gene targeting methods have changed from
    conventional gene targeting to high-throughput conditional gene
    targeting. The combined advantages of trapping and targeting elements
    are improving the gene trapping spectrum and gene targeting efficiency.
    As a newly-developed insertional mutation system, transposons have some
    advantages over retrovirus in trapping genes. Emergence of the
    international knockout mouse consortium (IKMP) is the beginning of a
    global collaboration to systematically knock out all the genes in the
    mouse genome for functional genomic research. genesis 48:73-85, 2010.
    (C) 2010 Wiley-Liss, Inc.
 C1 [Guan, Chunmei; Ye, Chao; Yang, Xiaomei; Gao, Jiangang] Shandong Univ, Coll Life Sci, Jinan 250100, Shandong, Peoples R China.
 RP Yang, XM, Shandong Univ, Coll Life Sci, South Bldg,Room 117, Jinan
    250100, Shandong, Peoples R China.
 EM yxm411@sdu.edu.cn
    jggao@sdu.edu.cn
 FU National Natural Sciences Foundation of China [30871436, 30973297]; 973
    Program [2010CB945002]; Ministry of Education of China [200804220011];
    Shandong Province Science and Technology Key Program [2009GG10003039]
 FX This work is supported by the National Natural Sciences Foundation of
    China (30871436, 30973297), the 973 Program (2010CB945002), grant from
    Ministry of Education of China (200804220011), grant for returned
    Chinese scholars, and Shandong Province Science and Technology Key
    Program (2009GG10003039).
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 NR 105
 TC 8
 PU WILEY-LISS
 PI HOBOKEN
 PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA
 SN 1526-954X
 J9 GENESIS
 JI Genesis
 PD FEB
 PY 2010
 VL 48
 IS 2
 BP 73
 EP 85
 DI 10.1002/dvg.20594
 PG 13
 SC Developmental Biology; Genetics & Heredity
 GA 558CZ
 UT ISI:000274719500001
 ER
 
 PT J
 AU Yang, Q
    Wu, SB
 AF Yang, Qing
    Wu, Shubin
 TI WHEAT STRAW PYROLYSIS ANALYSIS BY THERMOGRAVIMETRY AND GAS
    CHROMATOGRAPHY-MASS SPECTROMETRY
 SO CELLULOSE CHEMISTRY AND TECHNOLOGY
 LA English
 DT Article
 DE wheat straw; thermogravimetry; kinetics; Py-GC-MS; catalyst; pyrolysis
 ID BIOMASS
 AB The effect of the heating rates and the existence of a Ni-catalyst on
    the thermogravimetric characteristics of wheat straw were investigated
    by thermogravimetry and gas chromatography-mass spectrometry. The
    weight loss of wheat straw was not markedly by the heating rates, over
    a temperature range from 220.6 and 391.2 degrees C, although to obtain
    the same weight loss, the corresponding temperature was increased and
    the heating rates was enhanced. The thermogravimetric kinetic
    parameters of wheat straw were calculated both without catalyst and
    with 0.5% Ni-catalyst, by the method of Kissinger; the apparent
    activation energy values of wheat straw were of 93.92 and 119.80
    KJ.mol(-1) and the frequency factors lnA were 17.82 and 23.02 min(-1)
    respectively. The weight loss of wheat straw wasnot markedly influenced
    by the Ni-catalyst while pyrolysis-gas chromatography-mass spectrometry
    (Py-GC-MS) evidenced that at 800 degrees C, the presence of the
    catalyst influecned the peak intensities derived form cellulose,
    hemicellulose and lignin. It was concluded tat the Ni-catalyst favors a
    more analytic effect on wheat straw lignin that is the total value of
    the peak area from phenolic compounds and vanillin was higher than Mal
    from furfural and levoglucosan.
 C1 [Yang, Qing; Wu, Shubin] S China Univ Technol, State Key Lab Pulp Paper Engn, Guangzhou 510640, Guangdong, Peoples R China.
 RP Yang, Q, S China Univ Technol, State Key Lab Pulp Paper Engn, Guangzhou
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 NR 10
 TC 1
 PU EDITURA ACAD ROMANE
 PI BUCURESTI
 PA CALEA 13 SEPTEMBRIE NR 13, SECTOR 5, BUCURESTI 050711, ROMANIA
 SN 0576-9787
 J9 CELL CHEM TECHNOL
 JI Cell Chem. Technol.
 PD APR-JUN
 PY 2009
 VL 43
 IS 4-6
 BP 123
 EP 131
 PG 9
 SC Materials Science, Paper & Wood
 GA 556SR
 UT ISI:000274612700002
 ER
 
 PT J
 AU Yang, Q
    Wu, SB
 AF Yang, Qing
    Wu, Shubin
 TI THERMOGRAVIMETRIC CHARACTERISTICS OF WHEAT STRAW LIGNIN
 SO CELLULOSE CHEMISTRY AND TECHNOLOGY
 LA English
 DT Article
 DE wheat straw; thermogravimetry; dynamics; lignin
 ID THERMAL-ANALYSIS; PYROLYSIS; CELLULOSE; KINETICS; BIOMASS; WOOD; TG
 AB The thermogravimetric characteristics of wheat straw EMAL (Enzymatic
    Acidolysis Lignin) were analyzed. The effect of the heating rates on
    the thermogravimetric characteristics of wheat straw and the wheat
    straw influence on pyrolysis were investigated. The influence of
    various heating rates on wheat straw was significant, the pyrolysis
    rate of wheat straw EMAL increased at temperatures between 200 and 500
    degrees C. At a temperature above 200 degrees C the pyrolysis rate of
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    calculated by the methods of Kissinger and Ozawa, respectively; the
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    that of the Ozawa one. At a pyrolysis temperature over 400 degrees C,
    the influence of the lignin present in wheat straw on wheat straw
    thermal behaviour was very clear, lignin pyrolysis dominating over that
    of wheat straw.
 C1 [Yang, Qing; Wu, Shubin] S China Univ Technol, State Key Lab Pulp & Paper Engn, Guangzhou 510640, Guangdong, Peoples R China.
 RP Yang, Q, S China Univ Technol, State Key Lab Pulp & Paper Engn,
    Guangzhou 510640, Guangdong, Peoples R China.
 FU Major State Basic Research Development Program of China [2007CB210201];
    National High Technology Research and Development Program of China
    [2007AA05Z456]; National Natural Science Foundation of China [20576043]
 FX Investigations were supported by a grant from the Major State Basic
    Research Development Program of China (973 Program) No. 2007CB210201)
    the National High Technology Research and Development Program of China
    (863 Program) (No. 2007AA05Z456) and the National Natural Science
    Foundation of China (No. 20576043).
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 PI BUCURESTI
 PA CALEA 13 SEPTEMBRIE NR 13, SECTOR 5, BUCURESTI 050711, ROMANIA
 SN 0576-9787
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 PD APR-JUN
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 BP 133
 EP 139
 PG 7
 SC Materials Science, Paper & Wood
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    Kim, YI
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    Osteryoung, KW
    van Oudenaarden, A
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 AF Dong, Guogang
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 TI Elevated ATPase Activity of KaiC Applies a Circadian Checkpoint on Cell
    Division in Synechococcus elongatus
 SO CELL
 LA English
 DT Article
 ID GENE-EXPRESSION; BACILLUS-SUBTILIS; CLOCK SYSTEM; CYANOBACTERIA;
    PHOSPHORYLATION; PROTEIN; IDENTIFICATION; OSCILLATION; DOMAIN; FTSZ
 AB A circadian clock coordinates physiology and behavior in diverse groups
    of living organisms. Another major cyclic cellular event, the cell
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    Synechococcus elongatus, the circadian clock gates cell division by an
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    cell division in the wild-type and demonstrate the regulation of
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    activity closes the gate by acting through a known clock output pathway
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    stimulates KaiC phosphorylation independently of the KaiA protein was
    also uncovered. We propose a model that separates the functions of KaiC
    ATPase and phosphorylation in cell division gating and other circadian
    behaviors.
 C1 [Dong, Guogang; Wood, Thammajun L.; Golden, Susan S.] Texas A&M Univ, Dept Biol, Ctr Biol Clocks Res, College Stn, TX 77843 USA.
    [Dong, Guogang; Kim, Yong-Ick; Golden, Susan S.] Univ Calif San Diego, Div Biol Sci, Ctr Chronobiol, La Jolla, CA 92093 USA.
    [Wang, Qiang; Osteryoung, Katherine W.] Michigan State Univ, Dept Plant Biol, E Lansing, MI 48824 USA.
    [Yang, Qiong; van Oudenaarden, Alexander] MIT, Dept Phys, Cambridge, MA 02139 USA.
    [van Oudenaarden, Alexander] MIT, Dept Biol, Cambridge, MA 02139 USA.
 RP Golden, SS, Texas A&M Univ, Dept Biol, Ctr Biol Clocks Res, College
    Stn, TX 77843 USA.
 EM sgolden@ucsd.edu
 FU NIH [R01 GM62419, P01 NS39546, R01 GM068957]; American Recovery and
    Reinvestment Act ; NSF [PHY-0548484]; DOE [DE-FG-02-06ER15808]
 FX We thank P. Luitel for helpful discussions, A. LiWang for sharing
    instrumentation and unpublished data, C.-C. Zhang for providing the
    FtsZ antiserum, and A. Suescun for technical assistance. We are
    grateful to J. Xiao, T. Liu, and I. M. Axmann for constructive
    suggestions on the ATPase assays. This work was supported by grants
    from the NIH (R01 GM62419 and P01 NS39546 to S. S. G., R01 GM068957 to
    A.v.O.), the American Recovery and Reinvestment Act (S. S. G.), NSF
    (PHY-0548484 to A.v.O.), and DOE (DE-FG-02-06ER15808 to K.W.O.). The
    content is solely the responsibility of the authors and does not
    necessarily represent the official views of the National Institute of
    General Medical Sciences or the National Institutes of Health.
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 NR 49
 TC 7
 PU CELL PRESS
 PI CAMBRIDGE
 PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
 SN 0092-8674
 J9 CELL
 JI Cell
 PD FEB 19
 PY 2010
 VL 140
 IS 4
 BP 529
 EP 539
 DI 10.1016/j.cell.2009.12.042
 PG 11
 SC Biochemistry & Molecular Biology; Cell Biology
 GA 557KQ
 UT ISI:000274668400016
 ER
 
 PT J
 AU Kokubo, T
    Kakinuma, S
    Kobayashi, T
    Watanabe, F
    Iritani, R
    Tateno, K
    Nishimura, M
    Nishikawa, T
    Hino, O
    Shimada, Y
 AF Kokubo, Toshiaki
    Kakinuma, Shizuko
    Kobayashi, Toshiyuki
    Watanabe, Fumiko
    Iritani, Riichirou
    Tateno, Kaori
    Nishimura, Mayumi
    Nishikawa, Tetsu
    Hino, Okio
    Shimada, Yoshiya
 TI Age dependence of radiation-induced renal cell carcinomas in an Eker
    rat model
 SO CANCER SCIENCE
 LA English
 DT Article
 ID TUBEROUS SCLEROSIS COMPLEX; POSTNATAL-DEVELOPMENT; N-NITROSOETHYLUREA;
    SOMATIC MUTATIONS; GROWTH-FACTOR; IN-UTERO; 2ND HIT; KIDNEY; CANCER;
    TUMORS
 AB Exposure to carcinogens early in life may contribute to cancer
    development later in life. The amount of radiation exposure children
    experience during medical procedures has been increasing, so it is
    important to evaluate the radiation risk of cancer in developing
    organs. Toward this goal, we assessed the risk of developing renal cell
    carcinoma using Eker rats as a kidney tumor model. F1 hybrids of male
    Eker (Tsc2 mutant) and female F344 rats were irradiated with 0.5 or 2
    Gy gamma radiation on gestation days 15 and 19, and on postnatal days
    5, 20, and 49. At 27 weeks of age, kidneys were examined for
    proliferative lesions. Preneoplastic lesions such as phenotypically
    altered tubules increased after postnatal irradiation as a function of
    age-at-irradiation, and hyperplasia were greatly increased after
    perinatal and postnatal irradiation. In contrast, development of
    adenoma and adenocarcinoma were evident in animals irradiated at
    perinatal ages, being maximal at gestational day 19. The frequency of
    LOH at the Tsc2 locus was unexpectedly low - 0% (0 of 4) for the
    unirradiated control, and 17% (6 of 35) for the irradiated group.
    Irrespective of LOH, the mTOR (mammalian target of rapamycin) pathway,
    which is negatively regulated by the Tsc1/2 complex, was activated in
    both benign and malignant lesions, as evidenced by phosphorylation of
    S6 ribosomal protein and 4E-BP1. This suggests that the wild-type Tsc2
    allele may be functionally inactivated. In conclusion, actively growing
    kidneys in perinatal-aged (F344 x Eker) F1 rats (Tsc2(+/-)) are at risk
    for radiation-induced malignant transformation of the renal epithelium
    associated with mTOR activation. (Cancer Sci 2010; 101: 616-623)
 C1 [Kokubo, Toshiaki; Kakinuma, Shizuko; Watanabe, Fumiko; Nishimura, Mayumi; Shimada, Yoshiya] Natl Inst Radiol Sci, Res Ctr Radiat Protect, Expt Radiobiol Childrens Hlth Res Grp, Chiba 260, Japan.
    [Kokubo, Toshiaki; Kobayashi, Toshiyuki; Hino, Okio] Juntendo Univ, Sch Med, Dept Pathol & Oncol, Tokyo 113, Japan.
    [Kokubo, Toshiaki; Nishikawa, Tetsu] Natl Inst Radiol Sci, Fundamental Technol Ctr, Dept Tech Support & Dev, Lab Anim Sci Sect, Chiba 260, Japan.
    [Iritani, Riichirou; Tateno, Kaori] Sci Serv Co, Chiba, Japan.
 RP Shimada, Y, Natl Inst Radiol Sci, Res Ctr Radiat Protect, Expt
    Radiobiol Childrens Hlth Res Grp, Chiba 260, Japan.
 EM y_shimad@nirs.go.jp
 FU National Institute of Radiological Sciences ; Japan Chemical Industry
    Association ; Ministry of Health, Labor and Welfare of Japan 
 FX We thank Mr S. Tateno, Ms E. Kubo and all members of the Laboratory
    Animal Sciences Section of our institute for animal care. This work was
    supported by institute funds from the National Institute of
    Radiological Sciences, the LRI program of the Japan Chemical Industry
    Association, and a Grant-in-Aid for Cancer Research from the Ministry
    of Health, Labor and Welfare of Japan.
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 NR 43
 TC 0
 PU WILEY-BLACKWELL PUBLISHING, INC
 PI MALDEN
 PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
 SN 1347-9032
 J9 CANCER SCI
 JI Cancer Sci.
 PD MAR
 PY 2010
 VL 101
 IS 3
 BP 616
 EP 623
 DI 10.1111/j.1349-7006.2009.01456.x
 PG 8
 SC Oncology
 GA 556VQ
 UT ISI:000274621800007
 ER
 
 PT J
 AU Wang, XF
    Nagase, H
    Watanabe, T
    Nobusue, H
    Suzuki, T
    Asami, Y
    Shinojima, Y
    Kawashima, H
    Takagi, K
    Mishra, R
    Igarashi, J
    Kimura, M
    Takayama, T
    Fukuda, N
    Sugiyama, H
 AF Wang, Xiaofei
    Nagase, Hiroki
    Watanabe, Takayoshi
    Nobusue, Hiroyuki
    Suzuki, Tsukasa
    Asami, Yukihiro
    Shinojima, Yui
    Kawashima, Hiroyuki
    Takagi, Keiko
    Mishra, Rajeev
    Igarashi, Jun
    Kimura, Makoto
    Takayama, Tadatoshi
    Fukuda, Noboru
    Sugiyama, Hiroshi
 TI Inhibition of MMP-9 transcription and suppression of tumor metastasis
    by pyrrole-imidazole polyamide
 SO CANCER SCIENCE
 LA English
 DT Article
 ID MATRIX-METALLOPROTEINASE INHIBITORS; CELL-LINES; KAPPA-B; CANCER;
    EXPRESSION; INVASION; DNA; RECOGNITION; PROGRESSION; INDUCTION
 AB Matrix metalloproteinase (MMP)-9, the 92-kDa type IV collagenase,
    contributes to tumor invasion and metastases, and strategies to
    down-regulate its expression could ultimately be of clinical utility. A
    pyrrole-imidazole (PI) polyamide that targets the activator protein-1
    (AP-1)-binding site of the MMP-9 promoter was designed and synthesized
    as a gene-silencing agent for tumor metastases. The synthesized product
    showed selective DNA binding ability. The MMP-9 PI polyamide
    significantly inhibited MMP-9's mRNA expression, protein level, and
    enzymatic activity in human breast adenocarcinoma cells (MDA-MB-231).
    Furthermore, the MMP-9 PI polyamide inhibited migration and invasion by
    in vitro wound-healing and matrigel-invasion assay. The FITC-labeled PI
    polyamide was localized in nuclei in 45 min of incubation with an
    MDA-MB-231 cell and remained in the nuclei for up to 96 h after
    incubation in vitro. It was also quickly localized in the mouse
    cellular nuclei of many tissues, including liver, kidney, and spleen,
    after intravenous injection without using any drug-delivery system.
    Moreover, the polyamide treatment significantly decreased metastasis in
    a mouse model of liver metastasis. Our results suggest that this PI
    polyamide, which targets the MMP-9 gene promoter, can be a novel MMP-9
    downregulating molecule for antimetastasis. (Cancer Sci 2010; 101:
    759-766)
 C1 [Wang, Xiaofei; Nagase, Hiroki; Igarashi, Jun; Fukuda, Noboru] Nihon Univ, Adv Res Inst Sci & Humanities, Tokyo, Japan.
    [Nagase, Hiroki; Watanabe, Takayoshi; Nobusue, Hiroyuki; Suzuki, Tsukasa; Asami, Yukihiro; Shinojima, Yui; Kawashima, Hiroyuki; Mishra, Rajeev; Kimura, Makoto] Nihon Univ, Sch Med, Dept Adv Med Sci, Div Canc Genet, Tokyo, Japan.
    [Takagi, Keiko; Takayama, Tadatoshi] Nihon Univ, Sch Med, Dept Digest Surg, Tokyo, Japan.
    [Sugiyama, Hiroshi] Kyoto Univ, Grad Sch Sci, Dept Chem, Kyoto, Japan.
    [Nagase, Hiroki] Roswell Pk Canc Inst, Dept Canc Genet, Buffalo, NY 14263 USA.
 RP Nagase, H, Nihon Univ, Adv Res Inst Sci & Humanities, Tokyo, Japan.
 EM nagase.hiroki@nihon-u.ac.jp
 FU MEXT ; National Institute of Environmental Health Services [ES012249-01]
 FX We thank Mr Motoaki Kataba, Mr Shigeki Nakai, and Ms Yuki Yamada for
    their technical support. This work was supported by the Nihon
    University Multidisciplinary Research Grant for 2007; the Academic
    Frontier Project for 2006 for Private Universities: Matching fund
    subsidy from MEXT to H. N.; and a grant from the National Institute of
    Environmental Health Services to H. N. (no. ES012249-01).
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 NR 30
 TC 1
 PU WILEY-BLACKWELL PUBLISHING, INC
 PI MALDEN
 PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
 SN 1347-9032
 J9 CANCER SCI
 JI Cancer Sci.
 PD MAR
 PY 2010
 VL 101
 IS 3
 BP 759
 EP 766
 DI 10.1111/j.1349-7006.2009.01435.x
 PG 8
 SC Oncology
 GA 556VQ
 UT ISI:000274621800027
 ER
 
 PT J
 AU Tajima, N
    Fukui, K
    Uesato, N
    Maruhashi, J
    Yoshida, T
    Watanabe, Y
    Tojo, A
 AF Tajima, Nobuyuki
    Fukui, Kenji
    Uesato, Naofumi
    Maruhashi, Junji
    Yoshida, Takayuki
    Watanabe, Yoshihiro
    Tojo, Arinobu
 TI JTE-607, a multiple cytokine production inhibitor, induces apoptosis
    accompanied by an increase in p21(waf1/cip1) in acute myelogenous
    leukemia cells
 SO CANCER SCIENCE
 LA English
 DT Article
 ID ACUTE MYELOID-LEUKEMIA; ACUTE MYELOBLASTIC-LEUKEMIA; ENDOTHELIAL
    GROWTH-FACTOR; BLAST CELLS; BONE-MARROW; MYELODYSPLASTIC SYNDROMES;
    AUTOCRINE GROWTH; KAPPA-B; GM-CSF; EXPRESSION
 AB Proinflammatory cytokines and growth factors have been thought to play
    crucial roles in the pathology of acute myelogenous leukemia (AML) by
    supporting the proliferation and survival of AML cells in an autocrine
    and paracrine manner, although further elucidation is required. JTE-607
    was originally identified as a multiple cytokine inhibitor that
    suppresses production of proinflammatory cytokines from
    lipopolysaccharide (LPS)-stimulated peripheral blood mononuclear cells.
    Herein, we report that JTE-607 exhibits inhibitory activity on the
    growth of AML cell lines accompanying reduction of the proinflammatory
    cytokine and growth factor production. In in vitro studies, JTE-607
    suppressed expression and production of cytokines, which are
    spontaneously up-regulated in AML cell lines. JTE-607 also abrogated
    proliferation of AML cells in a concentration range in which colony
    formation of normal bone marrow cells was not affected. The growth
    inhibition by JTE-607 was characterized by induction of cell-cycle
    arrest at the S-phase and apoptosis, accompanied by a decrease in c-Myc
    and increase in p21(waf1/cip1). In a leukemia model engrafted with
    U-937 cells, JTE-607 significantly prolonged survival in mice and
    reduced human cytokine mRNA levels in the bone marrow. These results
    suggest the usefulness of JTE-607 in therapeutic applications for
    patients with hypercytokinemia and aggressive AML cell proliferation.
    (Cancer Sci 2010; 101: 774-781)
 C1 [Tajima, Nobuyuki; Fukui, Kenji; Uesato, Naofumi; Maruhashi, Junji] Japan Tobacco Inc, Cent Pharmaceut Res Inst, Biol & Pharmacol Labs, Osaka, Japan.
    [Yoshida, Takayuki; Watanabe, Yoshihiro] Japan Tobacco Inc, Cent Pharmaceut Res Inst, Pharmaceut Frontier Res Labs, Kanagawa, Japan.
    [Tojo, Arinobu] Univ Tokyo, Inst Med Sci, Adv Clin Res Ctr, Div Mol Therapy, Tokyo, Japan.
 RP Tajima, N, Japan Tobacco Inc, Cent Pharmaceut Res Inst, Biol &
    Pharmacol Labs, Osaka, Japan.
 EM nobuyuki.tajima@jt.com
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 NR 50
 TC 0
 PU WILEY-BLACKWELL PUBLISHING, INC
 PI MALDEN
 PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
 SN 1347-9032
 J9 CANCER SCI
 JI Cancer Sci.
 PD MAR
 PY 2010
 VL 101
 IS 3
 BP 774
 EP 781
 DI 10.1111/j.1349-7006.2009.01446.x
 PG 8
 SC Oncology
 GA 556VQ
 UT ISI:000274621800029
 ER
 
 PT J
 AU Watanabe, T
    Miura, T
    Degawa, Y
    Fujita, Y
    Inoue, M
    Kawaguchi, M
    Furihata, C
 AF Watanabe, Takashi
    Miura, Tomohiro
    Degawa, Yusuke
    Fujita, Yuna
    Inoue, Masaaki
    Kawaguchi, Makoto
    Furihata, Chie
 TI Comparison of lung cancer cell lines representing four
    histopathological subtypes with gene expression profiling using
    quantitative real-time PCR
 SO CANCER CELL INTERNATIONAL
 LA English
 DT Article
 ID COLON-CARCINOMA CELLS; FAMILY-MEMBERS; E-CADHERIN; ADENOCARCINOMA;
    CLASSIFICATION; BIOINFORMATICS; SENSITIVITY; METASTASIS; SUBCLASSES;
    BIOMARKERS
 AB Background: Lung cancers are the most common type of human malignancy
    and are intractable. Lung cancers are generally classified into four
    histopathological subtypes: adenocarcinoma (AD), squamous cell
    carcinoma (SQ), large cell carcinoma (LC), and small cell carcinoma
    (SC). Molecular biological characterization of these subtypes has been
    performed mainly using DNA microarrays. In this study, we compared the
    gene expression profiles of these four subtypes using twelve human lung
    cancer cell lines and the more reliable quantitative real-time PCR
    (qPCR).
    Results: We selected 100 genes from public DNA microarray data and
    examined them by DNA microarray analysis in eight test cell lines
    (A549, ABC-1, EBC-1, LK-2, LU65, LU99, STC 1, RERF-LC-MA) and a normal
    control lung cell line (MRC-9). From this, we extracted 19 candidate
    genes. We quantified the expression of the 19 genes and a housekeeping
    gene, GAPDH, with qPCR, using the same eight cell lines plus four
    additional validation lung cancer cell lines (RERF-LC-MS, LC-1/sq,
    86-2, and MS-1-L). Finally, we characterized the four subtypes of lung
    cancer cell lines using principal component analysis (PCA) of gene
    expression profiling for 12 of the 19 genes (AMY2A, CDH1, FOXG1, IGSF3,
    ISL1, MALL, PLAU, RAB25, S100P, SLCO4A1, STMN1, and TGM2). The combined
    PCA and gene pathway analyses suggested that these genes were related
    to cell adhesion, growth, and invasion. S100P in AD cells and CDH1 in
    AD and SQ cells were identified as candidate markers of these lung
    cancer subtypes based on their upregulation and the results of PCA
    analysis. Immunohistochemistry for S100P and RAB25 was closely
    correlated to gene expression.
    Conclusions: These results show that the four subtypes, represented by
    12 lung cancer cell lines, were well characterized using qPCR and PCA
    for the 12 genes examined. Certain genes, in particular S100P and CDH1,
    may be especially important for distinguishing the different subtypes.
    Our results confirm that qPCR and PCA analysis provide a useful tool
    for characterizing cancer cell subtypes, and we discuss the possible
    clinical applications of this approach.
 C1 [Watanabe, Takashi; Miura, Tomohiro; Degawa, Yusuke; Fujita, Yuna; Furihata, Chie] Aoyama Gakuin Univ, Sch Sci & Engn, Dept Chem & Biol Sci, Kanagawa 2298558, Japan.
    [Inoue, Masaaki] Japan Labor Hlth & Welf Org, Niigata Rosai Hosp, Dept Chest Surg, Niigata 9428502, Japan.
    [Kawaguchi, Makoto] Japan Labor Hlth & Welf Org, Niigata Rosai Hosp, Dept Pathol, Niigata 9428502, Japan.
 RP Furihata, C, Aoyama Gakuin Univ, Sch Sci & Engn, Dept Chem & Biol Sci,
    Kanagawa 2298558, Japan.
 EM chiefurihata@gmail.com
 FU Regional New Consortium RD Projects ; Ministry of Economy, Trade and
    Industry, Japan ; Ministry of Education, Culture, Sports, Science, and
    Technology, Japan 
 FX This work was supported in part by Regional New Consortium R&D
    Projects, The Ministry of Economy, Trade and Industry, Japan (C.
    Furihata), and a Grant-in-Aid from the Private School High-tech
    Research Center Program of the Ministry of Education, Culture, Sports,
    Science, and Technology, Japan (C. Furihata). We thank Dr. Takayuki
    Negishi, School of Science and Engineering, Aoyama Gakuin University,
    for collaboration with the Bioanalyzer experiment, and Dr. Kazuhiko
    Matsumoto, Torii Pharmaceutical Co. Ltd. for his advice on Dunnett's
    test.
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 TC 2
 PU BIOMED CENTRAL LTD
 PI LONDON
 PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
 SN 1475-2867
 J9 CANCER CELL INT
 JI Cancer Cell Int.
 PD JAN 21
 PY 2010
 VL 10
 AR 2
 DI 10.1186/1475-2867-10-2
 PG 12
 SC Oncology
 GA 557SS
 UT ISI:000274691000001
 ER
 
 PT J
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    Nichelatti, M
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    Colombo, C
    Veronese, S
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    Ricci, F
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 AF Trojani, Alessandra
    Montillo, Marco
    Nichelatti, Michele
    Tedeschi, Alessandra
    Colombo, Chiara
    Veronese, Silvio
    Mura, Maria Angela
    Ricci, Francesca
    Scarpati, Barbara
    Colosimo, Anna
    Lodola, Milena
    Morra, Enrica
 TI ZAP-70, IgVh, and cytogenetics for assessing prognosis in chronic
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 SO CANCER BIOMARKERS
 LA English
 DT Article
 DE CLL; biomarkers; ZAP-70; IgVh; cytogenetics
 ID MUTATION STATUS; GENOMIC ABERRATIONS; DISEASE PROGRESSION; 11Q
    DELETION; P53 GENE; IMMUNOGLOBULIN; EXPRESSION; SURVIVAL; DIAGNOSIS;
    PREDICTS
 AB Background: New prognostic factors such as IgVh mutational status,
    ZAP-70 protein expression and cytogenetic abnormalities have shown to
    offer important prognostic information for patients with chronic
    lymphocytic leukemia (CLL). Our aim was to evaluate the optimal cut-off
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    need for treatment within 3 years from diagnosis in 170 patients with
    B-CLL.
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    prognostic impact.
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    Conclusions: We assessed that IgVh mutational status, ZAP-70 protein
    and 6q- are powerful prognostic markers. Analyses of all these factors
    revealed that 11q deletion was the strongest predictor of disease
    progression in B-CLL.
 C1 [Trojani, Alessandra; Montillo, Marco; Tedeschi, Alessandra; Colombo, Chiara; Ricci, Francesca; Lodola, Milena; Morra, Enrica] Osped Niguarda Ca Granda, Div Hematol, I-20162 Milan, Italy.
    [Nichelatti, Michele] Osped Niguarda Ca Granda, Serv Biostat, I-20162 Milan, Italy.
    [Veronese, Silvio; Colosimo, Anna] Osped Niguarda Ca Granda, Mol Pathol Unit, Dept Lab Med, I-20162 Milan, Italy.
    [Scarpati, Barbara] Osped Niguarda Ca Granda, Dept Trasfus Med, I-20162 Milan, Italy.
    [Scarpati, Barbara] Osped Niguarda Ca Granda, Div Hematol, I-20162 Milan, Italy.
 RP Trojani, A, Osped Niguarda Ca Granda, Div Hematol, Piazza Osped
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 EM alessandra.trojani@ospedaleniguarda.it
 FU Associazione Malattie del Sangue (AMS, Milan, Italy) 
 FX This study was supported by Associazione Malattie del Sangue (AMS,
    Milan, Italy). The authors would like to thank Dr. Silvia Soriani who
    participated to the cytogenetic studies.
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 TC 2
 PU IOS PRESS
 PI AMSTERDAM
 PA NIEUWE HEMWEG 6B, 1013 BG AMSTERDAM, NETHERLANDS
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 PG 9
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 PU ROUTLEDGE JOURNALS, TAYLOR & FRANCIS LTD
 PI ABINGDON
 PA 4 PARK SQUARE, MILTON PARK, ABINGDON OX14 4RN, OXFORDSHIRE, ENGLAND
 SN 0039-6338
 J9 SURVIVAL
 JI Survival
 PY 2009
 VL 51
 IS 5
 BP 17
 EP 46
 DI 10.1080/00396330903309840
 PG 30
 SC International Relations; Political Science
 GA 552KN
 UT ISI:000274288800002
 ER
 
 PT J
 AU Lee, SH
    Kim, KY
    Ryu, SY
    Yoon, Y
    Hahm, DH
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 AF Lee, S. H.
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 SO CELLULAR AND MOLECULAR BIOLOGY
 LA English
 DT Article
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 ID HORMONE-SENSITIVE LIPASE; ADIPOSE TRIGLYCERIDE LIPASE; ACTIVATED
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 RP Yang, Y, Sookmyung Womens Univ, Dept Life Sci, Seoul 140742, South
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 EM yyang@sookmyung.ac.kr
 FU Rural Development Administration [20070301034031]; Korea Research
    Foundation [KRF-2008-313-C00708]; Korea government (MEST)
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 FX This work was supported by the Biogreen 21 project (20070301034031) of
    Rural Development Administration, and a Korea Research Foundation Grant
    KRF-2008-313-C00708 and the Korea Science and Engineering Foundation
    (KOSEF) grant funded by the Korea government (MEST)
    (R01-2008-000-20127-0).
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 NR 20
 TC 0
 PU C M B  ASSOC
 PI POITIERS
 PA 40 AVENUE  RECTEUR PINEAU,  BAT MECANIQUE, 86022 POITIERS, FRANCE
 SN 0145-5680
 J9 CELL MOL BIOL
 JI Cell. Mol. Biol.
 PY 2010
 VL 56
 SU Suppl. S
 BP OL1215
 EP OL1222
 DI 10.1170/138
 PG 8
 SC Biochemistry & Molecular Biology; Cell Biology
 GA 556DY
 UT ISI:000274570400001
 ER
 
 PT J
 AU Qiao, G
    Li, Z
    Minto, AW
    Shia, J
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 AF Qiao, G.
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 TI Altered thymic selection by overexpressing cellular FLICE inhibitory
    protein in T cells causes lupus-like syndrome in a BALB/c but not
    C57BL/6 strain
 SO CELL DEATH AND DIFFERENTIATION
 LA English
 DT Article
 DE signal transduction; autoimmunity; T-cell activation; apoptosis
 ID NF-KAPPA-B; C-FLIP; NEGATIVE SELECTION; POSITIVE SELECTION; ANTIGEN
    RECEPTOR; IN-VIVO; ACTIVATION; LYMPHOCYTES; CASPASE-8; AUTOIMMUNITY
 AB The cellular FLICE inhibitory protein (c-FLIP) is an endogenous
    inhibitor of the caspase-8 proapoptotic signaling pathway downstream of
    death receptors. Recent evidence indicates that the long form of c-FLIP
    (c-FLIPL) is required for proliferation and effector T-cell
    development. However, the role of c-FLIPL in triggering autoimmunity
    has not been carefully analyzed. We now report that c-FLIPL transgenic
    (Tg) mice develop splenomegaly, lymphadenopathy, multiorgan
    infiltration, high titers of autoantibodies, and proliferative
    glomerulonephritis with immune complex deposition in a strain-dependent
    manner. The development of autoimmunity requires CD4(+) T cells and may
    result from impaired thymic selection. At the molecular level, c-FLIPL
    overexpression inhibits the zeta chain-associated protein tyrosine
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    pathway derived from ZAP-70 required for thymic selection. Therefore,
    we have identified c-FLIPL as a susceptibility factor under the
    influence of epistatic modifiers for the development of autoimmunity.
    Cell Death and Differentiation (2010) 17, 522-533; doi:
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 C1 [Qiao, G.; Li, Z.; Minto, A. W.; Yang, L.; Bao, L.; Quigg, R. J.; Zhang, J.] Univ Chicago, Dept Med, Nephrol Sect, Chicago, IL 60637 USA.
    [Qiao, G.; Yang, L.; Zhang, J.] Univ Chicago, Comm Immunol, Chicago, IL 60637 USA.
    [Shia, J.] Mem Sloan Kettering Canc Ctr, Dept Pathol, New York, NY 10021 USA.
    [Tschopp, J.] Univ Lausanne, Dept Biochem, CH-1066 Epalinges, Switzerland.
    [Gao, J-X] Ohio State Univ, Dept Pathol, Columbus, OH 43210 USA.
    [Wang, J.] Invitrogen Corp, BioSource Cytokines & Signaling, Camarillo, CA USA.
    [Zhang, J.] Univ Chicago, Comm Mol Med, Chicago, IL 60637 USA.
 RP Zhang, J, Univ Chicago, Dept Med, Nephrol Sect, 5841 S Maryland Ave,
    Chicago, IL 60637 USA.
 EM jzhang@medicine.bsd.uchicago.edu
 FU National Institutes of Health (NIH) [R01 AR049775, DK055357]; American
    Heart Association [09GRNT2010084]; NIH independent scientist award [K02
    AR 049047]; American Lung Association Career Investigator 
 FX We thank Drs. Marcus Peter and Yang-Xin Fu for critical reading of the
    paper and discussion. This work is in part supported by a novel
    research grant from the Lupus Research Institute (to JZ) and a start-up
    fund from the University of Chicago. Additional support was provided by
    grants from the National Institutes of Health (NIH) (R01 AR049775 to JZ
    and DK055357 to RJQ) and from the American Heart Association
    (09GRNT2010084 to JZ). JZ was supported by a NIH independent scientist
    award (K02 AR 049047), and is an American Lung Association Career
    Investigator.
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 NR 43
 TC 0
 PU NATURE PUBLISHING GROUP
 PI LONDON
 PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
 SN 1350-9047
 J9 CELL DEATH DIFFERENTIATION
 JI Cell Death Differ.
 PD MAR
 PY 2010
 VL 17
 IS 3
 BP 522
 EP 533
 DI 10.1038/cdd.2009.143
 PG 12
 SC Biochemistry & Molecular Biology; Cell Biology
 GA 556CL
 UT ISI:000274565300015
 ER
 
 PT J
 AU Heng, JCD
    Feng, B
    Han, JY
    Jiang, JM
    Kraus, P
    Ng, JH
    Orlov, YL
    Huss, M
    Yang, L
    Lufkin, T
    Lim, B
    Ng, HH
 AF Heng, Jian-Chien Dominic
    Feng, Bo
    Han, Jianyong
    Jiang, Jianming
    Kraus, Petra
    Ng, Jia-Hui
    Orlov, Yuriy L.
    Huss, Mikael
    Yang, Lin
    Lufkin, Thomas
    Lim, Bing
    Ng, Huck-Hui
 TI The Nuclear Receptor Nr5a2 Can Replace Oct4 in the Reprogramming of
    Murine Somatic Cells to Pluripotent Cells
 SO CELL STEM CELL
 LA English
 DT Article
 ID STEM-CELLS; FIBROBLASTS; LRH-1; DOMAIN; MOUSE; MYC
 AB Somatic cells can be reprogrammed to induced pluripotent stem cells
    (iPSGs) with the introduction of Oct4, Sox2, Klf4, and c-Myc. Among
    these four factors, Oct4 is critical in inducing pluripotency because
    no transcription factor can substitute for Oct4, whereas Sox2, Klf4,
    and c-Myc can be replaced by other factors. Here we show that the
    orphan nuclear receptor Nr5a2 (also known as Lrh-1) can replace Oct4 in
    the derivation of iPSCs from mouse somatic cells, and it can also
    enhance reprogramming efficiency. Sumoylation mutants of Nr5a2 with
    enhanced transcriptional activity can further increase reprogramming
    efficiency. Genome-wide location analysis reveals that Nr5a2 shares
    many common gene targets with Sox2 and Klf4, which suggests that the
    transcription factor trio works in concert to mediate reprogramming. We
    also show that Nr5a2 works in part through activating Nanog. Together,
    we show that unrelated transcription factors can replace Oct4 and
    uncovers an exogenous Oct4-free reprogramming code.
 C1 [Heng, Jian-Chien Dominic; Feng, Bo; Jiang, Jianming; Ng, Jia-Hui; Yang, Lin; Ng, Huck-Hui] Genome Inst Singapore, Gene Regulat Lab, Singapore 138672, Singapore.
    [Orlov, Yuriy L.; Huss, Mikael] Genome Inst Singapore, Computat & Syst Biol Grp, Singapore 138672, Singapore.
    [Heng, Jian-Chien Dominic; Ng, Jia-Hui; Ng, Huck-Hui] NUS, Grad Sch Integrat Sci & Engn, Singapore 117597, Singapore.
    [Lufkin, Thomas; Ng, Huck-Hui] Natl Univ Singapore, Dept Biol Sci, Singapore 117543, Singapore.
    [Lim, Bing] Harvard Univ, Sch Med, Ctr Life Sci, Boston, MA 02115 USA.
 RP Ng, HH, Genome Inst Singapore, Gene Regulat Lab, Singapore 138672,
    Singapore.
 EM nghh@gis.a-star.edu.sg
 FU Biomedical Research Council, Agency for Science, Technology and
    Research and Singapore Stem Cell Consortium ; NUS Graduate School for
    Integrative Sciences and Engineering ; A STAR 
 FX We are grateful to the Biomedical Research Council, Agency for Science,
    Technology and Research and Singapore Stem Cell Consortium for funding.
    J.H. is supported by the NUS Graduate School for Integrative Sciences
    and Engineering Scholarship. J.-H.N. is supported by the A STAR
    graduate scholarship. We thank Xiangling Ng and Kuee-Theng Kuay for
    technical support and Meng-Chun Hu for plasmids. We acknowledge Valere
    Cacheux-Rataboul for karyotype analysis and GTB group for sequencing.
    We thank Andrew Hutchins and Felicia Huimei Hong for comments to the
    manuscript.
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 NR 19
 TC 29
 PU CELL PRESS
 PI CAMBRIDGE
 PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
 SN 1934-5909
 J9 CELL STEM CELL
 JI Cell Stem Cell
 PD FEB 5
 PY 2010
 VL 6
 IS 2
 BP 167
 EP 174
 DI 10.1016/j.stem.2009.12.009
 PG 8
 SC Cell & Tissue Engineering; Cell Biology
 GA 555OC
 UT ISI:000274520800011
 ER
 
 PT J
 AU Guo, J
    Liu, ML
    Yang, DH
    Bouxsein, ML
    Saito, H
    Galvin, RJS
    Kuhstoss, SA
    Thomas, CC
    Schipani, E
    Baron, R
    Bringhurst, FR
    Kronenberg, HM
 AF Guo, Jun
    Liu, Minlin
    Yang, Dehong
    Bouxsein, Mary L.
    Saito, Hiroaki
    Galvin, R. J. Sells
    Kuhstoss, Stuart A.
    Thomas, Clare C.
    Schipani, Ernestina
    Baron, Roland
    Bringhurst, F. Richard
    Kronenberg, Henry M.
 TI Suppression of Wnt Signaling by Dkk1 Attenuates PTH-Mediated Stromal
    Cell Response and New Bone Formation
 SO CELL METABOLISM
 LA English
 DT Article
 ID RECEPTOR-RELATED PROTEIN-5; PARATHYROID-HORMONE; BETA-CATENIN; IN-VIVO;
    OSTEOBLASTIC CELLS; HEAD INDUCTION; INHIBITION; DIFFERENTIATION;
    PHOSPHORYLATION; KINASE
 AB Parathyroid hormone (PTH) suppresses Dickkopf 1 (Dkk1) expression in
    osteoblasts. To determine whether this suppression is essential for
    PTH-mediated Wnt signaling and bone formation, we examined mice that
    overexpress Dkk1 in osteoblasts (Dkk1 mice). Dkk1 mice were osteopenic
    due to abnormal osteoblast and osteoclast activity. When fed a
    low-calcium diet, and in two other models of hyperparathyroidism, these
    mice failed to develop the peritrabecular stromal cell response
    ("osteitis fibrosis") and new bone formation seen in wild-type mice.
    Despite these effects of Dkk1 overexpression, PTH still activated Wnt
    signaling in Dkk1 mice and in osteoblastic cells cultured from these
    mice. In cultured MC3T3E1 preosteoblastic cells, PTH dramatically
    suppressed Dkk1 expression, induced PKA-mediated phosphorylation of
    beta-catenin, and significantly enhanced Lef1 expression. Our findings
    indicate that the full actions of PTH require intact Wnt signaling but
    that PTH can activate the Wnt pathway despite overexpression of Dkk1.
 C1 [Guo, Jun; Liu, Minlin; Yang, Dehong; Thomas, Clare C.; Schipani, Ernestina; Bringhurst, F. Richard; Kronenberg, Henry M.] Massachusetts Gen Hosp, Endocrine Unit, Boston, MA 02114 USA.
    [Bouxsein, Mary L.] Beth Israel Deaconess Med Ctr, Orthopaed Biomech Lab, Boston, MA 02215 USA.
    [Galvin, R. J. Sells; Baron, Roland] Harvard Univ, Sch Dent Med, Dept Oral Med, Boston, MA 02115 USA.
    [Galvin, R. J. Sells; Kuhstoss, Stuart A.] Eli Lilly & Co, Lilly Corp Ctr, Lilly Res Labs, Indianapolis, IN 46285 USA.
 RP Kronenberg, HM, Massachusetts Gen Hosp, Endocrine Unit, Boston, MA
    02114 USA.
 EM kronenberg.henry@mgh.harvard.edu
 FU National Heart, Lung, and Blood Institute (NHLBI) [HL081030]
 FX We thank Venkatesh Krishnan for useful discussion regarding the
    anti-Dkk1 study. This work was supported by a grant to H.M.K. from the
    National Heart, Lung, and Blood Institute (NHLBI) Specialized Center
    for Cell-Based Therapy (HL081030).
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 NR 40
 TC 10
 PU CELL PRESS
 PI CAMBRIDGE
 PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
 SN 1550-4131
 J9 CELL METAB
 JI Cell Metab.
 PD FEB 3
 PY 2010
 VL 11
 IS 2
 BP 161
 EP 171
 DI 10.1016/j.cmet.2009.12.007
 PG 11
 SC Cell Biology; Endocrinology & Metabolism
 GA 555ON
 UT ISI:000274521900008
 ER
 
 PT J
 AU Takai, H
    Ashihara, M
    Ishiguro, T
    Terashima, H
    Watanabe, T
    Kato, A
    Suzuki, M
 AF Takai, Hirotake
    Ashihara, Motohki
    Ishiguro, Takahiro
    Terashima, Hiromichi
    Watanabe, Takeshi
    Kato, Atsuhiko
    Suzuki, Masami
 TI Involvement of glypican-3 in the recruitment of M2-polarized
    tumor-associated macrophages in hepatocellular carcinoma
 SO CANCER BIOLOGY & THERAPY
 LA English
 DT Article
 DE GPC3; HCC; xenograft models; TAM; M2 macrophage; microarray analysis
 ID HEPARAN-SULFATE PROTEOGLYCANS; COLONY-STIMULATING FACTOR; BREAST-CANCER
    MODEL; XENOGRAFTS IN-VIVO; GENE-EXPRESSION; MICROARRAY ANALYSIS;
    T-CELLS; PROGRESSION; RANTES; LUNG
 AB Previously, we demonstrated that membrane expression of glypican-3
    (GPC3) stimulates the recruitment of macrophages into human
    hepatocellular carcinoma (HCC) tissues. however, functional
    polarization of the macrophages and the chemoattractant factors related
    to the recruitment has yet to be determined. In this study, to clarify
    the polarization (M1 or M2) of the macrophages and provide a clue as to
    the factors involved in the recruitment, we used xenograft models of
    SK-HEP-1 and SK03 cell lines with undetectable and high-level membrane
    expression of GPC3, respectively and analyzed the expression profiles
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    techniques. Clustering analyses with mouse genome arrays revealed that
    the SK-HEP-1 and SK03 xenografts showed different expression profiles
    for M2 macrophage-related genes but not for M1 macrophage-related
    genes. Many of the M2 macrophage-related genes were upregulated in the
    SK03 xenografts compared to the SK-HEP-1 xenografts. additionally, most
    of the macrophages infiltrating into the SK03 xenografts were positive
    for M2 macrophage-specific markers. Regarding the chemoattractant
    factors, the microarray and quantitative real-time PCR analyses
    revealed that, of the genes reportedly related to macrophage
    recruitment, CCL5, CCL3 and CSF1 were significantly upregulated in the
    SK03 xenograft. These findings suggest that the macrophages recruited
    into GPC3-overexpressing (with membrane expression) HCC are
    M2-polarized ones and, more specifically, M2 tumor-associated
    macrophages which are known to promote tumor progression and
    metastasis, and CCL5, CCL3 and CSF1 are possible candidate genes for
    the recruitment of macrophages.
 C1 [Takai, Hirotake; Watanabe, Takeshi; Kato, Atsuhiko; Suzuki, Masami] Chugai Pharmaceut Co Ltd, Dept Safety Assessment, Shizuoka, Japan.
    [Ashihara, Motohki; Terashima, Hiromichi] Chugai Pharmaceut Co Ltd, Dept Pharmaceut Technol, Kanagawa, Japan.
    [Ishiguro, Takahiro] Chugai Pharmaceut Co Ltd, Pharmaceut Res Dept 2, Kanagawa, Japan.
 RP Takai, H, Chugai Pharmaceut Co Ltd, Dept Safety Assessment, Shizuoka,
    Japan.
 EM takaihrt@chugai-pharm.co.jp
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    ZHU ZW, 2001, GUT, V48, P558
 NR 69
 TC 5
 PU LANDES BIOSCIENCE
 PI AUSTIN
 PA 1002 WEST AVENUE, 2ND FLOOR, AUSTIN, TX 78701 USA
 SN 1538-4047
 J9 CANCER BIOL THER
 JI Cancer Biol. Ther.
 PD DEC 15
 PY 2009
 VL 8
 IS 24
 BP 2329
 EP 2338
 PG 10
 SC Oncology
 GA 551RI
 UT ISI:000274226300010
 ER
 
 PT J
 AU Yang, FC
    Tso, AC
    Chen, CW
    Peng, GS
 AF Yang, Fu-Chi
    Tso, An-Chen
    Chen, Chun-Wen
    Peng, Giia-Sheun
 TI Cerebral venous thrombosis initially presenting with left occipital
    hemorrhage and headache
 SO BLOOD COAGULATION & FIBRINOLYSIS
 LA English
 DT Article
 DE anticoagulation; cerebral hemorrhage; cerebral venous thrombosis;
    headache
 ID DURAL SINUS THROMBOSIS
 AB Cerebral venous thrombosis (CVT) can be difficult to diagnose because
    of its wide spectrum of clinical manifestations. In the present
    article, we report a 58-year-old man coming to our emergency department
    presenting with left temporal throbbing headache and right hemianopia.
    Computed tomography of the brain revealed acute hemorrhages over the
    left occipital area. Due to the unusual location of hemorrhage,
    magnetic resonance venography was performed, revealing absence of
    venous flow over the superior sagittal and transverse sinuses
    suggestive of CVT. He received anticoagulant therapy for 6 months and
    the headache subsided. We feel that a high index of clinical suspicion
    is needed to diagnose an intracerebral hemorrhage in an uncommon site
    caused by CVT, even if risk factors of CVT are not present, so that
    appropriate treatment can be initiated as promptly as possible. Failure
    to recognize the signs of CVT could result in inappropriate management
    and suboptimal secondary prophylaxis strategies, which could affect the
    patient's clinical outcome. Blood Coagul Fibrinolysis 21:182-184 (C)
    2010 Wolters Kluwer Health vertical bar Lippincott Williams & Wilkins.
 C1 [Yang, Fu-Chi; Tso, An-Chen; Peng, Giia-Sheun] Triserv Gen Hosp, Dept Neurol, Natl Def Med Ctr, Taipei 114, Taiwan.
    [Chen, Chun-Wen] Triserv Gen Hosp, Dept Radiol, Natl Def Med Ctr, Taipei 114, Taiwan.
 RP Peng, GS, Triserv Gen Hosp, Dept Neurol, Natl Def Med Ctr, 325,Sect
    2,Cheng Kung Rd, Taipei 114, Taiwan.
 EM fuji-yang@yahoo.com.tw
    penggs@mail.ndmctsgh.edu.tw
 CR AGOSTONI E, 2004, NEUROL SCI S3, V25, S206, DOI
    10.1007/s10072-004-0287-3
    BOUSSER MG, 1985, STROKE, V16, P199
    BRETEAU G, 2003, J NEUROL, V250, P29, DOI 10.1007/s00415-003-0932-4
    CONNOR SEJ, 2002, CLIN RADIOL, V57, P449
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 NR 13
 TC 0
 PU LIPPINCOTT WILLIAMS & WILKINS
 PI PHILADELPHIA
 PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
 SN 0957-5235
 J9 BLOOD COAGULAT FIBRINOL
 JI Blood Coagul. Fibrinolysis
 PD MAR
 PY 2010
 VL 21
 IS 2
 BP 182
 EP 184
 DI 10.1097/MBC.0b013e328333782c
 PG 3
 SC Hematology
 GA 555LZ
 UT ISI:000274513600014
 ER
 
 PT J
 AU Yang, HC
    Chen, JW
    Liu, CM
    Wen, CC
    Liu, YL
    Chen, CH
    Hwu, HG
 AF Yang, Hsin-Chou
    Chen, Jia-Wei
    Liu, Chih-Min
    Wen, Chun-Chiang
    Liu, Yu-Li
    Chen, Chun-Houh
    Hwu, Hai-Gwo
 TI The Taiwan Schizophrenia Genetic Interaction Study
 SO GENETIC EPIDEMIOLOGY
 LA English
 DT Meeting Abstract
 CT 18th Annual Meeting of the International-Genetic-Epidemiology-Society
 CY OCT 10-20, 2009
 CL Honolulu, HI
 SP Int Genet Epidemiol Soc
 C1 [Yang, Hsin-Chou; Chen, Jia-Wei; Chen, Chun-Houh] Acad Sinica, Inst Stat Sci, Taipei, Taiwan.
    [Liu, Chih-Min; Wen, Chun-Chiang; Hwu, Hai-Gwo] Natl Taiwan Univ Hosp, Dept Psychiat, Taipei, Taiwan.
 NR 0
 TC 0
 PU WILEY-LISS
 PI HOBOKEN
 PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA
 SN 0741-0395
 J9 GENET EPIDEMIOL
 JI Genet. Epidemiol.
 PD DEC
 PY 2009
 VL 33
 IS 8
 BP 67         
 PG 1
 SC Genetics & Heredity; Public, Environmental & Occupational Health
 GA 529TK
 UT ISI:000272540600077
 ER
 
 PT J
 AU Levin, AM
    Datta, I
    Yang, J
    Iannuzzi, MC
    McKeigue, PM
    Rybicki, BA
    Gray-McGuire, CL
 AF Levin, Albert M.
    Datta, Indrani
    Yang, James
    Iannuzzi, Micheal C.
    McKeigue, Paul M.
    Rybicki, Benjamin A.
    Gray-McGuire, Courtney L.
 TI Ancestry Informative Markers and Family-Based Association
 SO GENETIC EPIDEMIOLOGY
 LA English
 DT Meeting Abstract
 CT 18th Annual Meeting of the International-Genetic-Epidemiology-Society
 CY OCT 10-20, 2009
 CL Honolulu, HI
 SP Int Genet Epidemiol Soc
 C1 [Levin, Albert M.; Datta, Indrani; Yang, James; Rybicki, Benjamin A.] Henry Ford Hlth Syst, Detroit, MI USA.
    [Iannuzzi, Micheal C.] SUNY Upstate Med Univ, Syracuse, NY USA.
    [McKeigue, Paul M.] Univ Edinburgh, Western Gen Hosp, Edinburgh EH8 9YL, Midlothian, Scotland.
    [Gray-McGuire, Courtney L.] Oklahoma Med Res Fdn, Oklahoma City, OK USA.
 NR 0
 TC 0
 PU WILEY-LISS
 PI HOBOKEN
 PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA
 SN 0741-0395
 J9 GENET EPIDEMIOL
 JI Genet. Epidemiol.
 PD DEC
 PY 2009
 VL 33
 IS 8
 BP 107        
 PG 1
 SC Genetics & Heredity; Public, Environmental & Occupational Health
 GA 529TK
 UT ISI:000272540600117
 ER
 
 PT J
 AU Yang, W
    Gu, CC
 AF Yang, Wei
    Gu, Chi C.
 TI A Whole-genome Simulator Capable of Modeling High-order Epistasis for
    GWAS Studies of Complex Disease
 SO GENETIC EPIDEMIOLOGY
 LA English
 DT Meeting Abstract
 CT 18th Annual Meeting of the International-Genetic-Epidemiology-Society
 CY OCT 10-20, 2009
 CL Honolulu, HI
 SP Int Genet Epidemiol Soc
 C1 [Gu, Chi C.] Washington Univ, Div Biostat, Dept Genet, St Louis, MO USA.
 NR 0
 TC 0
 PU WILEY-LISS
 PI HOBOKEN
 PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA
 SN 0741-0395
 J9 GENET EPIDEMIOL
 JI Genet. Epidemiol.
 PD DEC
 PY 2009
 VL 33
 IS 8
 BP 148        
 PG 1
 SC Genetics & Heredity; Public, Environmental & Occupational Health
 GA 529TK
 UT ISI:000272540600157
 ER
 
 PT J
 AU Chen, L
    Yang, G
 AF Chen, Lian
    Yang, Guang
 TI A genomic scanning using AFLP to detect candidate loci under selection
    in the finless porpoise (Neophocaena phocaenoides)
 SO GENES & GENETIC SYSTEMS
 LA English
 DT Article
 DE AFLP; finless porpoise; outlier loci; population genomics; selection
 ID BACKGROUND SELECTION; POPULATION-STRUCTURE; FUNCTIONAL GENOMICS;
    NATURAL-POPULATIONS; GENETIC-STRUCTURE; MARKERS; DIFFERENTIATION;
    POLYMORPHISM; ADAPTATION; DIVERGENCE
 AB Identifying loci under natural selection from genomic surveys is of
    great interest in different research areas, stimulated by the
    increasing ease with large numbers of markers to gain a genome-wide
    perspective on differentiation. In this study, we searched for the
    genetic signatures of selection by screening 114 amplified fragment
    length polymorphism (AFLP) markers in three finless porpoise
    populations inhabiting contrasting natural environments (freshwater and
    marine habitat). Comparing among three populations, four AFLP loci
    exhibited F-ST values higher than 0.975 quantile which might be
    inferred to be under divergent selection and two loci fell below the
    0.025 quantile which might be affected by balancing selection. Although
    these loci were not supported with statistical significance in false
    discovery rate (FDR) analysis, the present study illustrated the
    potential of genome-wide surveys to identify specific genome regions or
    genes associated with freshwater adaptation of the finless porpoise.
 C1 [Chen, Lian; Yang, Guang] Nanjing Normal Univ, Coll Life Sci, Jiangsu Key Lab Biodivers & Biotechnol, Nanjing 210046, Peoples R China.
 RP Yang, G, Nanjing Normal Univ, Coll Life Sci, Jiangsu Key Lab Biodivers
    & Biotechnol, Nanjing 210046, Peoples R China.
 EM gyang@njnu.edu.cn
 FU National Natural Science Foundation of China (NSFC) [30830016,
    30670294, 30470253]; Program for New Century Excellent Talents in
    University [NCET-07-0445]; Ministry of Education of China ; Specialized
    Research Fund for the Doctoral Program of Higher Education [SRFDP
    20060319002]; Natural Science Foundation of the Jiangsu Higher
    Education Institutions of China [07KJA18016]
 FX We thank Dr. Aurelie Bonin for her valuable advice and kind assistance
    on analytical issues. This research was financially supported by the
    National Natural Science Foundation of China (NSFC) key project grant
    no. 30830016, NSFC grant nos 30670294 and 30470253, the Program for New
    Century Excellent Talents in University (NCET-07-0445), the Ministry of
    Education of China, the Specialized Research Fund for the Doctoral
    Program of Higher Education (SRFDP 20060319002), the Ministry of
    Education of China, and the major project of the Natural Science
    Foundation of the Jiangsu Higher Education Institutions of China
    (07KJA18016).
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 NR 41
 TC 1
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 PI SHIZUOKA
 PA NATL INST GENETICS, YATA, MISHIMA,, SHIZUOKA, 411, JAPAN
 SN 1341-7568
 J9 GENES GENET SYST
 JI Genes Genet. Syst.
 PD AUG
 PY 2009
 VL 84
 IS 4
 BP 307
 EP 313
 PG 7
 SC Biochemistry & Molecular Biology; Genetics & Heredity
 GA 553OL
 UT ISI:000274376600006
 ER
 
 PT J
 AU Li, Z
    Zhao, B
    Wang, P
    Chen, F
    Dong, ZH
    Yang, HR
    Guan, KL
    Xu, YH
 AF Li, Ze
    Zhao, Bin
    Wang, Ping
    Chen, Fei
    Dong, Zhenghong
    Yang, Huirong
    Guan, Kun-Liang
    Xu, Yanhui
 TI Structural insights into the YAP and TEAD complex
 SO GENES & DEVELOPMENT
 LA English
 DT Article
 DE YAP; TEAD; structure; Hippo
 ID YES-ASSOCIATED PROTEIN; TRANSCRIPTION FACTOR; ONCOGENIC TRANSFORMATION;
    CELL-PROLIFERATION; CONTACT INHIBITION; GROWTH-CONTROL; SIZE-CONTROL;
    ORGAN SIZE; DOMAIN; COACTIVATOR
 AB The Yes-associated protein (YAP) transcriptional coactivator is a key
    regulator of organ size and a candidate human oncogene inhibited by the
    Hippo tumor suppressor pathway. The TEAD family of transcription
    factors binds directly to and mediates YAP-induced gene expression.
    Here we report the three-dimensional structure of the YAP (residues
    50-171)-TEAD1 (residues 194-411) complex, in which YAP wraps around the
    globular structure of TEAD1 and forms extensive interactions via three
    highly conserved interfaces. Interface 3, including YAP residues
    86-100, is most critical for complex formation. Our study reveals the
    biochemical nature of the YAP-TEAD interaction, and provides a basis
    for pharmacological intervention of YAP-TEAD hyperactivation in human
    diseases.
 C1 [Li, Ze; Wang, Ping; Chen, Fei; Dong, Zhenghong; Yang, Huirong; Xu, Yanhui] Fudan Univ, Sch Life Sci, Shanghai 200433, Peoples R China.
    [Li, Ze; Xu, Yanhui] Fudan Univ, Inst Biomed Sci, Shanghai 200032, Peoples R China.
    [Zhao, Bin; Guan, Kun-Liang] Univ Calif San Diego, Dept Pharmacol, La Jolla, CA 92093 USA.
    [Zhao, Bin; Guan, Kun-Liang] Univ Calif San Diego, Moores Canc Ctr, La Jolla, CA 92093 USA.
    [Xu, Yanhui] Fudan Univ, Dept Pathol, Canc Hosp, Shanghai 200032, Peoples R China.
 RP Xu, YH, Fudan Univ, Sch Life Sci, Shanghai 200433, Peoples R China.
 EM kuguan@ucsd.edu
    xuyh@fudan.edu.cn
 FU National Natural Science Foundation of China [30870493]; National Basic
    Research Program of China [2009CB918600]; Shanghai Pujiang Program
    [08PJ14010]; Shanghai Leading Academic Discipline Project [B111]; NIH 
 FX We thank all of the staff at the beamline BL17U at Shanghai Synchrotron
    Radiation Facility (China) and BL17A at Photon Factory (Japan) for
    assistance in data collection, and Karen Tumaneng for critical reading
    of the manuscript. This work was supported by grants from the National
    Natural Science Foundation of China (30870493), National Basic Research
    Program of China (2009CB918600), Shanghai Pujiang Program (08PJ14010),
    and Shanghai Leading Academic Discipline Project (B111) to Y.X., and
    grants from the NIH to K.L.G.
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 NR 38
 TC 7
 PU COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT
 PI WOODBURY
 PA 500 SUNNYSIDE BLVD, WOODBURY, NY 11797-2924 USA
 SN 0890-9369
 J9 GENE DEVELOP
 JI Genes Dev.
 PD FEB 1
 PY 2010
 VL 24
 IS 3
 BP 235
 EP 240
 DI 10.1101/gad.1865810
 PG 6
 SC Cell Biology; Developmental Biology; Genetics & Heredity
 GA 550UZ
 UT ISI:000274157300003
 ER
 
 PT J
 AU Yang, H
    Cui, GB
    Jiao, XY
    Wang, J
    Ju, G
    You, SW
 AF Yang, Hao
    Cui, Guang-Bin
    Jiao, Xi-Ying
    Wang, Jian
    Ju, Gong
    You, Si-Wei
 TI Thymosin-beta 4 Attenuates Ethanol-induced Neurotoxicity in Cultured
    Cerebral Cortical Astrocytes by Inhibiting Apoptosis
 SO CELLULAR AND MOLECULAR NEUROBIOLOGY
 LA English
 DT Article
 DE Thymosin-beta 4; Ethanol; Astrocyte; Cell culture; Apoptosis
 ID RAT HIPPOCAMPAL ASTROCYTES; CENTRAL-NERVOUS-SYSTEM; FETAL ALCOHOL
    SYNDROME; BETA(4) MESSENGER-RNA; INDUCED CELL-DEATH;
    ALZHEIMERS-DISEASE; IN-VITRO; CA2+ MOBILIZATION; OXIDATIVE DAMAGE;
    EPITHELIAL-CELLS
 AB Thymosin-beta 4 (T beta 4) is a major actin monomer-binding peptide in
    mammalian tissues and plays a crucial role in the nervous system in
    synaptogenesis, neuronal survival and migration, axonal growth, and
    plastic changes of dendritic spines. However, it is unknown whether T
    beta 4 is also involved in challenges with external stress such as
    ethanol-induced neurotoxicity. In the present study, we investigated
    the effects of T beta 4 on ethanol-induced neurotoxicity in cultured
    cerebral cortical astrocytes and the underlying mechanisms. Primarily
    cultured astrocytes were treated with 1 mu g/ml T beta 4 2 h prior to
    administration of 100 mM ethanol for 0.5, 1, 3 and 6 days,
    respectively. The results showed that ethanol caused neurotoxicity in
    cultured astrocytes, as shown by declined cell viability, distinct
    astroglial apoptosis and increased intracellular peroxidation. T beta 4
    markedly promoted cell viability, ameliorated the injury of
    intracellular glial fibrillary acidic protein-immunopositive
    cytoskeletal structures, reduced the percentage of apoptotic astrocyte
    and cellular DNA fragmentation, suppressed caspase-3 activity and
    upregulated Bcl-2 expression, inhibited the accumulation of reactive
    oxygen species and production of malondialdehyde in ethanol-treated
    astrocytes in a time-dependent manner. These data indicated that T beta
    4 attenuates ethanol-induced neurotoxicity in cultured cortical
    astrocytes through inhibition of apoptosis signaling, and one of the
    mechanisms underlying the capacity of T beta 4 to suppress apoptosis
    may in part be due to its effect of anti-peroxidation.
 C1 [Yang, Hao; Jiao, Xi-Ying; Wang, Jian; Ju, Gong; You, Si-Wei] Fourth Mil Med Univ, Inst Neurosci, Xian 710032, Peoples R China.
    [Cui, Guang-Bin] Fourth Mil Med Univ, Tangdu Hosp, Dept Radiol, Xian 710038, Peoples R China.
 RP Ju, G, Fourth Mil Med Univ, Inst Neurosci, Xian 710032, Peoples R China.
 EM yanghao71_99@yahoo.com
    jugong@fmmu.edu.cn
    yousiwei@fmmu.edu.cn
 FU Natural Science Foundation of China [30872829, 30571998]; Chinese PLA
    national scientific technological project [06G089]
 FX This work was supported by the Natural Science Foundation of China
    (30872829, 30571998) and Chinese PLA national scientific technological
    project (06G089).
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 NR 66
 TC 1
 PU SPRINGER/PLENUM PUBLISHERS
 PI NEW YORK
 PA 233 SPRING ST, NEW YORK, NY 10013 USA
 SN 0272-4340
 J9 CELL MOL NEUROBIOL
 JI Cell. Mol. Neurobiol.
 PD JAN
 PY 2010
 VL 30
 IS 1
 BP 149
 EP 160
 DI 10.1007/s10571-009-9439-6
 PG 12
 SC Cell Biology; Neurosciences
 GA 549XI
 UT ISI:000274087400015
 ER
 
 PT J
 AU Yang, WL
    Wu, CY
    Wu, J
    Lin, HK
 AF Yang, Wei-Lei
    Wu, Ching-Yuan
    Wu, Juan
    Lin, Hui-Kuan
 TI Regulation of Akt signaling activation by ubiquitination
 SO CELL CYCLE
 LA English
 DT Review
 DE Akt; kinase; ubiquitination; phosphorylation; TRAF6; E3 ligase; PDK1;
    mTORC2; NF kappa B; tumorigenesis
 ID NF-KAPPA-B; PLECKSTRIN HOMOLOGY DOMAIN; PROSTATE INTRAEPITHELIAL
    NEOPLASIA; PHOSPHOINOSITIDE 3-KINASE PATHWAY; SERINE-THREONINE KINASE;
    PROTEIN-KINASE; MOLECULAR-CLONING; TUMOR SUPPRESSION; CELL-MIGRATION;
    E17K MUTATION
 AB Akt (also known as PKB) signaling orchestrates many aspects of
    biological functions and, importantly, its deregulation is linked to
    cancer development. Akt activity is well-known regulated through its
    phosphorylation at T308 and S473 by PDK1 and mTORC2, respectively.
    Although in the last decade the research has been primarily focused on
    Akt phosphorylation and its role in Akt activation and functions, other
    posttranslational modifications on Akt have never been reported. Until
    very recently, a novel posttranslational modification on Akt termed
    ubiquitination was identified and shown to play an important role in
    Akt activation. The cancer-associated Akt mutant recently identified in
    a subset of human cancers displays enhanced Akt ubiquitination, in turn
    contributing to Akt hyperactivation, suggesting a potential role of Akt
    ubiquitination in cancers. Thus, this novel posttranslational
    modification on Akt reveals an exciting avenue that has advanced our
    current understandings of how Akt signaling activation is regulated.
 C1 [Yang, Wei-Lei; Wu, Ching-Yuan; Wu, Juan; Lin, Hui-Kuan] Univ Texas MD Anderson Canc Ctr, Dept Mol & Cellular Oncol, Houston, TX 77030 USA.
    [Yang, Wei-Lei; Lin, Hui-Kuan] Univ Texas Houston, Grad Sch Biomed Sci, Houston, TX USA.
    [Wu, Ching-Yuan] Chang Gung Univ, Coll Med, Chang Gung Mem Hosp, Kaohsiung Med Ctr,Dept Chinese Med, Kaohsiung, Taiwan.
    [Wu, Juan] Sun Yat Sen Univ, State Key Lab Oncol S China, Guangzhou 510275, Guangdong, Peoples R China.
    [Wu, Juan] Sun Yat Sen Univ, Dept Expt Res, Guangzhou 510275, Guangdong, Peoples R China.
 RP Lin, HK, Univ Texas MD Anderson Canc Ctr, Dept Mol & Cellular Oncol,
    Houston, TX 77030 USA.
 EM hklin@mdanderson.org
 FU National Science Council fund [NSC-97-2911-I-182-004-2]; China
    Scholarship Council fund 
 FX We thank the members of the Lin's lab for their critical reading and
    comments on our manuscript. We apologize to many investigators whose
    important works were not cited here due to space limitations. This work
    is supported by M. D. Anderson Research Trust Scholar Fund to H. K.
    Lin, a National Science Council fund (NSC-97-2911-I-182-004-2) from
    Taiwan to C.Y. Wu, and a China Scholarship Council fund to J. Wu.
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 NR 114
 TC 2
 PU LANDES BIOSCIENCE
 PI AUSTIN
 PA 1002 WEST AVENUE, 2ND FLOOR, AUSTIN, TX 78701 USA
 SN 1538-4101
 J9 CELL CYCLE
 JI Cell Cycle
 PD FEB 1
 PY 2010
 VL 9
 IS 3
 BP 486
 EP 497
 PG 12
 SC Cell Biology
 GA 550PI
 UT ISI:000274140000027
 ER
 
 PT J
 AU Tang, XF
    Bu, XK
    Hang, NH
    Li, XX
    Huang, HJ
    Bai, H
    Yang, X
 AF Tang, Xiaofei
    Bu, Xiaokun
    Zhang, Naihong
    Li, Xiaoxia
    Huang, Huanjun
    Bai, Hong
    Yang, Xi
 TI Inefficiency of C3H/HeN Mice to Control Chlamydial Lung Infection
    Correlates with Downregulation of Neutrophil Activation during the Late
    Stage of Infection
 SO CELLULAR & MOLECULAR IMMUNOLOGY
 LA English
 DT Article
 DE Chlamydia trachomatis; neutrophils; selectins; ICAM-1; CD11b
 ID CD11B/CD18 EXPRESSION; CROSS-LINKING; HOST-DEFENSE; P-SELECTIN;
    TRACHOMATIS; INFLAMMATION; INTEGRINS; HISTOPATHOLOGY; SEQUESTRATION;
    PHAGOCYTOSIS
 AB We previously reported that massive infiltration of neutrophils in
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    mice to lung infection. To further define the nature of neutrophil
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    expression of adhesion molecules and CD11b related to neutrophils
    infiltration and activation, respectively, following intranasal Cm
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    in C3H mice. In contrast, CD11b expression on peripheral blood and lung
    neutrophils in C3H mice exhibited a significant reduction compared with
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 C1 [Tang, Xiaofei; Bu, Xiaokun; Zhang, Naihong; Li, Xiaoxia; Huang, Huanjun; Bai, Hong; Yang, Xi] Tianjin Med Univ, Dept Immunol, Tianjin Key Lab Cellular & Mol Immunol, Key Lab Educ Minist China, Tianjin 300070, Peoples R China.
    [Yang, Xi] Univ Manitoba, Fac Med, Dept Med Microbiol, Lab Infect & Immun, Winnipeg, MB, Canada.
    [Yang, Xi] Univ Manitoba, Fac Med, Dept Immunol, Lab Infect & Immun, Winnipeg, MB R3E 0W3, Canada.
 RP Bai, H, Tianjin Med Univ, Dept Immunol, Tianjin Key Lab Cellular & Mol
    Immunol, Key Lab Educ Minist China, 22 Qixiangtai Rd, Tianjin 300070,
    Peoples R China.
 EM hongbai25@163.com
    yangxi@cc.umanitoba.ca
 FU Tianjin Municipal Science and Technology Commission [07JCYBJC 10600]
 FX This work was supported by fund from Tianjin Municipal Science and
    Technology Commission (07JCYBJC 10600).
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 PU CHINESE SOC IMMUNOLOGY
 PI BEIJING
 PA 5 SANTIAO DONGDAN, BEIJING, 10005, PEOPLES R CHINA
 SN 1672-7681
 J9 CELL MOL IMMUNOL
 JI Cell. Mol. Immunol.
 PD AUG
 PY 2009
 VL 6
 IS 4
 BP 253
 EP 260
 PG 8
 SC Immunology
 GA 552WH
 UT ISI:000274324000003
 ER
 
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 AF Lo, Cherry Kam Chun
    Lam, Queenie Lai Kwan
    Yang, Min
    Ko, King-Hung
    Sun, Lingyun
    Ma, Rui
    Wang, Shengjun
    Xu, Huaxi
    Tam, Sidney
    Wu, Chang-You
    Zheng, Bo-Jiang
    Lu, Liwei
 TI Leptin Signaling Protects NK Cells from Apoptosis During Development in
    Mouse Bone Marrow
 SO CELLULAR & MOLECULAR IMMUNOLOGY
 LA English
 DT Article
 DE NK cell; bone marrow; lymphocyte development
 ID NATURAL-KILLER-CELLS; TRANSCRIPTION FACTOR; DENDRITIC CELLS; B
    LYMPHOPOIESIS; MICE; RECEPTOR; ACTIVATION; IMMUNITY; HEMATOPOIESIS;
    DEFICIENCY
 AB Increasing evidence indicates a role of leptin in immune response, but
    it remains largely unclear whether leptin signaling is involved in
    regulating NK cell development in the bone marrow (BM). In this study,
    we have characterized NK cell differentiation and maturation in the BM
    of leptin-receptor deficient db/db mice at a prediabetic stage.
    Although the BM cellularity was similar to the control value, the total
    number of NK cells was severely reduced in mutant mice. Flow cytometric
    analysis of db/db BM cells revealed significantly decreased frequencies
    of developing NK cells at various stages of differentiation. BM db/db
    NK cells displayed markedly increased apoptosis but maintained normal
    cell cycling status and proliferative capacity. Moreover, recombinant
    leptin could significantly enhance the survival of NK cells from
    wild-type mice in cultures. Further examination on NK cell functional
    activity showed that db/db NK cells exhibited normal intrinsic
    cytotoxicity with significantly increased IL-10 production. Taken
    together, our findings suggest that leptin signaling regulates NK cell
    development via enhancing the survival of immature NK cells in mouse
    BM. Cellular & Molecular Immunology. 2009;6(5):353-360.
 C1 [Lo, Cherry Kam Chun; Lam, Queenie Lai Kwan; Yang, Min; Ko, King-Hung; Zheng, Bo-Jiang; Lu, Liwei] Univ Hong Kong, Dept Pathol, Hong Kong, Hong Kong, Peoples R China.
    [Lo, Cherry Kam Chun; Lam, Queenie Lai Kwan; Yang, Min; Ko, King-Hung; Zheng, Bo-Jiang; Lu, Liwei] Univ Hong Kong, Dept Microbiol, Hong Kong, Hong Kong, Peoples R China.
    [Lo, Cherry Kam Chun; Lam, Queenie Lai Kwan; Yang, Min; Ko, King-Hung; Zheng, Bo-Jiang; Lu, Liwei] Univ Hong Kong, Ctr Infect & Immunol, Hong Kong, Hong Kong, Peoples R China.
    [Sun, Lingyun] Nanjing Univ, Dept Rheumatol, Drum Tower Hosp, Sch Med, Nanjing 210008, Peoples R China.
    [Ma, Rui; Wang, Shengjun; Xu, Huaxi] Jiangsu Univ, Dept Immunol, Sch Med Sci & Lab Med, Zhenjiang, Peoples R China.
    [Tam, Sidney] Queen Mary Hosp, Dept Pathol, Hong Kong, Hong Kong, Peoples R China.
    [Wu, Chang-You] Sun Yat Sen Univ, Dept Immunol, Guangzhou 510275, Guangdong, Peoples R China.
 RP Lu, LW, Univ Hong Kong, Dept Pathol, Pokfulam Rd, Hong Kong, Hong Kong,
    Peoples R China.
 EM liweilu@hkucc.hku.hk
 FU Research Grants Council of Hong Kong 
 FX This work was supported by a grant to L Lu from the Research Grants
    Council of Hong Kong.
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 NR 30
 TC 5
 PU CHINESE SOC IMMUNOLOGY
 PI BEIJING
 PA 5 SANTIAO DONGDAN, BEIJING, 10005, PEOPLES R CHINA
 SN 1672-7681
 J9 CELL MOL IMMUNOL
 JI Cell. Mol. Immunol.
 PD OCT
 PY 2009
 VL 6
 IS 5
 BP 353
 EP 360
 PG 8
 SC Immunology
 GA 552WI
 UT ISI:000274324100005
 ER
 
 PT J
 AU Cai, ZJ
    Zhang, W
    Li, M
    Yue, YP
    Yang, F
    Yu, L
    Cao, XT
    Wang, JL
 AF Cai, Zhijian
    Zhang, Wei
    Li, Min
    Yue, Yinpu
    Yang, Fei
    Yu, Lei
    Cao, Xuetao
    Wang, Jianli
 TI TGF-beta 1 gene-modified, immature dendritic cells delay the
    development of inflammatory bowel disease by inducing CD4(+)Foxp3(+)
    regulatory T cells
 SO CELLULAR & MOLECULAR IMMUNOLOGY
 LA English
 DT Article
 DE DCs; IBD; TGF-beta 1; Treg
 ID EXPRESSION; TOLERANCE; IMMUNITY
 AB Inflammatory bowel disease (IBD) is caused by an uncontrolled immune
    response in the intestinal lumen, leading to inflammation in
    genetically predisposed individuals. Immunotherapy may be a promising
    approach to the treatment of IBD. Here, we show that transforming
    growth factor-beta 1 (TGF-beta 1) gene-modified immature dendritic
    cells (imDCs) could enhance the inhibitory function of imDCs and delay
    the progress of IBD induced by dextran sodium sulfate in mice. The
    results of fluorescence-activated cell sorter (FACS) demonstrated that
    this protective effect is mediated partially by inducing CD4(+)Foxp3(+)
    regulatory T cells (Tregs) in mesentery lymph nodes to control
    inflammation. In vitro experiments also supported this hypothesis. In
    conclusion, we provide evidence that TGF-beta 1-modified bone
    marrow-derived imDCs may have a therapeutic effect to IBD. Cellular &
    Molecular Immunology (2010) 7, 35-43; doi:10.1038/cmi.2009.107
 C1 [Cai, Zhijian; Zhang, Wei; Li, Min; Yue, Yinpu; Yang, Fei; Yu, Lei; Cao, Xuetao; Wang, Jianli] Zhejiang Univ, Sch Med, Inst Immunol, Hangzhou 310058, Zhejiang, Peoples R China.
    [Cao, Xuetao] Mil Med Coll 2, Inst Immunol, Shanghai, Peoples R China.
    [Cao, Xuetao] Mil Med Coll 2, Natl Key Lab Med Immunol, Shanghai, Peoples R China.
 RP Wang, JL, Zhejiang Univ, Sch Med, Inst Immunol, Hangzhou 310058,
    Zhejiang, Peoples R China.
 EM jlwang@zju.edu.cn
 FU National Key Basic Research Program of China [2007CB512400]; National
    High Technology Research and Development Program of China
    [2006AA02A239, 2007AA021102]; National Natural Science Foundation of
    China [30671909, 30972725]; Natural Science Foundation of Zhejiang
    Province [Z2090042]
 FX We thank Professor Lin-Rong Lu for his critical review of the
    manuscript. This work was supported by the National Key Basic Research
    Program of China (Grant 2007CB512400), the National High Technology
    Research and Development Program of China (Grants 2006AA02A239 and
    2007AA021102), the National Natural Science Foundation of China (Grant
    30671909 and 30972725) and Natural Science Foundation of Zhejiang
    Province (Z2090042).
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 NR 23
 TC 1
 PU NATURE PUBLISHING GROUP
 PI NEW YORK
 PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
 SN 1672-7681
 J9 CELL MOL IMMUNOL
 JI Cell. Mol. Immunol.
 PD JAN
 PY 2010
 VL 7
 IS 1
 BP 35
 EP 43
 DI 10.1038/cmi.2009.107
 PG 9
 SC Immunology
 GA 552WG
 UT ISI:000274323900005
 ER
 
 PT J
 AU Sun, JT
    Zhang, Y
    Yang, MX
    Zhang, Y
    Xie, Q
    Li, ZW
    Dong, ZG
    Yang, YM
    Deng, BP
    Feng, A
    Hu, WX
    Mao, HT
    Qu, X
 AF Sun, Jintang
    Zhang, Yan
    Yang, Meixiang
    Zhang, Yun
    Xie, Qi
    Li, Zewu
    Dong, Zhaogang
    Yang, Yongmei
    Deng, Biping
    Feng, Alei
    Hu, Weixu
    Mao, Haiting
    Qu, Xun
 TI Hypoxia induces T-cell apoptosis by inhibiting chemokine C receptor 7
    expression: the role of adenosine receptor A(2)
 SO CELLULAR & MOLECULAR IMMUNOLOGY
 LA English
 DT Article
 DE adenosine receptor; apoptosis; CCR7; T cells
 ID DENDRITIC CELLS; EFFECTOR FUNCTIONS; DEAMINASE DEFICIENCY; LYMPHOCYTES;
    PROLIFERATION; SUPPRESSES; ACTIVATION; MECHANISMS; PROTECTION; SUBSETS
 AB Hypoxia is a major characteristic of the tumor microenvironment, and
    its effects on immune cells are proposed to be important factors for
    the process of tumor immune escape. It has been reported that hypoxia
    affects the function of dendritic cells and the antitumor function of T
    cells. Here we discuss the effects of hypoxia on T-cell survival. Our
    results showed that hypoxia induced apoptosis of T cells. Adenosine and
    adenosine receptors (AR) are important to the hypoxia-related signaling
    pathway. Using AR agonists and antagonists, we demonstrated that
    hypoxia-induced apoptosis of T cells was mediated by A(2a) and A(2b)
    receptors. Furthermore, we are the first, to our knowledge, to report
    that hypoxia significantly inhibited the expression of chemokine C
    receptor 7 (CCR7) of T cells via the A(2)R signal pathway, perhaps
    representing a mechanism of hypoxia-induced apoptosis of T cells.
    Collectively, our research demonstrated that hypoxia induces T-cell
    apoptosis by the A(2)R signaling pathway partly by suppressing CCR7.
    Blocking the A(2)R signaling pathway and/or activation of CCR7 can
    increase the anti-apoptosis function of T cells and may become a new
    strategy to improve antitumor potential. Cellular & Molecular
    Immunology (2010) 7, 77-82; doi:10.1038/cmi.2009.105; published online
    23 December 2009
 C1 [Sun, Jintang; Zhang, Yan; Yang, Meixiang; Zhang, Yun; Xie, Qi; Li, Zewu; Dong, Zhaogang; Yang, Yongmei; Deng, Biping; Feng, Alei; Hu, Weixu; Mao, Haiting; Qu, Xun] Shandong Univ, Qilu Hosp, Inst Basic Med Sci, Jinan 250012, Peoples R China.
    [Zhang, Yan] Shandong Ctr Dis Control & Prevent, Jinan, Peoples R China.
 RP Qu, X, Shandong Univ, Qilu Hosp, Inst Basic Med Sci, Jinan 250012,
    Peoples R China.
 EM quxun@sdu.edu.cn
 FU National Natural Science Foundation of China [30671902, 30872321];
    Natural Science Foundation of Shandong Province [Y2008C02, Y2006C122]
 FX This work was supported by grants from the National Natural Science
    Foundation of China (No. 30671902 and No. 30872321) and the Natural
    Science Foundation of Shandong Province (No. Y2008C02 and No.
    Y2006C122).
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 NR 31
 TC 0
 PU NATURE PUBLISHING GROUP
 PI NEW YORK
 PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
 SN 1672-7681
 J9 CELL MOL IMMUNOL
 JI Cell. Mol. Immunol.
 PD JAN
 PY 2010
 VL 7
 IS 1
 BP 77
 EP 82
 DI 10.1038/cmi.2009.105
 PG 6
 SC Immunology
 GA 552WG
 UT ISI:000274323900010
 ER
 
 PT J
 AU Yoshida, C
    Hishiyama, K
    Miyazaki, K
    Watanabe, M
    Kanbe, M
    Yamada, Y
    Matsuzaki, K
    Miyashita, K
    Kitanaka, S
    Miyata, S
 AF Yoshida, Chisato
    Hishiyama, Kazsuyoshi
    Miyazaki, Khosuke
    Watanabe, Manami
    Kanbe, Masahiro
    Yamada, Yuta
    Matsuzaki, Keiithi
    Miyashita, Kiichi
    Kitanaka, Susumu
    Miyata, Shohei
 TI Analysis of inhibition of topoisomerase II alpha and cancer cell
    proliferation by ingenolEZ
 SO CANCER SCIENCE
 LA English
 DT Article
 ID DNA TOPOISOMERASE; EUPHORBIA-KANSUI; INDUCE APOPTOSIS; DECATENATION;
    CHECKPOINT; ENZYME; ESTERS; CYTOTOXICITY; DERIVATIVES; DITERPENES
 AB We previously reported that many ingenol compounds derived from
    Euphorbia kansui exhibit topoisomerase inhibitory activity and/or
    inhibitory activity of cell proliferation. The inhibitory effects of
    20-O-(2'E,4'Z-decadienoyl) ingenol and
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    topoisomerase II activity and on the cell proliferative activity and
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    (MMT) cell line. Although 20-O-ingenolEZ exerted inhibitory effects on
    both topoisomerase II activity and cell proliferative activity,
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    cell cycle arrest in the G2/M phase. Topoisomerase II inhibition can be
    divided into the poison and catalytic inhibitor types. A checkpoint
    mechanism is activated when cells are treated with these topoisomerase
    II inhibitors. Poison-type inhibition occurs via induction of the DNA
    damage checkpoint and the catalytic-type inhibition occurs via
    induction of the DNA-decatenation checkpoint, suggestive of distinct
    checkpoint reactions. 20-O-ingenolEZ inhibited topoisomerase II alpha
    activity through inhibition of ATPase, and induced DNA-decatenation
    checkpoint without signaling for phosphorylation of H2AX. (Cancer Sci
    2010; 101: 374-378).
 C1 [Yoshida, Chisato; Miyazaki, Khosuke; Watanabe, Manami; Kanbe, Masahiro; Yamada, Yuta; Miyata, Shohei] Nihon Univ, Coll Humanities & Sci, Dept Chem, Tokyo, Japan.
    [Hishiyama, Kazsuyoshi; Matsuzaki, Keiithi; Kitanaka, Susumu] Nihon Univ, Coll Pharm, Chiba, Japan.
    [Miyashita, Kiichi] Keio Univ, Sch Med, Inst Adv Med Res, Tokyo, Japan.
 RP Miyata, S, Nihon Univ, Coll Humanities & Sci, Dept Chem, Tokyo, Japan.
 EM miyata@chs.nihon-u.ac.jp
 FU Nihon University 
 FX This investigation was supported in part by a grant from Nihon
    University to S. Miyata.
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 NR 26
 TC 0
 PU WILEY-BLACKWELL PUBLISHING, INC
 PI MALDEN
 PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
 SN 1347-9032
 J9 CANCER SCI
 JI Cancer Sci.
 PD FEB
 PY 2010
 VL 101
 IS 2
 BP 374
 EP 378
 DI 10.1111/j.1349-7006.2009.01408.x
 PG 5
 SC Oncology
 GA 550UR
 UT ISI:000274156400013
 ER
 
 PT J
 AU Tatsuwaki, H
    Tanigawa, T
    Watanabe, T
    Machida, H
    Okazaki, H
    Yamagami, H
    Shiba, M
    Watanabe, K
    Tominaga, K
    Fujiwara, Y
    Oshitani, N
    Muguruma, K
    Sawada, T
    Hirakawa, K
    Higuchi, K
    Arakawa, T
 AF Tatsuwaki, Hiroshi
    Tanigawa, Tetsuya
    Watanabe, Toshio
    Machida, Hirohisa
    Okazaki, Hirotoshi
    Yamagami, Hirokazu
    Shiba, Masatsugu
    Watanabe, Kenji
    Tominaga, Kazunari
    Fujiwara, Yasuhiro
    Oshitani, Nobuhide
    Muguruma, Kazuya
    Sawada, Tetsuji
    Hirakawa, Kosei
    Higuchi, Kazuhide
    Arakawa, Tetsuo
 TI Reduction of 15-hydroxyprostaglandin dehydrogenase expression is an
    independent predictor of poor survival associated with enhanced cell
    proliferation in gastric adenocarcinoma
 SO CANCER SCIENCE
 LA English
 DT Article
 ID NONSTEROIDAL ANTIINFLAMMATORY DRUGS; EPIDERMAL-GROWTH-FACTOR;
    COLORECTAL-CANCER; CYCLOOXYGENASE-2 EXPRESSION; TUMOR-SUPPRESSOR;
    PROSTAGLANDIN E-2; PROSTATE-CANCER; LUNG-CANCER; CARCINOMAS;
    OVEREXPRESSION
 AB Prostaglandin (PG) E-2 promotes gastrointestinal carcinogenesis and
    tumor progression. We determined the correlations between pattern of
    expression of 15-hydroxyprostaglandin dehydrogenase (15-PGDH), a
    catabolic enzyme for biological inactivation of PGE(2), in gastric
    adenocarcinoma and various clinicopathological factors and patient
    outcome in an attempt to elucidate its biological significance. In 35
    of 71 cases of gastric adenocarcinoma, expression of 15-PGDH protein
    was reduced in tumor tissues. Multivariate analysis revealed reduction
    of 15-PGDH expression to be an independent predictor of poor survival.
    The proportion of Ki67-positive cells in 15-PGDH-negative
    adenocarcinoma was higher than that in 15-PGDH-positive adenocarcinoma.
    No differences were found in clinicopathological parameters between
    patients with cyclooxygenase-2 (COX-2)-positive tumors and those with
    COX-2 negative tumors. In an in vitro study, use of specific siRNA to
    silence 15-PGDH or a specific inhibitor of 15-PGDH enhanced cell
    proliferation in the gastric cancer cell line AGS, which expresses
    15-PGDH. These findings suggest that reduction of 15-PGDH is an
    independent predictor of poor survival associated with enhancement of
    cell proliferation in gastric adenocarcinoma. (Cancer Sci 2010; 101:
    550-558)
 C1 [Tatsuwaki, Hiroshi; Tanigawa, Tetsuya; Watanabe, Toshio; Machida, Hirohisa; Okazaki, Hirotoshi; Yamagami, Hirokazu; Shiba, Masatsugu; Watanabe, Kenji; Tominaga, Kazunari; Fujiwara, Yasuhiro; Oshitani, Nobuhide; Arakawa, Tetsuo] Osaka City Univ, Dept Gastroenterol, Grad Sch Med, Osaka 558, Japan.
    [Muguruma, Kazuya; Sawada, Tetsuji; Hirakawa, Kosei] Osaka City Univ, Grad Sch Med, Dept Surg Oncol, Osaka 558, Japan.
    [Shiba, Masatsugu] Osaka City Gen Hosp, Dept Gastroenterol, Osaka, Japan.
    [Higuchi, Kazuhide] Osaka Med Coll, Dept Internal Med 2, Takatsuki, Osaka 569, Japan.
 RP Tanigawa, T, Osaka City Univ, Dept Gastroenterol, Grad Sch Med, Osaka
    558, Japan.
 EM ttanigawa@med.osaka-cu.ac.jp
 FU Ministry of Education, Science, and Culture of Japan 
 FX This study was supported by a Grant-in-Aid from the Ministry of
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 NR 45
 TC 1
 PU WILEY-BLACKWELL PUBLISHING, INC
 PI MALDEN
 PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
 SN 1347-9032
 J9 CANCER SCI
 JI Cancer Sci.
 PD FEB
 PY 2010
 VL 101
 IS 2
 BP 550
 EP 558
 DI 10.1111/j.1349-7006.2009.01390.x
 PG 9
 SC Oncology
 GA 550UR
 UT ISI:000274156400038
 ER
 
 PT J
 AU Lorbeck, MT
    Singh, N
    Zervos, A
    Dhatta, M
    Lapchenko, M
    Yang, C
    Elefant, F
 AF Lorbeck, Meridith T.
    Singh, Neetu
    Zervos, Ashley
    Dhatta, Madhusmita
    Lapchenko, Maria
    Yang, Chen
    Elefant, Felice
 TI The histone demethylase Dmel\Kdm4A controls genes required for life
    span and male-specific sex determination in Drosophila
 SO GENE
 LA English
 DT Article
 DE Chromatin; Histone demethylase; Epigenetics; Drosophila; Gene control;
    Life span; Male-specific sex determination; Kdm4A
 ID DOMAIN-CONTAINING PROTEINS; ANDROGEN-RECEPTOR; FRUITLESS GENE;
    METHYLATION; DISEASE; H3; MUTANTS; FAMILY; MODEL; PHOSPHORYLATION
 AB Histone methylation plays an important role in regulating
    chromatin-mediated gene control and epigenetic-based memory systems
    that direct cell fate. Enzymes termed histone demethylases directly
    remove the methyl marks from histones, thus contributing to a
    dynamically regulated histone methylated genome; however. the
    biological functions of these newly identified enzymes remain unclear.
    The JMJD2-AD family belongs to the JmjC domain-containing family of
    histone demethylases (JHDMs). Here, we report the cloning and
    functional characterization of the Drosophila HDM gene Dmel\Kdm4A that
    is a homolog of the human JMJD2 family. We show that homologs for three
    human JHDM families, JHDM1, JHDM2, and JMJD2, are present in Drosophila
    and that each is expressed during the Drosophila lifecycle. Disruption
    of Dmel/Kdm4A results in a reduction of the male life span and a
    male-specific wing extension/twitching phenotype that occurs in
    response to other males and is reminiscent of an inter-male courtship
    phenotype involving the courtship song. Remarkably, certain genes
    associated with each of these phenotypes are significantly
    downregulated in response to Dmel\Kdm4A loss, most notably the
    longevity associated Hsp22 gene and the male sex-determination
    fruitless gene. Our results have implications for the role of the
    epigenetic regulator Dmel\Kdm4A in the control of genes involved in
    life span and male-specific sex determination in the fly. (C) 2009
    Elsevier B.V. All rights reserved.
 C1 [Lorbeck, Meridith T.; Singh, Neetu; Zervos, Ashley; Dhatta, Madhusmita; Lapchenko, Maria; Yang, Chen; Elefant, Felice] Drexel Univ, Dept Biol, Philadelphia, PA 19104 USA.
 RP Elefant, F, Drexel Univ, Dept Biol, Philadelphia, PA 19104 USA.
 EM fe22@drexel.edu
 FU National Institute of Health [1R01HD057939]
 FX The authors gratefully acknowledge Dr. Daniel Marenda and Dr. Xianmin
    Zhu for their invaluable advice and technical support. This work was
    supported by a National Institute of Health grant 1R01HD057939 to F.E.
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 NR 61
 TC 4
 PU ELSEVIER SCIENCE BV
 PI AMSTERDAM
 PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
 SN 0378-1119
 J9 GENE
 JI Gene
 PD JAN 15
 PY 2010
 VL 450
 IS 1-2
 BP 8
 EP 17
 DI 10.1016/j.gene.2009.09.007
 PG 10
 SC Genetics & Heredity
 GA 547YF
 UT ISI:000273925100002
 ER
 
 PT J
 AU Lin, Q
    Zhu, FC
    Yang, WN
 AF Lin, Qiong
    Zhu, Fengchang
    Yang, Wannian
 TI Coupling cellular mitogenesis to apoptosis by designed biomolecules
 SO CELLULAR SIGNALLING
 LA English
 DT Article
 DE Signaling rewiring; Ras; Raf; Caspase 3; Mitogenesis; Apoptosis
 ID GENE-THERAPY; RETROVIRAL VECTORS; CASPASE ACTIVATION; CYSTEINE
    PROTEASE; MECHANISMS; PATHWAYS; CANCER; CPP32; KINASES; DOMAINS
 AB Cellular signal transduction pathways transduce input signals to
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    biomolecules that couple mitogenesis to apoptosis are designated as
    "mitogenesis coupled-apoptosis molecular device" (MCAMD). As
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    potential applications for cancer gene therapy. (C) 2009 Elsevier B.V.
    All rights reserved.
 C1 [Lin, Qiong; Zhu, Fengchang; Yang, Wannian] Weis Ctr Res, Geisinger Clin, Danville, PA 17822 USA.
 RP Yang, WN, Weis Ctr Res, Geisinger Clin, 100 N Acad Ave, Danville, PA
    17822 USA.
 EM wyang1@geisinger.edu
 FU Congress-directed Medical Research Programs-Prostate Cancer Research
    Program [W81XWH-05-1-0178, W81XWH-07-1-0084]
 FX This work was supported by research grants (W81XWH-05-1-0178 and
    W81XWH-07-1-0084; to W.Y.) from Congress-directed Medical Research
    Programs-Prostate Cancer Research Program.
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 NR 30
 TC 0
 PU ELSEVIER SCIENCE INC
 PI NEW YORK
 PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
 SN 0898-6568
 J9 CELL SIGNAL
 JI Cell. Signal.
 PD FEB
 PY 2010
 VL 22
 IS 2
 BP 190
 EP 196
 DI 10.1016/j.cellsig.2009.09.005
 PG 7
 SC Cell Biology
 GA 548LR
 UT ISI:000273964800003
 ER
 
 PT J
 AU Tung, WH
    Hsieh, HL
    Yang, CM
 AF Tung, Wei-Hsuan
    Hsieh, Hsi-Lung
    Yang, Chuen-Mao
 TI Enterovirus 71 induces COX-2 expression via MAPKs, NF-kappa B, and AP-1
    in SK-N-SH cells: Role of PGE(2) in viral replication
 SO CELLULAR SIGNALLING
 LA English
 DT Article
 DE Viral infection; COX-2; PGE(2); Neurons; MAPKs; Transcription factors
 ID SMOOTH-MUSCLE-CELLS; HEPATITIS-C VIRUS; PROSTAGLANDIN E-2;
    EPITHELIAL-CELLS; P42/P44 MAPK; REGULATING CYCLOOXYGENASE-2; SIGNALING
    PATHWAY; MESSENGER-RNA; T-CELLS; ACTIVATION
 AB The enterovirus 71 (EV71) causes severe neurological diseases that were
    mediated through cyclooxygenase-2 (COX-2) expression in brain. However,
    the mechanisms underlying EV71-initiated intracellular signaling
    pathways leading to COX-2 expression remain unknown in neurons. Here we
    report that exposure of SK-N-SH cells to EV71 increased COX-2
    expression and PGE(2) generation in a time- and virus titer-dependent
    manner, revealed by Western blots real-time PCR, and PGE(2) analyses.
    These EV71-induced responses were mediated through activation of
    p42/p44 MAPK, p38 MAPK, JNK, NF-kappa B, and AP-1, revealed by using
    selective pharmacological inhibitors or transfection with respective
    siRNAs. Consistently, EV71-stimulated translocation of NF-kappa B into
    the nucleus and degradation of I kappa B alpha in the cytosol was
    blocked by pretreatment with the selective inhibitors of MEK1/2 (U0126)
    and NF-kappa B (Bay11-7085), respectively, suggesting that
    MEK1/2-p42/p44 MAPK cascade linking to NF-kappa B was involved in COX-2
    expression. In addition, EV71-induced AP-1 subunits (c-jun and c-fos
    mRNA) expression was also attenuated by pretreatment with a selective
    JNK inhibitor SP600125, suggesting that JNK cascade linking to AP-1 was
    involved in COX-2 expression induced by EV71. These findings suggested
    that up-regulation of COX-2 associated with the release of PGE2 from
    EV71-infected SK-N-SH cells which was mediated through activation of
    p38 MAPK, JNK, p42/p44 MAPK NF-kappa B. and AP-1 pathways. (C) 2009
    Elsevier Inc. All rights reserved.
 C1 [Tung, Wei-Hsuan; Yang, Chuen-Mao] Chang Gung Univ, Dept Physiol & Pharmacol, Tao Yuan, Taiwan.
    [Hsieh, Hsi-Lung] Chang Gung Inst Technol, Dept Nursing, Div Basic Med Sci, Tao Yuan, Taiwan.
 RP Yang, CM, Chang Gung Univ, Dept Pharmacol, 259 Wen Hwa 1st Rd, Tao
    Yuan, Taiwan.
 EM chuenmao@mail.cgu.edu.tw
 FU Chang Gung Medical Research Foundation [CMRPD150253, CMRPD150313,
    CMRPD170491]; National Science Council, Taiwan [NSC96-2320-B-182-003,
    NSC96-2320-B-182-047-MY3, NSC972321-B-182-007]
 FX This work was supported by grants CMRPD150253, CMRPD150313, and
    CMRPD170491 from Chang Gung Medical Research Foundation and
    NSC96-2320-B-182-003, NSC96-2320-B-182-047-MY3, and NSC972321-B-182-007
    from National Science Council, Taiwan.
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 NR 43
 TC 5
 PU ELSEVIER SCIENCE INC
 PI NEW YORK
 PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
 SN 0898-6568
 J9 CELL SIGNAL
 JI Cell. Signal.
 PD FEB
 PY 2010
 VL 22
 IS 2
 BP 234
 EP 246
 DI 10.1016/j.cellsig.2009.09.018
 PG 13
 SC Cell Biology
 GA 548LR
 UT ISI:000273964800007
 ER
 
 PT J
 AU Sun, WJ
    Tan, XJ
    Shi, Y
    Xu, GF
    Mao, RF
    Gu, X
    Fan, YH
    Yu, Y
    Burlingame, S
    Zhang, H
    Rednam, SP
    Lu, XB
    Zhang, T
    Fu, SB
    Cao, GW
    Qin, J
    Yang, JH
 AF Sun, Wenjing
    Tan, Xiaojie
    Shi, Yi
    Xu, Gufeng
    Mao, Renfang
    Gu, Xue
    Fan, Yihui
    Yu, Yang
    Burlingame, Susan
    Zhang, Hong
    Rednam, Surya P.
    Lu, Xiongbin
    Zhang, Ting
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    Cao, Guangwen
    Qin, Jun
    Yang, Jianhua
 TI USP11 negatively regulates TNF alpha-induced NF-kappa B activation by
    targeting on I kappa B alpha
 SO CELLULAR SIGNALLING
 LA English
 DT Article
 DE I kappa B alpha; NF-kappa B; USP11; IKK beta; TNF alpha
 ID IKK-BETA; DEUBIQUITINATING ENZYME; TRANSCRIPTION FACTOR; KINASE
    COMPLEX; SIGNAL-TRANSDUCTION; INTERLEUKIN-6 GENE; DNA-DAMAGE;
    PHOSPHORYLATION; INTERACTS; PROTEINS
 AB I kappa B alpha serves as a central anchoring molecule in the
    sequestration of NF-kappa B transcription factor in the cytoplasm.
    Ubiquitination-mediated I kappa B alpha degradation immediately
    precedes and is required for NF-kappa B nuclear translocation and
    activation. However, the precise mechanism for the deubiquitination Of
    I kappa B alpha is still not fully understood. Using a proteomic
    approach, we have identified Ubiquitin Specific Pepticlase 11 (USP11)
    as an I kappa B alpha associated deubiquitinase. Overexpression of
    USP11 inhibits I kappa B alpha ubiquitination. Recombinant USP11
    catalyzes deubiquitination Of I kappa B alpha in vitro. Moreover,
    knockdown of USP11 expression enhances TNF alpha-induced I kappa B
    alpha ubiquitination and NF-kappa B activation. These data demonstrate
    that USP11 plays an important role in the downregulation of TNF
    alpha-mediated NF-kappa B activation through modulating I kappa B alpha
    stability. In addition, overexpression of a catalytically inactive
    USP11 mutant partially inhibits TNF alpha- and IKK beta-induced
    NF-kappa B activation, suggesting that USP11 also exerts a
    non-catalytic function in its negative regulation of TNF alpha-mediated
    NF-kappa B activation. Thus. I kappa B alpha ubiquitination and
    deubiquitination processes function as a Yin-Yang regulatory mechanism
    on TNF alpha-induced NF-kappa B activation. (C) 2009 Elsevier Inc. All
    rights reserved.
 C1 [Sun, Wenjing; Tan, Xiaojie; Xu, Gufeng; Gu, Xue; Fan, Yihui; Yu, Yang; Burlingame, Susan; Rednam, Surya P.; Yang, Jianhua] Baylor Coll Med, Dept Pediat, Texas Childrens Canc Ctr, Houston, TX 77030 USA.
    [Shi, Yi; Qin, Jun] Baylor Coll Med, Dept Mol & Cellular Biol, Verna & Marrs Mclean Dept Biochem & Mol Biol, Ctr Mol Discovery, Houston, TX 77030 USA.
    [Mao, Renfang; Zhang, Hong] Baylor Coll Med, Dan L Duncan Canc Ctr, Dept Pathol, Houston, TX 77030 USA.
    [Lu, Xiongbin] Univ S Carolina, Dept Biol Sci, Columbia, SC 29208 USA.
    [Tan, Xiaojie; Cao, Guangwen] Mil Med Coll 2, Dept Epidemiol, Shanghai 200433, Peoples R China.
    [Sun, Wenjing; Fu, Songbin] Harbin Med Coll, Med Genet Lab, Harbin 150081, Peoples R China.
    [Gu, Xue; Zhang, Ting] Capital Inst Pediat, Beijing 100020, Peoples R China.
 RP Yang, JH, Baylor Coll Med, Dept Pediat, Texas Childrens Canc Ctr,
    Houston, TX 77030 USA.
 EM jianhuay@bcm.edu
 FU Diabetes Endocrinology Research Center (DERC) [DK079638]; NIH/NCI
    [IR21CA106513-OIA2]; American Cancer Society [RSG-06-070-01-TBE];
    Fleming and Davenport Award ; National Basic Research Program
    [2007CB511900]
 FX We thank the proteomics core of Diabetes Endocrinology Research Center
    (DERC) supported by DK079638 for protein identification. We are very
    grateful to Dr. Paul Chiao for providing Flag-IKBot expression
    construct, Dr. Xinhua Feng for HA-ubiquitin expression plasmid, and Dr.
    Zhijian Chen for GST-Control and GST-IKBOt plasmids. This work was
    supported by thegrants; from the NIH/NCI IR21CA106513-OIA2 (toj.Y.),
    the American Cancer Society grant RSG-06-070-01-TBE (to j.Y.), the
    Fleming and Davenport Award (to HZ), and the National Basic Research
    Program (973 Program) of China grant 2007CB511900 (to TZ).
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 NR 30
 TC 1
 PU ELSEVIER SCIENCE INC
 PI NEW YORK
 PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
 SN 0898-6568
 J9 CELL SIGNAL
 JI Cell. Signal.
 PD MAR
 PY 2010
 VL 22
 IS 3
 BP 386
 EP 394
 DI 10.1016/j.cellsig.2009.10.008
 PG 9
 SC Cell Biology
 GA 548CD
 UT ISI:000273935700006
 ER
 
 PT J
 AU Esteban, MA
    Wang, T
    Qin, BM
    Yang, JY
    Qin, DJ
    Cai, JL
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 AF Esteban, Miguel Angel
    Wang, Tao
    Qin, Baoming
    Yang, Jiayin
    Qin, Dajiang
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    Li, Wen
    Weng, Zhihui
    Chen, Jiekai
    Ni, Su
    Chen, Keshi
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    Xu, Jianyong
    Zhang, Shiqiang
    Li, Feng
    He, Wenzhi
    Labuda, Krystyna
    Song, Yancheng
    Peterbauer, Anja
    Wolbank, Susanne
    Redl, Heinz
    Zhong, Mei
    Cai, Daozhang
    Zeng, Lingwen
    Pei, Duanqing
 TI Vitamin C Enhances the Generation of Mouse and Human Induced
    Pluripotent Stem Cells
 SO CELL STEM CELL
 LA English
 DT Article
 ID IPS CELLS; HUMAN FIBROBLASTS; DEFINED FACTORS; DISEASE; DEMETHYLASES;
    EFFICIENCY; INDUCTION; PATHWAY; LIMITS; LINES
 AB Somatic cells can be reprogrammed into induced pluripotent stem cells
    (iPSCs) by defined factors. However, the low efficiency and slow
    kinetics of the reprogramming process have hampered progress with this
    technology. Here we report that a natural compound, vitamin C (Vc),
    enhances iPSC: generation from both mouse and human somatic cells. Vc
    acts at least in part by alleviating cell senescence, a recently
    identified roadblock for reprogramming. In addition, Vc accelerates
    gene expression changes and promotes the transition of pre-iPSC
    colonies to a fully reprogrammed state. Our results therefore highlight
    a straightforward method for improving the speed and efficiency of iPSC
    generation and provide additional insights into the mechanistic basis
    of the reprogramming process.
 C1 [Esteban, Miguel Angel; Wang, Tao; Qin, Baoming; Yang, Jiayin; Qin, Dajiang; Cai, Jinglei; Li, Wen; Weng, Zhihui; Chen, Jiekai; Ni, Su; Chen, Keshi; Li, Yuan; Liu, Xiaopeng; Xu, Jianyong; Zhang, Shiqiang; Li, Feng; He, Wenzhi; Zeng, Lingwen; Pei, Duanqing] Chinese Acad Sci, Guangzhou Inst Biomed, S China Inst Stem Cell Biol & Regenerat Med, Stem Cell & Canc Biol Grp,Key Lab Regenerat Biol, Guangzhou 510663, Guangdong, Peoples R China.
    [Esteban, Miguel Angel; Wang, Tao; Qin, Baoming; Yang, Jiayin; Qin, Dajiang; Cai, Jinglei; Li, Wen; Weng, Zhihui; Chen, Jiekai; Ni, Su; Chen, Keshi; Li, Yuan; Liu, Xiaopeng; Xu, Jianyong; Zhang, Shiqiang; Li, Feng; He, Wenzhi; Zeng, Lingwen; Pei, Duanqing] Chinese Acad Sci, Guangzhou Inst Hlth, Guangzhou 510663, Guangdong, Peoples R China.
    [Labuda, Krystyna; Wolbank, Susanne; Redl, Heinz] Ludwig Boltzmann Inst Clin & Expt Traumatol, A-1200 Vienna, Austria.
    [Song, Yancheng; Cai, Daozhang] Sun Yat Sen Univ, Affiliated Hosp 3, Guangzhou 510630, Guangdong, Peoples R China.
    [Peterbauer, Anja] Red Cross Blood Transfus Serv Upper Austria, A-4020 Linz, Austria.
    [Zhong, Mei] Nanfang Hosp, Ctr Prenatal & Hereditary Dis Diag, Guangzhou 510515, Guangdong, Peoples R China.
 RP Pei, DQ, Chinese Acad Sci, Guangzhou Inst Biomed, S China Inst Stem
    Cell Biol & Regenerat Med, Stem Cell & Canc Biol Grp,Key Lab Regenerat
    Biol, Guangzhou 510663, Guangdong, Peoples R China.
 EM pei_duanqing@gibh.ac.cn
 FU National Natural Science Foundation of China [30630039, 90813033];
    National Science Fund for Distinguished Young Scholars [30725012];
    Knowledge Innovation Project of The Chinese Academy of Sciences
    [KSCX2-YW-R-48, KSCX1-YW-02-1]; Bureau of Science and Technology of
    Guangzhou Municipality, China [2008A1-E4011]; Key Technologies R&D
    Program, 973 Program of China [2006CB701504, 2006CB943600,
    2007CB948002, 2009CB941102, 2009CB940902]; EFBIC RED travel grant ;
    Chinese Academy of Sciences/SAFEA International Partnership [230725012]
 FX Supported by National Natural Science Foundation of China (grant
    numbers 30630039 and 90813033), National Science Fund for Distinguished
    Young Scholars (30725012), Knowledge Innovation Project of The Chinese
    Academy of Sciences (grant numbers KSCX2-YW-R-48, KSCX1-YW-02-1),
    Bureau of Science and Technology of Guangzhou Municipality, China
    (grant 2008A1-E4011), Key Technologies R&D Program, 973 Program of
    China (grant numbers 2006CB701504, 2006CB943600, 2007CB948002,
    2009CB941102, 2009CB940902), an EFBIC RED travel grant, and the Chinese
    Academy of Sciences/SAFEA International Partnership Program for
    Creative Research Teams (grant number 230725012). We wish to thank
    members of our laboratories for their support.
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 NR 32
 TC 50
 PU CELL PRESS
 PI CAMBRIDGE
 PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
 SN 1934-5909
 J9 CELL STEM CELL
 JI Cell Stem Cell
 PD JAN 8
 PY 2010
 VL 6
 IS 1
 BP 71
 EP 79
 DI 10.1016/j.stem.2009.12.001
 PG 9
 SC Cell & Tissue Engineering; Cell Biology
 GA 549EW
 UT ISI:000274029700013
 ER
 
 PT J
 AU Huang, YW
    Liao, YT
    Chen, W
    Chen, CL
    Hu, JT
    Liu, CJ
    Lai, MY
    Chen, PJ
    Chen, DS
    Yang, SS
    Kao, JH
 AF Huang, Y-W
    Liao, Y-T
    Chen, W.
    Chen, C-L
    Hu, J-T
    Liu, C-J
    Lai, M-Y
    Chen, P-J
    Chen, D-S
    Yang, S-S
    Kao, J-H
 TI Vitamin D receptor gene polymorphisms and distinct clinical phenotypes
    of hepatitis B carriers in Taiwan
 SO GENES AND IMMUNITY
 LA English
 DT Article
 DE vitamin D receptor; polymorphism; hepatitis B virus; chronic carrier;
    hepatocellular carcinoma
 ID VIRUS-INFECTION; 1,25-DIHYDROXYVITAMIN D-3; HEPATOCELLULAR-CARCINOMA;
    AMINOTRANSFERASE LEVELS; VIRAL-HEPATITIS; NATURAL-HISTORY;
    LIVER-DISEASE; HBV INFECTION; E-ANTIGEN; CIRRHOSIS
 AB Vitamin D exhibits immunomodulatory and antiproliferative effects
    through vitamin D receptor (VDR) in chronic infections and cancers. We
    genotyped the BsmI (rs1544410), ApaI (rs7975232) and TaqI (rs731236)
    polymorphisms of VDR gene in 250 Taiwanese chronic hepatitis B virus
    (HBV) carriers who were categorized into six phenotypes. After
    adjustment for age and sex, the frequencies of the VDR B/b, B/a, B/T,
    B/a/T in patients with hepatitis flare(s) were lower than those without
    (7 vs 20%, P = 0.009; 1 vs 9%, P = 0.004; 3 vs 10%, P = 0.007; 1 vs 9%,
    P = 0.005, respectively); in contrast, T/t, A/T, A/t, b/A/t were higher
    in flare(s) (8 vs 3%, P = 0.003; 49 vs 34%, P = 0.027; 2 vs 1%, P =
    0.004; 0.5 vs 0%, P = 0.001, respectively). In addition, B/b, B/B, T/t,
    b/A, B/a, B/A, B/T, B/t, A/t, b/A/T, B/a/T, B/A/T, B/A/t, b/A/t were
    higher in patients positive for HBeAg. The distribution of VDR
    genotypes was comparable between patients with and without
    hepatocellular carcinoma (HCC). VDR gene polymorphisms are associated
    with distinct clinical phenotypes in Taiwanese HBV carriers but not
    with HCC development. Genes and Immunity (2010) 11, 87-93;
    doi:10.1038/gene.2009.65; published online 20 August 2009
 C1 [Kao, J-H] Natl Taiwan Univ Hosp, Hepatitis Res Ctr, Dept Internal Med, Div Gastroenterol, Taipei 10002, Taiwan.
    [Huang, Y-W; Liu, C-J; Lai, M-Y; Chen, P-J; Chen, D-S; Kao, J-H] Natl Taiwan Univ, Coll Med, Dept Internal Med, Div Gastroenterol, Taipei, Taiwan.
    [Huang, Y-W; Hu, J-T; Yang, S-S] Cathay Gen Hosp, Med Ctr, Liver Unit, Taipei, Taiwan.
    [Liao, Y-T] Natl Taiwan Univ, Coll Publ Hlth, Grad Inst Epidemiol, Taipei 10764, Taiwan.
    [Chen, W.; Chen, D-S; Kao, J-H] Natl Taiwan Univ Hosp, Hepatitis Res Ctr, Taipei, Taiwan.
    [Chen, C-L; Liu, C-J; Lai, M-Y; Chen, P-J; Chen, D-S; Kao, J-H] Natl Taiwan Univ, Coll Med, Grad Inst Clin Med, Taipei 10764, Taiwan.
    [Hu, J-T; Yang, S-S] Fu Jen Catholic Univ, Coll Med, Sch Med, Taipei, Taiwan.
    [Lai, M-Y; Chen, P-J; Kao, J-H] Natl Taiwan Univ Hosp, Dept Med Res, Taipei, Taiwan.
 RP Kao, JH, Natl Taiwan Univ Hosp, Hepatitis Res Ctr, Dept Internal Med,
    Div Gastroenterol, 1 Chang Te St, Taipei 10002, Taiwan.
 EM kaojh@ntu.edu.tw
 FU National Taiwan University Hospital ; Cathay General Hospital
    [97-CGN01]; Department of Health ; National Science Council, Taiwan ;
    National Health Research Institutes, Taiwan ; Liver Disease Prevention
    and Treatment Research Foundation 
 FX This study was supported by grants from the National Taiwan University
    Hospital; Cathay General Hospital (97-CGN01), Department of Health and
    the National Science Council, Executive Yuan, Taiwan; National Health
    Research Institutes, Taiwan; and Liver Disease Prevention and Treatment
    Research Foundation.
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 NR 39
 TC 3
 PU NATURE PUBLISHING GROUP
 PI LONDON
 PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
 SN 1466-4879
 J9 GENES IMMUN
 JI Genes Immun.
 PD JAN
 PY 2010
 VL 11
 IS 1
 BP 87
 EP 93
 DI 10.1038/gene.2009.65
 PG 7
 SC Genetics & Heredity; Immunology
 GA 546CE
 UT ISI:000273785200009
 ER
 
 PT J
 AU Cho, DY
    Lin, SZ
    Yang, WK
    Hsu, DM
    Lee, HC
    Lee, WY
    Liu, SP
 AF Cho, Der-Yang
    Lin, Shinn-Zong
    Yang, Wen-Kuang
    Hsu, Den-Mei
    Lee, Han-Chung
    Lee, Wen-Yeun
    Liu, Shih-Ping
 TI Recent Advances of Dendritic Cells (DCs)-Based Immunotherapy for
    Malignant Gliomas
 SO CELL TRANSPLANTATION
 LA English
 DT Proceedings Paper
 CT 1st Pan Pacific Sympsoium of Cell Stem Research
 CY JUN, 2008
 CL Taichung, TAIWAN
 HO China Med Univ & Hosp
 DE Anaplastic astrocytoma; Cancer stem cells; Cytotoxic T lymphocytes
    (CTLs); Dendritic cells (DCs); Glioblastoma multiforme (GBM);
    Immunotherapy; Malignant gliomas; Tumor vaccine
 ID CYTOTOXIC T-CELLS; GROWTH-FACTOR RECEPTOR; CANCER STEM-CELLS;
    PHASE-I/II TRIAL; BRAIN-TUMORS; GLIOBLASTOMA-MULTIFORME;
    IMMUNE-RESPONSES; MURINE GLIOMA; INTRACRANIAL GLIOMAS;
    MONOCLONAL-ANTIBODY
 AB Immunotherapy is a new light of hope for the treatment of malignant
    gliomas. The brain is no longer believed to be an immunologically
    privileged organ. The major advantage of immunotherapy is the
    tumor-specific cytotoxic effect on the tumor cells with minimal side
    effects. Autologous dendritic cells (DCs)-based immunotherapy is a
    promising and feasible method. DCs are the most potent
    antigen-presenting cells (APCs). DCs prime T lymphocytes by epitopic
    major histocompatibility (MHC) class I and II for CD8(+) cytotoxic T
    lymphocytes (CTLs) and CD4(+) T helper cells, respectively. From the
    tissue specimen examination after DCs-based immunotherapy, CD8(+) CTLs
    have replaced T regulatory cells (Tregs) as the major dominant tissue
    infiltrating lymphocytes (TILs). CD8(+) CTLs play a key role in the
    tumor response, which may also be effective against cancer stem cells.
    DCs themselves also produce many cytokines including interferon-gamma
    and interleukin (IL-2) to kill the tumor cells. From the preliminary
    better outcomes in the literature for malignant gliomas, DC-based
    immunotherapy may improve tumor response by increasing the survival
    rate and time. It is recommended that DC-based immunotherapy is applied
    as soon as possible with conjunctive radiotherapy and chemotherapy.
    Malignant gliomas have heterogeneity of tissue-associated antigens
    (TAAs). To find universal common antigens through different kinds of
    tumor culture may be the essential issue for tumor vaccine development
    in the future.
 C1 [Cho, Der-Yang; Lin, Shinn-Zong; Yang, Wen-Kuang; Hsu, Den-Mei; Lee, Han-Chung; Lee, Wen-Yeun; Liu, Shih-Ping] China Med Univ & Hosp, Dept Neurosurg, Ctr Neuropsychiat, Cell Gene Therapy Res Lab, Taichung, Taiwan.
    [Cho, Der-Yang; Lin, Shinn-Zong] China Med Univ, Grad Inst Immunol, Taichung, Taiwan.
 RP Yang, WK, China Med Univ Hosp, Cell Gene Therapy Res Lab, 2 Yu Der Rd,
    Taichung, Taiwan.
 EM d5057@mail.cmuh.org.tw
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 NR 62
 TC 6
 PU COGNIZANT COMMUNICATION CORP
 PI ELMSFORD
 PA 3 HARTSDALE ROAD, ELMSFORD, NY 10523-3701 USA
 SN 0963-6897
 J9 CELL TRANSPLANT
 JI Cell Transplant.
 PY 2009
 VL 18
 IS 9
 BP 977
 EP 983
 DI 10.3727/096368909X12483162196962
 PG 7
 SC Cell & Tissue Engineering; Medicine, Research & Experimental;
    Transplantation
 GA 544ZA
 UT ISI:000273699100003
 ER
 
 PT J
 AU Hong, Z
    Yang, YR
    Zhang, C
    Niu, Y
    Li, K
    Zhao, X
    Liu, JJ
 AF Hong, Zhi
    Yang, Yanrui
    Zhang, Cheng
    Niu, Yang
    Li, Ke
    Zhao, Xi
    Liu, Jia-Jia
 TI The retromer component SNX6 interacts with dynactin p150(Glued) and
    mediates endosome-to-TGN transport
 SO CELL RESEARCH
 LA English
 DT Article
 DE sorting nexin; retromer; p150(Glued); retrograde transport;
    dynein/dynactin; CI-MPR
 ID BETA-III-SPECTRIN; SORTING NEXIN-1; MAMMALIAN RETROMER; PX-DOMAIN;
    COMPLEX; RECEPTOR; SUBUNIT; MOTOR; MICROTUBULES; ASSOCIATION
 AB The retromer is a protein complex that mediates retrograde transport of
    transmembrane cargoes from endosomes to the trans-Golgi network (TGN).
    It is comprised of a cargo-selection subcomplex of Vps26, Vps29 and
    Vps35 and a membrane-binding coat subcomplex of sorting nexins (SNXs).
    Previous studies identified SNX1/2 as one of the components of the SNX
    subcomplex, and SNX5/6 as candidates for the second SNX. How the
    retromer-associated cargoes are recognized and transported by molecular
    motors are largely unknown. In this study, we found that one of
    SNX1/2's dimerization partners, SNX6, interacts with the p150(Glued)
    subunit of the dynein/dynactin motor complex. We present evidence that
    SNX6 is a component of the retromer, and that recruitment of the motor
    complex to the membrane-associated retromer requires the
    SNX6-p150(Glued) interaction. Disruption of the SNX6-p150Glued
    interaction causes failure in formation and detachment of the
    tubulovesicular sorting structures from endosomes and results in block
    of CI-MPR retrieval from endosomes to the TGN. These observations
    indicate that in addition to SNX1/2, SNX6 in association with the
    dynein/dynactin complex drives the formation and movement of tubular
    retrograde intermediates.
 C1 [Hong, Zhi; Yang, Yanrui; Zhang, Cheng; Niu, Yang; Li, Ke; Zhao, Xi; Liu, Jia-Jia] Chinese Acad Sci, Inst Genet & Dev Biol, Key Lab Mol & Dev Biol, Beijing 100101, Peoples R China.
    [Hong, Zhi; Niu, Yang; Li, Ke; Zhao, Xi] Chinese Acad Sci, Grad Sch, Beijing 100039, Peoples R China.
 RP Liu, JJ, Chinese Acad Sci, Inst Genet & Dev Biol, Key Lab Mol & Dev
    Biol, Beijing 100101, Peoples R China.
 EM jjliu@genetics.ac.cn
 FU National Natural Science Foundation of China [30770675]; Chinese
    Academy of Sciences [KSCX1-YW-R-37]; CAS 
 FX We thank Yingfang Liu (Institute of Biophysics, Chinese Academy of
    Sciences) for advice on PX domain structure and SNX6 mutations. We are
    particularly grateful to Yanmin Yang (Stanford University, USA) for
    insightful discussions and the Flag-MAP1B LC construct. We also thank
    Juan S Bonifacino (NIH, USA) for the rabbit anti- CI- MPR antibody,
    Hiroyoshi Ariga (Hokkaido University, Japan) for Flag- and HA-tagged
    human SNX6 overexpression constructs, and Li Yu (Tsinghua University,
    China) for the YFP- EEA1 expression construct. We thank Chonglin Yang
    (Institute of Genetics and Developmental Biology, Chinese Academy of
    Sciences), Dahua Chen (Institute of Zoology, Chinese Academy of
    Sciences) and Li Yu for critical reading of the manuscript. This work
    was supported by grants from the National Natural Science Foundation of
    China (30770675) and Chinese Academy of Sciences (KSCX1-YW-R-37). J-J
    Liu is supported by the CAS 100-Talents Program.
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 NR 41
 TC 2
 PU INST BIOCHEMISTRY & CELL BIOLOGY
 PI SHANGHAI
 PA SIBS, CAS, 319 YUEYAND ROAD, SHANGHAI, 200031, PEOPLES R CHINA
 SN 1001-0602
 J9 CELL RES
 JI Cell Res.
 PD DEC
 PY 2009
 VL 19
 IS 12
 BP 1334
 EP 1349
 DI 10.1038/cr.2009.130
 PG 16
 SC Cell Biology
 GA 546CD
 UT ISI:000273785100006
 ER
 
 PT J
 AU Chen, RQ
    Sun, SL
    Wang, C
    Li, YS
    Liang, Y
    An, FY
    Li, C
    Dong, HL
    Yang, XH
    Zhang, J
    Zuo, JR
 AF Chen, Ruiqiang
    Sun, Shulan
    Wang, Chun
    Li, Yansha
    Liang, Yan
    An, Fengying
    Li, Chao
    Dong, Haili
    Yang, Xiaohui
    Zhang, Jian
    Zuo, Jianru
 TI The Arabidopsis PARAQUAT RESISTANT2 gene encodes an
    S-nitrosoglutathione reductase that is a key regulator of cell death
 SO CELL RESEARCH
 LA English
 DT Article
 DE GSNOR1/HOT5/PAR2; nitric oxide; paraquat; cell death; superoxide
 ID DEPENDENT FORMALDEHYDE DEHYDROGENASE; DISEASE RESISTANCE RESPONSE;
    PLANT-PATHOGEN INTERACTIONS; NITRIC-OXIDE; ARABIDOPSIS-THALIANA;
    SUPEROXIDE-DISMUTASE; METHYL VIOLOGEN; HYPERSENSITIVE RESPONSE;
    NITROSYLATED PROTEINS; ASCORBATE PEROXIDASE
 AB Metabolism of S-nitrosoglutathione (GSNO), a major biologically active
    nitric oxide (NO) species, is catalyzed by the evolutionally conserved
    GSNO reductase (GSNOR). Previous studies showed that the Arabidopsis
    GSNOR1/HOT5 gene regulates salicylic acid signaling and thermotolerance
    by modulating the intracellular S-nitrosothiol level. Here, we report
    the characterization of the Arabidopsis paraquat resistant2-1 (par2-1)
    mutant that shows an anti-cell death phenotype. The production of
    superoxide in par2-1 is comparable to that of wild-type plants when
    treated by paraquat (1,1'-dimethyl-4,4'-bipyridinium dichloride),
    suggesting that PAR2 acts downstream of superoxide to regulate cell
    death. PAR2, identified by positional cloning, is shown to be identical
    to GSNOR1/HOT5. The par2-1 mutant carries a missense mutation in a
    highly conserved glycine, which renders the mutant protein unstable.
    Compared to wild type, par2-1 mutant has a higher NO level, as revealed
    by staining with 4,5-diaminofluorescein diacetate. Consistent with this
    result, wild-type plants treated with an NO donor display resistance to
    paraquat. Interestingly, the GSNOR1/HOT5/PAR2 protein level, other than
    its steady-state mRNA level, is induced by paraquat, but is reduced by
    NO donors. Taken together, these results suggest that GSNOR1/HOT5/PAR2
    plays an important role in regulating cell death in plant cells through
    modulating intracellular NO level.
 C1 [Chen, Ruiqiang; Sun, Shulan; Wang, Chun; Li, Yansha; Liang, Yan; An, Fengying; Li, Chao; Dong, Haili; Yang, Xiaohui; Zhang, Jian; Zuo, Jianru] Chinese Acad Sci, State Key Lab Plant Genom, Beijing 100101, Peoples R China.
    [Chen, Ruiqiang; Sun, Shulan; Wang, Chun; Li, Yansha; Liang, Yan; An, Fengying; Li, Chao; Dong, Haili; Yang, Xiaohui; Zhang, Jian; Zuo, Jianru] Chinese Acad Sci, Inst Genet & Dev Biol, Natl Plant Gene Res Ctr Beijing, Beijing 100101, Peoples R China.
    [Chen, Ruiqiang; Sun, Shulan; Wang, Chun; Li, Yansha; An, Fengying; Li, Chao; Dong, Haili] Chinese Acad Sci, Grad Sch, Beijing 100049, Peoples R China.
 RP Zuo, JR, Chinese Acad Sci, State Key Lab Plant Genom, Beijing 100101,
    Peoples R China.
 EM jrzuo@genetics.ac.cn
 FU National Natural Science Foundation of China [30330360]; Ministry of
    Science and Technology of China [2006AA10A112]; Chinese Academy of
    Sciences [KSCX2-YW-N-015]
 FX We thank Dr Gary Loake (University of Edinburgh, UK) for providing
    gsnor1-3 seeds. We are grateful to Drs Chuanyou Li, Shuhua Yang and
    Yiqin Wang for critically reading the manuscript. This study was
    supported by grants from the National Natural Science Foundation of
    China (30330360), the Ministry of Science and Technology of China
    (2006AA10A112) and the Chinese Academy of Sciences (KSCX2-YW-N-015).
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 NR 62
 TC 3
 PU INST BIOCHEMISTRY & CELL BIOLOGY
 PI SHANGHAI
 PA SIBS, CAS, 319 YUEYAND ROAD, SHANGHAI, 200031, PEOPLES R CHINA
 SN 1001-0602
 J9 CELL RES
 JI Cell Res.
 PD DEC
 PY 2009
 VL 19
 IS 12
 BP 1377
 EP 1387
 DI 10.1038/cr.2009.117
 PG 11
 SC Cell Biology
 GA 546CD
 UT ISI:000273785100009
 ER
 
 PT J
 AU Wang, HZ
    Gao, XL
    Huang, Y
    Yang, JN
    Liu, ZR
 AF Wang, Haizhen
    Gao, Xueliang
    Huang, Yun
    Yang, Jenny
    Liu, Zhi-Ren
 TI P68 RNA helicase is a nucleocytoplasmic shuttling protein
 SO CELL RESEARCH
 LA English
 DT Article
 DE P68 RNA helicase; nucleocytoplasm shuttle; NLS; NES; DEAD box
 ID ESTROGEN-RECEPTOR-ALPHA; STRUCTURE PREDICTION SERVER; NUCLEAR EXPORT;
    MESSENGER-RNA; CELL-PROLIFERATION; TRANSCRIPTIONAL COACTIVATOR;
    IMPORTIN-ALPHA; SMAD PROTEINS; T-ANTIGEN; TRANSPORT
 AB P68 RNA helicase is a prototypical DEAD box RNA helicase. The protein
    plays a very important role in early organ development and maturation.
    Consistent with the function of the protein in transcriptional
    regulation and pre-mRNA splicing, p68 was found to predominately
    localize in the cell nucleus. However, recent experiments demonstrate a
    transient cytoplasmic localization of the protein. We report here that
    p68 shuttles between the nucleus and the cytoplasm. The
    nucleocytoplasmic shuttling of p68 is mediated by two nuclear
    localization signal and two nuclear exporting signal sequence elements.
    Our experiments reveal that p68 shuttles via a classical
    RanGTPase-dependent pathway.
 C1 [Wang, Haizhen; Gao, Xueliang; Liu, Zhi-Ren] Georgia State Univ, Dept Biol, Atlanta, GA 30303 USA.
    [Huang, Yun; Yang, Jenny] Georgia State Univ, Dept Chem, Atlanta, GA 30303 USA.
 RP Liu, ZR, Georgia State Univ, Dept Biol, POB 4010, Atlanta, GA 30303 USA.
 EM biozrl@langate.gsu.edu
 FU National Institutes of Health [GM063874, CA118113]; Georgia Cancer
    Coalition ; MBD fellowship ; GSU 
 FX We thank Drs Joan A Steitz (Yale University School of Medicine),
    Melissa J Moore (University of Massachusetts medical school) and
    Hung-Ying Kao (Case Western Reserve University) for providing the
    vectors for expression of MS2-DEK and human CRM1. We are grateful to
    Professor Peter Stockley (University of Leeds) for providing antibody
    against MS2-DEK. We also thank Birgit Neuhaus (Georgia State
    University) for assistance in confocal imaging. This manuscript is
    greatly improved by comments from Christie Carter, Michael Kirberger
    and Heena Dey (Georgia State University). This work is supported in
    part by research grants from National Institutes of Health (GM063874
    and CA118113) and Georgia Cancer Coalition to ZR Liu. X Gao is
    supported by an MBD fellowship, GSU.
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 NR 62
 TC 3
 PU INST BIOCHEMISTRY & CELL BIOLOGY
 PI SHANGHAI
 PA SIBS, CAS, 319 YUEYAND ROAD, SHANGHAI, 200031, PEOPLES R CHINA
 SN 1001-0602
 J9 CELL RES
 JI Cell Res.
 PD DEC
 PY 2009
 VL 19
 IS 12
 BP 1388
 EP 1400
 DI 10.1038/cr.2009.113
 PG 13
 SC Cell Biology
 GA 546CD
 UT ISI:000273785100010
 ER
 
 PT J
 AU Peng, J
    Yang, XO
    Chang, SH
    Yang, J
    Dong, C
 AF Peng, Juan
    Yang, Xuexian O.
    Chang, Seon Hee
    Yang, Jiong
    Dong, Chen
 TI IL-23 signaling enhances Th2 polarization and regulates allergic airway
    inflammation
 SO CELL RESEARCH
 LA English
 DT Article
 DE cytokines; helper T cells; T cell differentiation; allergic airway
    inflammation
 ID CD4 T-CELLS; AUTOIMMUNE INFLAMMATION; TH17 CELLS; ASTHMA;
    INTERLEUKIN-17; INNATE; IL-17; CYTOKINE; DISTINCT; MICE
 AB IL-23/IL-17 axis is an important regulator in various inflammatory
    diseases. However, the role of IL-23 in allergic airway inflammation is
    not well understood. In this study, we show that in an allergen-induced
    asthma model, mice with transgenic overexpression of IL-23R exhibited
    increased airway infiltration of eosinophils and Th2 cytokine
    production, whereas those deficient in IL-23 displayed reduced airway
    inflammation. In vitro, IL-23-IL-23R signaling promoted GATA-3
    expression and enhanced Th2 cytokine expression. Conversely, in the
    absence of this signal, Th2 cell differentiation was partially
    inhibited. Therefore, IL-23 signaling may regulate allergic asthma
    through modulation of Th2 cell differentiation.
 C1 [Peng, Juan; Yang, Xuexian O.; Chang, Seon Hee; Dong, Chen] Univ Texas Houston, MD Anderson Canc Ctr, Dept Immunol, Houston, TX 77030 USA.
    [Peng, Juan; Yang, Jiong] Wuhan Univ, Renmin Hosp, Dept Resp Dis, Wuhan 430060, Peoples R China.
    [Peng, Juan; Yang, Jiong] Wuhan Univ, Zhongnan Hosp, Dept Resp Dis, Wuhan 430071, Peoples R China.
 RP Dong, C, Univ Texas Houston, MD Anderson Canc Ctr, Dept Immunol,
    Houston, TX 77030 USA.
 EM xoyang@mdanderson.org
    cdong@mdanderson.org
 FU NIH ; MD Anderson Center for Targeted Therapy ; American Heart
    Association ; Ministry of Education of China 
 FX We thank Dr Jan Parker-Thornburg (MD Anderson Cancer Center, USA) for
    her help in the generation of IL-23R transgenic animals and the Dong
    lab members for their help and discussion. The work was supported by
    research grants from the NIH, and the MD Anderson Center for Targeted
    Therapy (to CD) and from the American Heart Association (to XOY). JP
    receives a fellowship from the Ministry of Education of China, and CD
    is a Trust Fellow of the MD Anderson Cancer Center and a Leukemia and
    Lymphoma Society Scholar.
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 NR 31
 TC 8
 PU INST BIOCHEMISTRY & CELL BIOLOGY
 PI SHANGHAI
 PA SIBS, CAS, 319 YUEYAND ROAD, SHANGHAI, 200031, PEOPLES R CHINA
 SN 1001-0602
 J9 CELL RES
 JI Cell Res.
 PD JAN
 PY 2010
 VL 20
 IS 1
 BP 62
 EP 71
 DI 10.1038/cr.2009.128
 PG 10
 SC Cell Biology
 GA 546DT
 UT ISI:000273790500008
 ER
 
 PT J
 AU Ohsumi, S
    Shimozuma, K
    Ohashi, Y
    Takeuchi, A
    Nomura, Y
    Suemasu, K
    Kuranami, M
    Ohno, S
    Watanabe, T
 AF Ohsumi, S.
    Shimozuma, K.
    Ohashi, Y.
    Takeuchi, A.
    Nomura, Y.
    Suemasu, K.
    Kuranami, M.
    Ohno, S.
    Watanabe, T.
 TI Objective and Subjective Assessment of Edema during Adjuvant
    Chemotherapy Using Taxane-Containing Regimens in a Randomized
    Controlled Trial: National Surgical Adjuvant Study of Breast Cancer
    (NSAS-BC) 02
 SO CANCER RESEARCH
 LA English
 DT Meeting Abstract
 CT 32nd Annual San Antonio Breast Cancer Symposium
 CY DEC 09-13, 2009
 CL San Antonio, TX
 C1 NHO Shikoku Canc Ctr, Matsuyama, Ehime, Japan.
    Ritsumeikan Univ, Shiga, Japan.
    Univ Tokyo, Tokyo, Japan.
    Comprehens Support Project Orcol Res, Tokyo, Japan.
    Arche Clin, Saitama, Japan.
    Kitasato Univ, Kanagawa, Japan.
    NHO Kyushu Canc Ctr, Fukuoka, Japan.
    Hamamatsu Oncol Ctr, Shizuoka, Japan.
 NR 0
 TC 0
 PU AMER ASSOC CANCER RESEARCH
 PI PHILADELPHIA
 PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
 SN 0008-5472
 J9 CANCER RES
 JI Cancer Res.
 PD DEC 15
 PY 2009
 VL 69
 IS 24
 SU Suppl. 3
 BP 622S
 EP 622S
 PG 1
 SC Oncology
 GA 534TR
 UT ISI:000272920701123
 ER
 
 PT J
 AU Peng, C
    Chen, YY
    Yang, ZF
    Zhang, HJ
    Osterby, L
    Rosmarin, AG
    Li, SG
 AF Peng, Cong
    Chen, Yaoyu
    Yang, Zhongfa
    Zhang, Haojian
    Osterby, Lori
    Rosmarin, Alan G.
    Li, Shaoguang
 TI PTEN is a tumor suppressor in CML stem cells and BCR-ABL-induced
    leukemias in mice
 SO BLOOD
 LA English
 DT Article
 ID CHRONIC MYELOID-LEUKEMIA; KINASE INHIBITOR STI571; TYROSINE KINASE;
    CHRONIC PHASE; PROTEIN; MUTATION; CANCER; GENE; EXPRESSION; RESISTANCE
 AB The tumor suppressor gene phosphatase and tensin homolog (PTEN) is
    inactivated in many human cancers. However, it is unknown whether PTEN
    functions as a tumor suppressor in human Philadelphia
    chromosome-positive leukemia that includes chronic myeloid leukemia
    (CML) and B-cell acute lymphoblastic leukemia (B-ALL) and is induced by
    the BCR-ABL oncogene. By using our mouse model of BCR-ABL-induced
    leukemias, we show that Pten is down-regulated by BCR-ABL in leukemia
    stem cells in CML and that PTEN deletion causes acceleration of CML
    development. In addition, overexpression of PTEN delays the development
    of CML and B-ALL and prolongs survival of leukemia mice. PTEN
    suppresses leukemia stem cells and induces cell-cycle arrest of
    leukemia cells. Moreover, PTEN suppresses B-ALL development through
    regulating its downstream gene Akt1. These results demonstrate a
    critical role of PTEN in BCR-ABL-induced leukemias and suggest a
    potential strategy for the treatment of Philadelphia chromosome
    positive leukemia. (Blood. 2010; 115: 626-635)
 C1 [Peng, Cong; Chen, Yaoyu; Yang, Zhongfa; Zhang, Haojian; Osterby, Lori; Rosmarin, Alan G.; Li, Shaoguang] Univ Massachusetts, Sch Med, Dept Med, Div Hematol Oncol, Worcester, MA USA.
 RP Li, SG, 364 Plantat St,LRB 315, Worcester, MA 01604 USA.
 EM Shaoguang.Li@umassmed.edu
 FU Leukemia & Lymphoma Society ; National Institutes of Health
    [R01CA122142, R01-CA114199]; Scholar of the Leukemia & Lymphoma Society 
 FX This work was supported by the grants from the Leukemia & Lymphoma
    Society and the National Institutes of Health (R01-CA122142,
    R01-CA114199) to S. L. S. L. is a Scholar of the Leukemia & Lymphoma
    Society.
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 NR 49
 TC 9
 PU AMER SOC HEMATOLOGY
 PI WASHINGTON
 PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
 SN 0006-4971
 J9 BLOOD
 JI Blood
 PD JAN 21
 PY 2010
 VL 115
 IS 3
 BP 626
 EP 635
 DI 10.1182/blood-2009-06-228130
 PG 10
 SC Hematology
 GA 546OR
 UT ISI:000273820600024
 ER
 
 PT J
 AU Yang, LP
    Meng, ZN
    Liu, Y
    Zhang, Y
    Liu, XC
    Lu, DQ
    Huang, JH
    Lin, HR
 AF Yang, Liping
    Meng, Zining
    Liu, Yun
    Zhang, Yong
    Liu, Xiaochun
    Lu, Danqi
    Huang, Junhai
    Lin, Haoran
 TI Growth hormone and prolactin in Andrias davidianus: cDNA cloning,
    tissue distribution and phylogenetic analysis
 SO GENERAL AND COMPARATIVE ENDOCRINOLOGY
 LA English
 DT Article
 DE Growth hormone; Prolactin; Andrias davidianus; Phylogeny
 ID MESSENGER-RNA EXPRESSION; SEQUENCE ALIGNMENT; MOLECULAR EVOLUTION;
    GENES; FISHES; SALAMANDERS; AMPHIBIA; CAUDATA; DNA
 AB The Chinese giant salamander (Andrias davidianus) is one of the largest
    and 'living fossil' species of amphibian. To obtain genetic information
    for this species, the cDNAs encoding growth hormone (adGH) and
    prolactin (adPRL) were cloned from a pituitary cDNA library. The
    isolated adGH cDNA consisted of 864 bp and encoded a propeptide of 215
    amino acids, while the cDNA of adPRL was 1106 bp in length and encoded
    a putative peptide of 229 amino acids. Expression of the GH and PRL
    mRNA was only detected in the pituitary. Phylogenetic analyses were
    performed based on the isolated pituitary hormone sequences using
    maximum parsimony and neighbor-joining algorithms. The clustering
    results are similar to that based on the morphological characteristics
    or the rRNA genes, which indicate that the two orders (Anura and
    Caudata) of amphibian were monophyletic, and that A. davidianus was
    diverged early in the Caudate clade. These results indicated that both
    the GH and PRL sequence might be useful to study the phylogenies of
    relatively moderate evolved groups. Crown Copyright (C) 2009 Published
    by Elsevier Inc. All rights reserved.
 C1 [Yang, Liping; Meng, Zining; Liu, Yun; Zhang, Yong; Liu, Xiaochun; Lu, Danqi; Lin, Haoran] Sun Yat Sen Univ, Sch Life Sci, Inst Aquat Econ Anim, State Key Lab Biocontrol, Guangzhou 510275, Guangdong, Peoples R China.
    [Yang, Liping; Meng, Zining; Liu, Yun; Zhang, Yong; Liu, Xiaochun; Lu, Danqi; Lin, Haoran] Sun Yat Sen Univ, Sch Life Sci, Guangdong Prov Key Lab Aquat Econ Anim, Guangzhou 510275, Guangdong, Peoples R China.
    [Yang, Liping] Chinese Acad Fishery Sci, Pearl River Fisheries Res Inst, Guangzhou 510380, Guangdong, Peoples R China.
    [Huang, Junhai] Zhuhai Doumen Jinni Fishery Sci & Technol Co LTD, Doumen 519100, Peoples R China.
    [Lin, Haoran] Hainan Univ, Coll Ocean, Haikou 570228, Peoples R China.
 RP Lin, HR, Sun Yat Sen Univ, Sch Life Sci, Inst Aquat Econ Anim, State
    Key Lab Biocontrol, Guangzhou 510275, Guangdong, Peoples R China.
 EM lsslhr@mail.sysu.edu.cn
 FU Ministry of Education, Guangdong [2006D90204002]; Guangdong Provincial
    Scientific and Technical Program [20041326001183]
 FX This work was supported by Combination Projects on Production,
    Education and Research, Ministry of Education, Guangdong (No.
    2006D90204002), the grants from Guangdong Provincial Scientific and
    Technical Program (No. 20041326001183) and the priming scientific
    research foundation for the junior teachers in Sun Yat-Sen University.
    Thanks to Pei Zhu Ph.D. for improvements on an earlier draft of this
    paper.
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 NR 29
 TC 0
 PU ACADEMIC PRESS INC ELSEVIER SCIENCE
 PI SAN DIEGO
 PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
 SN 0016-6480
 J9 GEN COMP ENDOCRINOL
 JI Gen. Comp. Endocrinol.
 PD JAN 15
 PY 2010
 VL 165
 IS 2
 BP 177
 EP 180
 DI 10.1016/j.ygcen.2009.07.010
 PG 4
 SC Endocrinology & Metabolism
 GA 542TD
 UT ISI:000273517500001
 ER
 
 PT J
 AU Ke, XY
    Wang, J
    Gao, ZF
    Zhao, LZ
    Li, M
    Jing, HM
    Wang, JJ
    Zhao, W
    Gilbert, H
    Yang, XF
 AF Ke, Xiaoyan
    Wang, Jing
    Gao, Zifen
    Zhao, Lingzhi
    Li, Min
    Jing, Hongmei
    Wang, Jijun
    Zhao, Wei
    Gilbert, Heather
    Yang, Xiao-Feng
 TI Clinical characteristics and prognostic analysis of Chinese patients
    with diffuse large B-cell lymphoma
 SO BLOOD CELLS MOLECULES AND DISEASES
 LA English
 DT Article
 DE Diffuse large B-cell lymphoma; Prognostic analysis; Cell origin of
    tumor; Lactate dehydrogenase; International prognostic index
 ID GERMINAL CENTER; EXPRESSION PATTERNS; GENE REARRANGEMENT; HLA ALLELES;
    CHOP; IMMUNOHISTOCHEMISTRY; CHEMOTHERAPY; PREDICTOR; RITUXIMAB; DISEASE
 AB Diffuse large B-cell lymphoma (DLBCL) is the most common type of
    lymphoma in adults. As it is a highly heterogenous disease, many
    studies have focused on finding useful prognostic factors to help guide
    therapy. In this report, we examine several biological markers in 83
    patients with DLBCL enrolled in our hospital, including cell origin,
    serum lactate dehydrogenase (LDH) levels, and international prognostic
    index (IPI), in order to find the best combination of prognostic
    factors. We also examined whether DLBCL has a significant geographic
    difference. since several studies have suggested that the prevalence
    and potential etiological factors of lymphomas in China may be
    different from those in other countries. Our results demonstrate that:
    (1) patients in China have higher extranodal tissue involvement and
    different extranodal organ distribution than patients reported from
    other countries; (2) Chinese patients have higher rates of germinal
    center (GC) cell origin: and (3) among nine prognostic variables, lower
    IPI scores, GC cell origin determined by immunohistochemical staining,
    and no more than 1.5 times of normal levels of LDH are statistically
    significant good prognostic factors in Chinese patients with DLBCL,
    whereas age at the time of diagnosis, clinical stage,
    beta(2)-microglobulin levels, extranodal tissue involvement, and
    expression levels of Bcl-6 protein were not useful in determining
    prognosis. (C) 2009 Elsevier Inc. All rights reserved.
 C1 [Ke, Xiaoyan; Wang, Jing; Zhao, Lingzhi; Jing, Hongmei; Wang, Jijun; Zhao, Wei] Peking Univ, Hosp 3, Dept Hematol, Beijing 100191, Peoples R China.
    [Ke, Xiaoyan; Wang, Jing; Zhao, Lingzhi; Jing, Hongmei; Wang, Jijun; Zhao, Wei] Peking Univ, Hosp 3, Lymphoma Res Ctr, Beijing 100191, Peoples R China.
    [Gao, Zifen; Li, Min] Peking Univ, Dept Pathol, Hlth Sci Ctr, Beijing 100191, Peoples R China.
    [Gilbert, Heather] Univ Utah, Special Genet Lab, ARUP Labs, Sect Hematol,Dept Internal Med,Sch Med, Salt Lake City, UT 84132 USA.
    [Yang, Xiao-Feng] Temple Univ, Dept Pharmacol, Sch Med, Philadelphia, PA 19140 USA.
 RP Ke, XY, Peking Univ, Hosp 3, Dept Hematol, Beijing 100191, Peoples R
    China.
 EM xiaoyank@yahoo.com
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 NR 29
 TC 0
 PU ACADEMIC PRESS INC ELSEVIER SCIENCE
 PI SAN DIEGO
 PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
 SN 1079-9796
 J9 BLOOD CELLS MOLECULES DIS
 JI Blood Cells Mol. Dis.
 PD JAN 15
 PY 2010
 VL 44
 IS 1
 BP 55
 EP 61
 DI 10.1016/j.bcmd.2009.09.002
 PG 7
 SC Hematology
 GA 544XY
 UT ISI:000273695100010
 ER
 
 PT J
 AU Degenhardt, Y
    Huang, J
    Greshock, J
    Horiates, G
    Nathanson, K
    Yang, XL
    Herlyn, M
    Weber, B
 AF Degenhardt, Yan
    Huang, Jia
    Greshock, Joel
    Horiates, Galene
    Nathanson, Katherine
    Yang, Xiaolu
    Herlyn, Meenhard
    Weber, Barbara
 TI Distinct MHC Gene Expression Patterns During Progression of Melanoma
 SO GENES CHROMOSOMES & CANCER
 LA English
 DT Article
 ID SQUAMOUS-CELL CARCINOMA; ANTIGEN-PROCESSING MACHINERY; CLASS-II GENES;
    T-CELLS; DOWN-REGULATION; BRAF MUTATIONS; TUMOR-CELLS; CANCER; LINES;
    ASSOCIATION
 AB Abnormal expression of major histocompatibility complex l molecules in
    melanoma has been reported previously. However, the MHC molecule
    expression patterns in different growth phases of melanoma and the
    underlying mechanisms are not well understood. Here, we demonstrate
    that in vertical growth phase (VGP) melanomas, MHC genes are subject to
    increased rates of DNA copy number gains, accompanied by increased
    expression, in comparison to normal melanocytes. In contrast, MHC
    expression in metastatic melanomas drastically decreased compared to
    VGP melanomas, despite still prevalent DNA copy number gains.
    Subsequent investigations found that the master transactivator of MHC
    genes, CIITA, was also significantly downregulated in metastatic
    melanomas when compared to VGP melanomas. This could be one of the
    mechanisms accounting for the discrepancy between DNA copy number and
    expression level in metastatic melanomas, a potentially separate
    mechanism of gene regulation. These results infer a dynamic role of MHC
    function in melanoma progression. We propose potential mechanisms for
    the overexpression of MHC molecules in earlier stages of melanoma as
    well as for its downregulation in metastatic melanomas. (C) 2009
    Wiley-Liss, Inc.
 C1 [Degenhardt, Yan; Greshock, Joel; Horiates, Galene] GlaxoSmithKline Inc, Canc Metab DPU, King Of Prussia, PA 19406 USA.
    [Huang, Jia] Univ Miami, Miami Inst Human Genom, Miami, FL USA.
    [Nathanson, Katherine; Yang, Xiaolu] Univ Penn, Dept Canc Biol, Philadelphia, PA 19104 USA.
    [Nathanson, Katherine; Yang, Xiaolu] Univ Penn, Abramson Family Canc Res Inst, Philadelphia, PA 19104 USA.
    [Herlyn, Meenhard] Wistar Inst Anat & Biol, Philadelphia, PA 19104 USA.
    [Weber, Barbara] Novartis Inst Biomed Res, Boston, MA USA.
 RP Degenhardt, Y, GlaxoSmithKline Inc, Canc Metab DPU, Mail Stop
    UW2109,709 Swedeland Rd, King Of Prussia, PA 19406 USA.
 EM yan.y.degenhardt@gsk.com
 FU National Cancer Institute Melanoma [P50CA093372]
 FX Supported by: National Cancer Institute Melanoma Specialized Program of
    Research Excellence (SPORE), Grant number: P50CA093372.
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 NR 47
 TC 1
 PU WILEY-LISS
 PI HOBOKEN
 PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA
 SN 1045-2257
 J9 GENE CHROMOSOME CANCER
 JI Gene Chromosomes Cancer
 PD FEB
 PY 2010
 VL 49
 IS 2
 BP 144
 EP 154
 DI 10.1002/gcc.20728
 PG 11
 SC Oncology; Genetics & Heredity
 GA 539XX
 UT ISI:000273293700006
 ER
 
 PT J
 AU Yang, B
    Jiang, Q
    Chan, T
    Ko, WKW
    Wong, AOL
 AF Yang, Bo
    Jiang, Quan
    Chan, Ting
    Ko, Wendy K. W.
    Wong, Anderson O. L.
 TI Goldfish kisspeptin: Molecular cloning, tissue distribution of
    transcript expression, and stimulatory effects on prolactin, growth
    hormone and luteinizing hormone secretion and gene expression via
    direct actions at the pituitary level
 SO GENERAL AND COMPARATIVE ENDOCRINOLOGY
 LA English
 DT Article
 DE Kisspeptin-10; Kisspeptin receptor; Growth hormone; Prolactin;
    Gonadotropin; Laser capture microdissection; Pituitary cells; Goldfish
 ID GONADOTROPIN-RELEASING-HORMONE; METASTASIS-SUPPRESSOR GENE;
    PROTEIN-COUPLED-RECEPTOR; CARASSIUS-AURATUS; KISS-1 PEPTIDE; NATURAL
    LIGAND; IN-VIVO; CELLS; GPR54; RAT
 AB Kisspeptin, the product of Kiss1 gene, is a novel regulator of the
    gonadotropic axis. In mammals, its stimulatory effect on gonadotropin
    secretion is well documented and mediated mainly by hypothalamic
    release of gonadotropin-releasing hormone. Although the pituitary
    actions of kisspeptin have been reported, the effects of kisspeptin on
    gonadotropin release via direct action on pituitary cells are still
    controversial. Using goldfish as a model, here we examined the direct
    actions of kisspeptin on pituitary functions in modern-day bony fish.
    As a first step, the structural identity of goldfish Kiss1 was
    established by T/TRACE and Kiss1 transcript was shown to be widely
    expressed in various tissues in goldfish. At the pituitary level, Kiss1
    receptor (Kissi1r) expression was detected in immuno-identified
    gonadotrophs, lactotrophs, and somatotrophs. Kiss1 transcript was also
    located in goldfish somatotrophs but not in lactotrophs or
    gonadotrophs. In parallel studies, goldfish kisspeptin-10 was
    synthesized and used to test the pituitary actions of kisspeptin in
    vitro. In goldfish pituitary cell cultures, 30-min incubation with
    kisspeptin-10 increased basal release of luteinizing hormone (LH),
    prolactin (PRL), and growth hormone (GH). Transcript expression of LH,
    PRL, and GH were also elevated by prolonging kisspeptin-10 treatment to
    24 h. These results taken together suggest that kisspeptin via Kiss1r
    activation can act directly at the pituitary level to trigger LH, PRL,
    and GH secretion and gene expression in goldfish. Our finding of Kiss1
    expression in somatotrophs also rises the possibility that kisspeptin
    may be produced locally in the fish pituitary and serve as an
    autocrine/paracrine regulator. (C) 2009 Elsevier Inc. All rights
    reserved.
 C1 [Yang, Bo; Jiang, Quan; Chan, Ting; Ko, Wendy K. W.; Wong, Anderson O. L.] Univ Hong Kong, Div Endocrinol, Sch Biol Sci, Hong Kong, Hong Kong, Peoples R China.
 RP Wong, AOL, Univ Hong Kong, Div Endocrinol, Sch Biol Sci, 4S-12 Kadoorie
    Biol Sci Bldg,Pokfulam Rd, Hong Kong, Hong Kong, Peoples R China.
 EM olwong@hkucc.hku.hk
 FU Research Grant Council (Hong Kong) ; National 973 Program (China) ;
    University Research Committee (University of Hong Kong) ; School of
    Biological Sciences (University of Hong Kong) 
 FX The project was supported by grants (to A.O.L.W.) from Research Grant
    Council (Hong Kong), National 973 Program (China), and University
    Research Committee (University of Hong Kong). Financial support from
    the School of Biological Sciences (University of Hong Kong) in the form
    of postgraduate studentship is also acknowledged (to BY., Q.J., and
    T.Q. Special thanks are given to Dr. R.E. Peter (University of Alberta,
    Canada) for the supply of antisera used in GH, PRL, and LH measurement.
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 NR 50
 TC 5
 PU ACADEMIC PRESS INC ELSEVIER SCIENCE
 PI SAN DIEGO
 PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
 SN 0016-6480
 J9 GEN COMP ENDOCRINOL
 JI Gen. Comp. Endocrinol.
 PD JAN 1
 PY 2010
 VL 165
 IS 1
 BP 60
 EP 71
 DI 10.1016/j.ygcen.2009.06.001
 PG 12
 SC Endocrinology & Metabolism
 GA 542HP
 UT ISI:000273483900009
 ER
 
 PT J
 AU Zheng, CL
    Yang, SG
    Guo, ZX
    Liao, WB
    Zhang, L
    Yang, RC
    Han, ZC
 AF Zheng, Cuiling
    Yang, Shaoguang
    Guo, Zhenxing
    Liao, Wenbin
    Zhang, Lei
    Yang, Renchi
    Han, Zhong Chao
 TI Human Multipotent Mesenchymal Stromal Cells From Fetal Lung Expressing
    Pluripotent Markers and Differentiating Into Cell Types of Three Germ
    Layers
 SO CELL TRANSPLANTATION
 LA English
 DT Article
 DE Multipotent mesenchymal stromal cells; Fetal lung; Pluripotent markers;
    Differentiation capacity
 ID HUMAN BONE-MARROW; UMBILICAL-CORD BLOOD; STEM-CELLS; ADIPOSE-TISSUE;
    IN-VITRO; THERAPY; IDENTIFICATION; EXPANSION; MSC; TRANSPLANTATION
 AB Multipotent mesenchymal stromal cells (MSCs) are a promising cell type
    for cell transplantation; however, their utilization remains limited
    until the availability of adequate alternative sources of MSCs and the
    thorough understanding of the biology of MSCs isolated from various
    sources are realized. Fetal lung has been identified as a rich source
    of MSCs. To explore the therapeutic potential of passaged fetal lung
    MSCs (FLMSCs), the present study evaluated their growth kinetics,
    telomere length, karyotype, immunophenotype, and the differentiation
    potential during in vitro expansion. FLMSCs could be easily amplified
    in vitro with no significant shorting of telomere length and had a
    normal karyotype. No significant differences between passage 5 or
    passage 25 were observed in the immunophenotype analysis using flow
    cytometry. Moreover, flow cytometry results provided the first
    demonstration, to our knowledge, that FLMSCs stably expressed
    pluripotent markers including Oct4, Nanog, Sox2, TRA-1-60, c-Myc, and
    SSEA-4 through 25 passages. In vitro differentiation studies as
    identified by confocal microscopy, flow cytometry, RT-PCR, and
    immunohistochemistry showed that FLMSCs had extended capacity of
    differentiating into mesodermal, ectodermal, and endodermal lineages,
    and that their potential for adipogenic, osteogenic, and chondrogenic
    differentiation may be maintained over 25 passages. Furthermore,
    osteogenic and chondrogenic differentiation was used as an indicator of
    their differentiation capability in vivo, as evidenced by ectopic bone
    and cartilage formation. In summary, these results suggest that FLMSCs
    are a primitive population and that their extensive in vitro expansion
    does not involve significant functional modification of the cells,
    including morphology, growth, karyotype, immunophenotype, and
    mesodermal differentiation potential. Hence, FLMSCs might constitute an
    attractive cell resource for cell transplantation to induce
    regeneration of damaged tissues/organs.
 C1 [Zheng, Cuiling; Yang, Shaoguang; Guo, Zhenxing; Liao, Wenbin; Zhang, Lei; Yang, Renchi; Han, Zhong Chao] Chinese Acad Med Sci, Inst Hematol & Blood Dis Hosp, State Key Lab Expt Hematol, Tianjin 300020, Peoples R China.
    [Zheng, Cuiling; Yang, Shaoguang; Guo, Zhenxing; Liao, Wenbin; Zhang, Lei; Yang, Renchi; Han, Zhong Chao] Peking Union Med Coll, Tianjin 300020, Peoples R China.
    [Guo, Zhenxing] Tsinghua Univ, Hosp 1, Dept Hematol Oncol, Beijing 100084, Peoples R China.
 RP Han, ZC, Chinese Acad Med Sci, Inst Hematol & Blood Dis Hosp, State Key
    Lab Expt Hematol, 288 Nanjing Rd, Tianjin 300020, Peoples R China.
 EM tihzchan@public.tpt.tj.cn
 FU Ministry Science & Technology of China [2006AA02A110]; National Natural
    Science Foundation of China [30600238]; Tianjin Municipal Science and
    Technology Commission [07JCYBJC11200, 08ZCKFSF03200]
 FX The authors would like to thank HUES Cell Facility/Melton Laboratory
    (Harvard Universityl HHMI, Cambridge, MA, USA) for kindly providing
    Human ES cell line. The authors would like to thank Dr. Shihong Lu,
    Qian ren, and Qinjun Zhao for their discussion and help with the
    writing of the manuscript. This study was supported by 863 projects
    from Ministry Science & Technology of China (2006AA02A110), National
    Natural Science Foundation of China (30600238), and Tianjin Municipal
    Science and Technology Commission (07JCYBJC11200 and 08ZCKFSF03200).
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 NR 49
 TC 3
 PU COGNIZANT COMMUNICATION CORP
 PI ELMSFORD
 PA 3 HARTSDALE ROAD, ELMSFORD, NY 10523-3701 USA
 SN 0963-6897
 J9 CELL TRANSPLANT
 JI Cell Transplant.
 PY 2009
 VL 18
 IS 10-11
 BP 1093
 EP 1109
 DI 10.3727/096368909X12483162197042
 PG 17
 SC Cell & Tissue Engineering; Medicine, Research & Experimental;
    Transplantation
 GA 541QU
 UT ISI:000273434500004
 ER
 
 PT J
 AU Yang, J
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    Nyland, SB
    Zhang, RR
    Ryland, LK
    Broeg, K
    Baab, KT
    Jarbadan, NR
    Irby, R
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 AF Yang, Jun
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    Zhang, Ranran
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    Irby, Rosalyn
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    granular lymphocytes via an autocrine regulatory pathway
 SO BLOOD
 LA English
 DT Article
 ID KILLER-CELL-ACTIVITY; PDGF BETA-RECEPTOR; LYMPHOPROLIFERATIVE DISEASE;
    SIGNAL-TRANSDUCTION; MEMBRANE-BINDING; LGL LEUKEMIA; T-CELLS;
    EXPRESSION; INHIBITION; ALPHA
 AB Large granular lymphocyte (LGL) leukemia results from chronic expansion
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    identified platelet-derived growth factor (PDGF) as a key master switch
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    show that an autocrine PDGF regulatory loop mediates survival of
    leukemic LGLs of both T- and NK-cell origin. We found high levels of
    circulating PDGF-BB in platelet-poor plasma samples from LGL leukemia
    patients. Production of PDGF-BB by leukemic LGLs was demonstrated by
    immunocytochemical staining. Leukemic cells expressed much higher
    levels of PDGFR-beta transcripts than purified normal CD8(+) T cells or
    NK cells. We observed that phosphatidylinositol-3-kinase (PI3 kinase),
    Src family kinase (SFK), and downstream protein kinase B (PKB)/AKT
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    Pharmacologic blockade of these pathways led to apoptosis of leukemic
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    that targeting of PDGF-BB, a pivotal regulator for the long-term
    survival of leukemic LGLs, may be an important therapeutic strategy.
    (Blood. 2010;115:51-60)
 C1 [Yang, Jun; Liu, Xin; Nyland, Susan B.; Zhang, Ranran; Ryland, Lindsay K.; Broeg, Kathleen; Baab, Kendall Thomas; Jarbadan, Nancy Ruth; Irby, Rosalyn; Loughran, Thomas P., Jr.] Penn State Univ, Coll Med, Penn State Hershey Canc Inst, Dept Med, Hershey, PA 17033 USA.
 RP Yang, J, Penn State Univ, Coll Med, Penn State Hershey Canc Inst, Dept
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 EM jyang@psu.edu
 FU National Institutes of Health [R01 CA112112]
 FX This work was supported by National Institutes of Health grant R01
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 TC 6
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 PI WASHINGTON
 PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
 SN 0006-4971
 J9 BLOOD
 JI Blood
 PD JAN 7
 PY 2010
 VL 115
 IS 1
 BP 51
 EP 60
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 PG 10
 SC Hematology
 GA 541CE
 UT ISI:000273389600012
 ER
 
 PT J
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 TI Generation of Mouse Conditional and Null Alleles of the Type III
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 SO GENESIS
 LA English
 DT Article
 DE PiT-1; Slc20a1; yolk sac vasculature; anemia; knockout; conditional;
    mouse; embryonic lethal; type III sodium-dependent phosphate
    cotransporter
 ID INORGANIC-PHOSPHATE; TRANSPORT FUNCTION; CALCIFICATION; FAMILY
 AB Accelerated vascular calcification occurs in several human diseases
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 RP Giachelli, CM, Univ Washington, Dept Bioengn, Box 355061, Seattle, WA
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 EM ceci@uw.edu
 FU NIH [HL07828, HL62329]
 FX NIH, Contract grant numbers: HL07828, HL62329
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 VL 47
 IS 12
 BP 858
 EP 863
 DI 10.1002/dvg.20577
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 SC Developmental Biology; Genetics & Heredity
 GA 537JG
 UT ISI:000273108600009
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 C1 [Gamble, Matthew J.; Frizzell, Kristine M.; Yang, Christine; Krishnakumar, Raga; Kraus, W. Lee] Cornell Univ, Dept Mol Biol & Genet, Ithaca, NY 14853 USA.
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 RP Kraus, WL, Cornell Univ, Dept Mol Biol & Genet, Ithaca, NY 14853 USA.
 EM wlk5@cornell.edu
 FU NIH/NIDDK [DK069710, DK079847-01]; Cornell University Center for
    Vertebrate Genomics ; Endocrine Society ; American Heart Association
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    NIH/NIDDK (DK069710), the Cornell University Center for Vertebrate
    Genomics, and the Endocrine Society to W. L. K.; a post-doctoral
    fellowship from the American Heart Association (AHA) and from the
    NIH/NIDDK (DK079847-01) to M. J. G.; and a predoctoral fellowship from
    the AHA to K. M. F.
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 NR 45
 TC 11
 PU COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT
 PI WOODBURY
 PA 500 SUNNYSIDE BLVD, WOODBURY, NY 11797-2924 USA
 SN 0890-9369
 J9 GENE DEVELOP
 JI Genes Dev.
 PD JAN 1
 PY 2010
 VL 24
 IS 1
 BP 21
 EP 32
 DI 10.1101/gad.1876110
 PG 12
 SC Cell Biology; Developmental Biology; Genetics & Heredity
 GA 539JD
 UT ISI:000273249300005
 ER
 
 PT J
 AU Zheng, JF
    Mercado-Uribe, I
    Rosen, DG
    Chang, B
    Liu, PS
    Yang, G
    Malpica, A
    Naora, H
    Auersperg, N
    Mills, GB
    Bast, RC
    Liu, JS
 AF Zheng, Jingfang
    Mercado-Uribe, Imelda
    Rosen, Daniel G.
    Chang, Bin
    Liu, Peishu
    Yang, Gong
    Malpica, Anais
    Naora, Honami
    Auersperg, Nelly
    Mills, Gordon B.
    Bast, Robert C.
    Liu, Jinsong
 TI Induction of papillary carcinoma in human ovarian surface epithelial
    cells using combined genetic elements and peritoneal microenvironment
 SO CELL CYCLE
 LA English
 DT Article
 DE high grade serous carcinoma; HER2/neu; human ovarian surface epithelial
    cells; transformation
 ID SEROUS CARCINOMA; HUMAN-BREAST; FALLOPIAN-TUBE; MOUSE MODEL; CANCER;
    CARCINOGENESIS; TRANSITION; EXPRESSION; BIOLOGY; TUMORS
 AB Papillary differentiation is one of the most common histological
    features of ovarian cancer, although the underlying mechanism that
    leads to such differentiation is not known. We hypothesized that human
    ovarian surface epithelial cells can be transformed into carcinoma with
    papillary differentiation by overexpressing HeR2/neu in these cells.
    Mice were injected either subcutaneously or intraperitoneally with two
    immortalized human ovarian surface epithelial cell lines after enforced
    expression of HeR-2/neu. Mice subcutaneously injected with tumor cells
    from either the T29Nt or T80Nt developed undifferentiated carcinomas.
    In contrast, mice injected intraperitoneally with T29Nt cells developed
    papillary carcinoma, and those injected intraperitoneally with T80Nt
    cells developed undifferentiated carcinoma. our results demonstrate
    that ovarian surface epithelial cells can develop into papillary
    carcinoma in mice, and that the induction of papillary differentiation
    depends not only on specific genetic modifications but also on the
    tumor microenvironment and epithelial cell type from ovary from
    different patients.
 C1 [Zheng, Jingfang; Mercado-Uribe, Imelda; Rosen, Daniel G.; Chang, Bin; Yang, Gong; Malpica, Anais; Liu, Jinsong] Univ Texas MD Anderson Canc Ctr, Dept Pathol, Houston, TX 77030 USA.
    [Naora, Honami; Mills, Gordon B.] Univ Texas MD Anderson Canc Ctr, Dept Syst Biol, Houston, TX 77030 USA.
    [Zheng, Jingfang; Bast, Robert C.] Univ Texas MD Anderson Canc Ctr, Dept Expt Therapeut, Houston, TX 77030 USA.
    [Zheng, Jingfang; Liu, Peishu] Shandong Univ, Dept Obstet & Gynecol, Qilu Hosp, Jinan 250100, Shandong, Peoples R China.
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 RP Liu, JS, Univ Texas MD Anderson Canc Ctr, Dept Pathol, Houston, TX
    77030 USA.
 EM jliu@mdanderson.org
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 NR 23
 TC 2
 PU LANDES BIOSCIENCE
 PI AUSTIN
 PA 1002 WEST AVENUE, 2ND FLOOR, AUSTIN, TX 78701 USA
 SN 1538-4101
 J9 CELL CYCLE
 JI Cell Cycle
 PD JAN 1
 PY 2010
 VL 9
 IS 1
 BP 140
 EP 146
 PG 7
 SC Cell Biology
 GA 539EQ
 UT ISI:000273236800033
 ER
 
 PT J
 AU Zhu, XY
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    Cai, JG
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    Liang, SH
    Ren, DM
 AF Zhu, Xiangying
    Yang, Nan
    Cai, Jianguo
    Yang, Guimei
    Liang, Shenghua
    Ren, Daming
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    cells
 SO CELLULAR & MOLECULAR BIOLOGY LETTERS
 LA English
 DT Article
 DE Cancer; Intrabody; Anti-hTERT ScFv; Immortality
 ID TELOMERASE CATALYTIC SUBUNIT; REVERSE-TRANSCRIPTASE; INTRACELLULAR
    EXPRESSION; TUMOR-CELLS; INHIBITION; CARCINOMA; PROLIFERATION;
    PROSPECTS; IMMUNITY; THERAPY
 AB hTERT (human telomerase reverse transcriptase) plays a key role in the
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    implicated in 85% of malignant tumors and offers a specific target for
    cancer therapy. In this paper, we describe an effective approach using
    a single-chain variable fragment (scFv) intrabody derived from
    monoclonal hybridoma directed against hTERT to attenuate the
    immortalization of human uterine cervix and hepatoma cells. The scFv we
    constructed had a high affinity to hTERT, and specifically neutralized
    over 70% of telomere synthesis activity, thereby inhibiting the
    viability and proliferation of the cancer cells. Our results indicate
    that this anti-hTERT intrabody is a promising tool to target hTERT and
    intervene in the immortalization process of cancer cells.
 C1 [Zhu, Xiangying; Yang, Nan; Cai, Jianguo; Yang, Guimei; Liang, Shenghua; Ren, Daming] Fudan Univ, Sch Life Sci, State Key Lab Genet Engn, Shanghai, Peoples R China.
 RP Ren, DM, Fudan Univ, Sch Life Sci, State Key Lab Genet Engn, Shanghai,
    Peoples R China.
 EM dmren@fudan.edu.cn
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 NR 43
 TC 0
 PU VERSITA
 PI WARSAW
 PA SOLIPSKA 14A-1, 02-482 WARSAW, POLAND
 SN 1425-8153
 J9 CELL MOL BIOL LETT
 JI Cell. Mol. Biol. Lett.
 PD MAR
 PY 2010
 VL 15
 IS 1
 BP 32
 EP 45
 DI 10.2478/s11658-009-0032-2
 PG 14
 SC Biochemistry & Molecular Biology; Cell Biology
 GA 535LB
 UT ISI:000272968600003
 ER
 
 PT J
 AU Wang, F
    Yang, W
 AF Wang, Feng
    Yang, Wei
 TI Structural Insight into Translesion Synthesis by DNA Pol II
 SO CELL
 LA English
 DT Article
 ID ESCHERICHIA-COLI; POLYMERASE-II; SPONTANEOUS MUTAGENESIS; FAMILY
    POLYMERASES; DAMAGE TOLERANCE; GENOME STABILITY; ABASIC LESION;
    Y-FAMILY; B-FAMILY; IN-VIVO
 AB E. coli DNA Pol II and eukaryotic Rev3 are B-family polymerases that
    can extend primers past a damaged or mismatched site when the
    high-fidelity replicative polymerases in the same family are
    ineffective. We report here the biochemical and structural properties
    of DNA Pol II that facilitate this translesion synthesis. DNA Pol II
    can extend primers past lesions either directly or by template
    skipping, in which small protein cavities outside of the active site
    accommodate looped-out template nucleotides 1 or 2 bp upstream. Because
    of multiple looping-out alternatives, mutation spectra of bypass
    synthesis are complicated. Moreover, translesion synthesis is enhanced
    by altered partitioning of DNA substrate between the polymerase active
    site and the proofreading exonuclease site. Compared to the replicative
    B family polymerases, DNA Pol II has subtle amino acid changes remote
    from the active site that allow it to replicate normal DNA with high
    efficiency yet conduct translesion synthesis when needed.
 C1 [Wang, Feng; Yang, Wei] NIDDK, Mol Biol Lab, NIH, Bethesda, MD 20892 USA.
 RP Yang, W, NIDDK, Mol Biol Lab, NIH, 9000 Rockville Pike,Bldg 5,Room
    B1-03, Bethesda, MD 20892 USA.
 EM wei.yang@nih.gov
 FU National Institute of Diabetes and Digestive and Kidney Diseases
    intramural research program at National Institutes of Health 
 FX We thank S. Doublie for purified gp43 protein and the gp43-beta- clone,
    W. Konigsberg for the gp43 exo- clone, our labmates for technical
    support, D. Leahy and R. Craigie for critical reading of the
    manuscript, and F. Dyda for maintaining the X-ray equipment. The
    research is funded by the National Institute of Diabetes and Digestive
    and Kidney Diseases intramural research program at National Institutes
    of Health.
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 NR 56
 TC 8
 PU CELL PRESS
 PI CAMBRIDGE
 PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
 SN 0092-8674
 J9 CELL
 JI Cell
 PD DEC 24
 PY 2009
 VL 139
 IS 7
 BP 1279
 EP 1289
 DI 10.1016/j.cell.2009.11.043
 PG 11
 SC Biochemistry & Molecular Biology; Cell Biology
 GA 536MO
 UT ISI:000273048700016
 ER
 
 PT J
 AU Sun, J
    Yu, EY
    Yang, YT
    Confer, LA
    Sun, SH
    Wan, K
    Lue, NF
    Lei, M
 AF Sun, Jia
    Yu, Eun Young
    Yang, Yuting
    Confer, Laura A.
    Sun, Steven H.
    Wan, Ke
    Lue, Neal F.
    Lei, Ming
 TI Stn1-Ten1 is an Rpa2-Rpa3-like complex at telomeres
 SO GENES & DEVELOPMENT
 LA English
 DT Article
 DE Telomere; telomere-binding protein; telomerase; homologous recombination
 ID SINGLE-STRANDED-DNA; REPLICATION PROTEIN-A; CHROMOSOME END-PROTECTION;
    CANDIDA-ALBICANS; BINDING-PROTEIN; CRYSTAL-STRUCTURE; LENGTH
    REGULATION; FISSION YEAST; OB-FOLD; POT1
 AB In budding yeast, Cdc13, Stn1, and Ten1 form a heterotrimeric complex
    (CST) that is essential for telomere protection and maintenance.
    Previous bioinformatics analysis revealed a putative
    oligonucleotide/oligosaccharide-binding (OB) fold at the N terminus of
    Stn1 (Stn1N) that shows limited sequence similarity to the OB fold of
    Rpa2, a subunit of the eukaryotic ssDNA-binding protein complex
    replication protein A (RPA). Here we present functional and structural
    analyses of Stn1 and Ten1 from multiple budding and fission yeast. The
    crystal structure of the Candida tropicalis Stn1N complexed with Ten1
    demonstrates an Rpa2N-Rpa3-like complex. In both structures, the OB
    folds of the two components pack against each other through
    interactions between two C-terminal helices. The structure of the
    C-terminal domain of Saccharomyces cerevisiae Stn1 (Stn1C) was found to
    comprise two related winged helix-turn-helix (WH) motifs, one of which
    is most similar to the WH motif at the C terminus of Rpa2, again
    supporting the notion that Stn1 resembles Rpa2. The crystal structure
    of the fission yeast Schizosaccharomyces pombe Stn1N-Ten1 complex
    exhibits a virtually identical architecture as the C. tropicalis
    Stn1N-Ten1. Functional analyses of the Candida albicans Stn1 and Ten1
    proteins revealed critical roles for these proteins in suppressing
    aberrant telomerase and recombination activities at telomeres.
    Mutations that disrupt the Stn1-Ten1 interaction induce telomere
    uncapping and abolish the telomere localization of Ten1. Collectively,
    our structural and functional studies illustrate that, instead of being
    confined to budding yeast telomeres, the CST complex may represent an
    evolutionarily conserved RPA-like telomeric complex at the 3' overhangs
    that works in parallel with or instead of the well-characterized
    POT1-TPP1/TEBP alpha-beta complex.
 C1 [Sun, Jia; Yang, Yuting; Confer, Laura A.; Wan, Ke; Lei, Ming] Univ Michigan, Sch Med, Howard Hughes Med Inst, Ann Arbor, MI 48109 USA.
    [Sun, Jia; Yang, Yuting; Confer, Laura A.; Sun, Steven H.; Wan, Ke; Lei, Ming] Univ Michigan, Sch Med, Dept Biol Chem, Ann Arbor, MI 48109 USA.
    [Yu, Eun Young; Lue, Neal F.] Cornell Univ, Dept Microbiol & Immunol, WR Hearst Microbiol Res Ctr, Weill Med Coll, New York, NY 10065 USA.
 RP Lei, M, Univ Michigan, Sch Med, Howard Hughes Med Inst, Ann Arbor, MI
    48109 USA.
 EM nflue@med.cornell.edu
    leim@umich.edu
 FU NIH [GM 083015-01, GM069507]; American Cancer Society Research Scholar
    ; Sidney Kimmel Scholar Award ; Michigan Economic Development
    Corporation ; Michigan Technology Tri-Corridor [085P1000817]; U. S.
    Department of Energy, Office of Science, Office of Basic Energy
    Sciences [DE-AC02-06CH11357]
 FX We thank Y. Chen and F. Wang for help at various stages of the project.
    This work was supported by NIH grants (GM 083015-01 to M. L. and
    GM069507 to N. L.), an American Cancer Society Research Scholar grant,
    and a Sidney Kimmel Scholar Award (to M. L.). M. L. is a Howard Hughes
    Medical Institute Early Career Scientist. N. F. L. thanks Drs.
    Ting-Fang Wang and Chung Wang (Academia Sinica, Taiwan) for support
    during his summer 2007 visit, on which occasion some of the works
    described here were initiated. Use of Life Sciences Collaborative
    Access Team Sector 21 was supported by the Michigan Economic
    Development Corporation and the Michigan Technology Tri-Corridor (grant
    085P1000817). Use of the Advanced Photon Source was supported by the U.
    S. Department of Energy, Office of Science, Office of Basic Energy
    Sciences, under contract number DE-AC02-06CH11357.
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 NR 62
 TC 16
 PU COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT
 PI WOODBURY
 PA 500 SUNNYSIDE BLVD, WOODBURY, NY 11797-2924 USA
 SN 0890-9369
 J9 GENE DEVELOP
 JI Genes Dev.
 PD DEC 15
 PY 2009
 VL 23
 IS 24
 BP 2900
 EP 2914
 DI 10.1101/gad.1851909
 PG 15
 SC Cell Biology; Developmental Biology; Genetics & Heredity
 GA 532YB
 UT ISI:000272785500012
 ER
 
 PT J
 AU Dou, BD
    Hou, BW
    Xu, HM
    Lou, XY
    Chi, XF
    Yang, JB
    Wang, F
    Ni, ZF
    Sun, QX
 AF Dou, Bingde
    Hou, Beiwei
    Xu, Haiming
    Lou, Xiangyang
    Chi, Xiaofei
    Yang, Jinbin
    Wang, Fang
    Ni, Zhongfu
    Sun, Qixin
 TI Efficient mapping of a female sterile gene in wheat (Triticum aestivum
    L.)
 SO GENETICS RESEARCH
 LA English
 DT Article
 ID HYBRID SEED PRODUCTION; LOCI; POPULATIONS; INHERITANCE; POLLENIZER;
    FERTILITY; EVOLUTION; SYSTEM; MAP
 AB Studies on inheritance of fertility are of great importance in wheat
    breeding. Although Substantial progress has been achieved in molecular
    characterization or male sterility and fertility restoration recently,
    little effort has been devoted to female sterility. To identify the
    gene(s) controlling female sterility in wheat efficiently, an
    investigation was conducted for the seed setting ratio using a set of
    F-2 populations derived from the cross between a female sterile line
    XND126 and an elite cultivar Gaocheng 8901. Bulked segregation analysis
    (BSA) method and recessive class approach were adopted to screen for
    SSR markers potentially linked to female fertility gene loci in 2005.
    Out of 1080 SSRs in wheat genome, eight markers on chromosome 2D showed
    a clear difference between two disparate bulks and small recombination
    frequency values, suggesting a strong linkage signal to the sterility
    gene. Based on the candidate linked markers, partial linkage maps were
    constructed with Mapmaker 3.0 (EXP) instead of whole genome maps, and
    quantitative trait locus (QTL) mapping was implemented with software
    QTLNetwork 2.0. A major gene locus designated as taf1, was located on
    chromosome 2DS. The above result was confirmed by the analysis for 2007
    data, and taf1 was identified on the same chromosome 2DS with a
    confidence interval of 2.4 cM, which Could explain 44-99 % of
    phenotypic variation. These results provided fundamental information
    for fine mapping studies and laid the groundwork for wheat fertility
    genetic studies.
 C1 [Dou, Bingde; Hou, Beiwei; Yang, Jinbin] Huaiyin Normal Univ, Inst Plant Biotechnol, Jiangsu Key Lab Ecoagr Biotechnol Hongze Lake, Huaian 223300, Peoples R China.
    [Dou, Bingde; Hou, Beiwei; Yang, Jinbin; Wang, Fang] Xinjiang Agr Univ, Agron Coll, Urumqi 830052, Peoples R China.
    [Xu, Haiming; Lou, Xiangyang; Chi, Xiaofei] Zhejiang Univ, Coll Agr & Biotechnol, Hangzhou 310029, Zhejiang, Peoples R China.
    [Ni, Zhongfu; Sun, Qixin] China Agr Univ, Dept Plant Genet & Breeding, Beijing 100094, Peoples R China.
 RP Dou, BD, Huaiyin Normal Univ, Inst Plant Biotechnol, Jiangsu Key Lab
    Ecoagr Biotechnol Hongze Lake, Huaian 223300, Peoples R China.
 EM doubd@163.com
 FU National Natural Science Foundation of China [30771380]; Qing Lan
    Project in Jiangsu Province 
 FX We are grateful to Professor Dr Zhiyong Liu, Department of Plant
    Genetics and Breeding, China Agricultural University for their
    technical support on this program. This research was sponsored by the
    National Natural Science Foundation of China (No. 30771380) and Qing
    Lan Project in Jiangsu Province.
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 NR 46
 TC 4
 PU CAMBRIDGE UNIV PRESS
 PI NEW YORK
 PA 32 AVENUE OF THE AMERICAS, NEW YORK, NY 10013-2473 USA
 SN 0016-6723
 J9 GENET RES
 JI Genet. Res.
 PD OCT
 PY 2009
 VL 91
 IS 5
 BP 337
 EP 343
 DI 10.1017/S0016672309990218
 PG 7
 SC Genetics & Heredity
 GA 534DP
 UT ISI:000272876000004
 ER
 
 PT J
 AU Sharma, G
    Mirza, S
    Yang, YH
    Parshad, R
    Hazrah, P
    Gupta, SD
    Ralhan, R
 AF Sharma, Gayatri
    Mirza, Sameer
    Yang, Yi-Hsin
    Parshad, Rajinder
    Hazrah, Priya
    Gupta, Siddartha Datta
    Ralhan, Ranju
 TI Prognostic relevance of promoter hypermethylation of multiple genes in
    breast cancer patients
 SO CELLULAR ONCOLOGY
 LA English
 DT Article
 DE Breast cancer; methylation; prognosis; RAR beta; GSTP1; BRCA1
 ID METHYLATION-SPECIFIC PCR; DNA METHYLATION; CELL-LINES; CPG-ISLAND;
    ESTROGEN-RECEPTOR; OVARIAN-TUMORS; RAR-BETA; BRCA1; EXPRESSION; RASSF1A
 AB Background: Methylation-mediated suppression of detoxification, DNA
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    disease prognosis and patients' survival.
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 C1 [Sharma, Gayatri; Mirza, Sameer; Ralhan, Ranju] All India Inst Med Sci, Dept Biochem, New Delhi 110029, India.
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 NR 54
 TC 3
 PU IOS PRESS
 PI AMSTERDAM
 PA NIEUWE HEMWEG 6B, 1013 BG AMSTERDAM, NETHERLANDS
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 VL 31
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 BP 487
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 PG 14
 SC Oncology; Cell Biology; Pathology
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 UT ISI:000272854400007
 ER
 
 PT J
 AU Yang, B
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 AF Yang, B.
    Kumar, S.
 TI Nedd4 and Nedd4-2: closely related ubiquitin-protein ligases with
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 SO CELL DEATH AND DIFFERENTIATION
 LA English
 DT Review
 DE ubiquitylation; endocytosis; trafficking; receptor; signaling
 ID EPITHELIAL NA+ CHANNEL; FACTOR-I RECEPTOR; INDUCIBLE KINASE ISOFORMS;
    YEAST METAL TRANSPORTER; GROWTH-FACTOR RECEPTOR; SODIUM-CHANNEL; WW
    DOMAINS; PROTEASOMAL DEGRADATION; MULTIVESICULAR BODIES; MEDIATED
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 AB The Nedd4 (neural precursor cell-expressed developmentally
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 C1 [Yang, B.] Univ Iowa, Carver Coll Med, Iowa City, IA 52242 USA.
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    [Kumar, S.] Hanson Inst, Adelaide, SA 5000, Australia.
 RP Yang, B, Univ Iowa, Carver Coll Med, 200 Hawkins Dr,46 MRF, Iowa City,
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 EM baoli-yang@uiowa.edu
    Sharad.Kumar@health.sa.gov.au
 FU NIH [DK52617, AR052647, DE16215]; National Health and Medical Research
    Council [508086]; Australian Research Council [DP0880571]
 FX The work in the Yang laboratory is supported by the NIH (DK52617,
    AR052647, and DE16215 to BY), and in the Kumar Laboratory by the
    National Health and Medical Research Council (508086), and the
    Australian Research Council (DP0880571). We thank the members of our
    respective laboratories and Dr. Paula Oliver (Children's Hospital of
    Philadelphia) for helpful comments.
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 NR 118
 TC 12
 PU NATURE PUBLISHING GROUP
 PI LONDON
 PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
 SN 1350-9047
 J9 CELL DEATH DIFFERENTIATION
 JI Cell Death Differ.
 PD JAN
 PY 2010
 VL 17
 IS 1
 BP 68
 EP 77
 DI 10.1038/cdd.2009.84
 PG 10
 SC Biochemistry & Molecular Biology; Cell Biology
 GA 533JC
 UT ISI:000272818700009
 ER
 
 PT J
 AU Watanabe, T
    Kato, H
    Kobayashi, Y
    Yamasaki, S
    Morita-Hoshi, Y
    Yokoyama, H
    Morishima, Y
    Ricker, JL
    Otsuki, T
    Miyagi-Maesima, A
    Matsuno, Y
    Tobinai, K
 AF Watanabe, Takashi
    Kato, Harumi
    Kobayashi, Yukio
    Yamasaki, Satoshi
    Morita-Hoshi, Yuriko
    Yokoyama, Hiroki
    Morishima, Yasuo
    Ricker, Justin L.
    Otsuki, Tetsuya
    Miyagi-Maesima, Akiko
    Matsuno, Yoshihiro
    Tobinai, Kensei
 TI Potential efficacy of the oral histone deacetylase inhibitor vorinostat
    in a phase I trial in follicular and mantle cell lymphoma
 SO CANCER SCIENCE
 LA English
 DT Article
 ID SUBEROYLANILIDE HYDROXAMIC ACID; ADVANCED CANCER; SAHA; DEPSIPEPTIDE;
    APOPTOSIS; TUMORS
 AB Vorinostat (suberoylanilide hydroxamic acid, SAHA, Zolinza) is a
    histone deacetylase inhibitor with clinical activity in cutaneous
    T-cell lymphoma (CTCL). A phase I trial of oral vorinostat was
    conducted in Japanese patients with malignant lymphoma. Vorinostat 100
    or 200 mg was administered twice daily for 14 consecutive days followed
    by a 1-week rest interval. Of 10 patients enrolled, four had follicular
    lymphoma (FL), two mantle cell lymphoma (MCL), two diffuse large B-cell
    lymphoma, and two CTCL (median age, 60 years; median number of prior
    regimens, 3). Vorinostat was well tolerated up to 200 mg with only one
    of six patients developing a dose-limiting toxicity (DLT; Grade 3
    anorexia/hypokalemia). Common Grade 3 events were reversible
    neutropenia (30%), thrombocytopenia, and hypermagnesemia (20% each).
    The median number of treatment cycles was five (range, 1-36); two
    patients were continuing treatment. The overall response rate was 40%,
    with two complete responses/unconfirmed (CRu) and one partial response
    among FL patients and one CRu among MCL patients. One FL patient
    maintained CRu for 18.0 months. The median time to achieve CRu among
    the three patients was 8 months. These data suggest that further
    investigations of vorinostat in non-Hodgkin lymphoma, focusing on FL
    and MCL, are warranted. (Cancer Sci 2009).
 C1 [Watanabe, Takashi; Kobayashi, Yukio; Yamasaki, Satoshi; Morita-Hoshi, Yuriko; Yokoyama, Hiroki; Tobinai, Kensei] Natl Canc Ctr, Hematol & Stem Cell Transplantat Div, Tokyo, Japan.
    [Kato, Harumi; Morishima, Yasuo] Aichi Canc Ctr Hosp, Dept Hematol & Cell Therapy, Nagoya, Aichi 464, Japan.
    [Ricker, Justin L.] Merck Res Labs, N Wales, PA USA.
    [Otsuki, Tetsuya] Banyu Pharmaceut Co Ltd, Tokyo, Japan.
    [Miyagi-Maesima, Akiko; Matsuno, Yoshihiro] Natl Canc Ctr, Clin Lab, Tokyo, Japan.
 RP Watanabe, T, Natl Canc Ctr, Hematol & Stem Cell Transplantat Div, 1-1
    Tsukiji 5 Chome, Tokyo, Japan.
 EM takawata@ncc.go.jp
 FU Merck Research Laboratories, Rahway, NJ, USA ; Banyu Pharmaceutical,
    Tokyo, Japan 
 FX \We thank all of the investigators including Drs Takashi Terauchi
    (Diagnostic Division, Research Center for Cancer Prevention and
    Screening, National Cancer Center) and Teruhisa Azuma and Masakazu Mori
    (Hematology Division, National Cancer Center Hospital) for their
    response assessment by reviews of serial computed tomography performed
    every 3 months; and a clinical research coordinator, Ms Tamami Yamano,
    at National Cancer Center Hospital, for her data collection. We also
    thank Dr Shinichi Kanazu (Banyu Pharmaceutical) and Dr James S.
    Hardwick (Merck Research Laboratories) for their support in preparing
    this manuscript and thank Ms Mary Flynn (Merck Research Laboratories)
    for her assistance with the histone acetylation assays. This trial was
    supported by research funding from Merck Research Laboratories, Rahway,
    NJ, USA, and Banyu Pharmaceutical, Tokyo, Japan.
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 NR 19
 TC 10
 PU WILEY-BLACKWELL PUBLISHING, INC
 PI MALDEN
 PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
 SN 1347-9032
 J9 CANCER SCI
 JI Cancer Sci.
 PD JAN
 PY 2010
 VL 101
 IS 1
 BP 196
 EP 200
 DI 10.1111/j.1349-7006.2009.01360.x
 PG 5
 SC Oncology
 GA 530ZM
 UT ISI:000272631500028
 ER
 
 PT J
 AU Chi, HT
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    Iwasaki, R
    Thao, LB
    Hara, Y
    Taguchi, T
    Watanabe, T
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 AF Chi, Hoang Thanh
    Vu, Hoang Anh
    Iwasaki, Reo
    Thao, Le Ba
    Hara, Yukihiko
    Taguchi, Takahiro
    Watanabe, Toshiki
    Sato, Yuko
 TI Green tea (-)-epigalocatechin-3-gallate inhibits KIT activity and
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    including imatinib-resistant cells
 SO CANCER BIOLOGY & THERAPY
 LA English
 DT Article
 DE GIST-T1; GIST-T1 IR; EGCG; MAPK; AKT
 ID GROWTH-FACTOR RECEPTOR; TYROSINE KINASE INHIBITOR; COLON-CANCER CELLS;
    C-KIT; (-)-EPIGALLOCATECHIN GALLATE; SIGNALING PATHWAYS; MUTATIONS;
    MESYLATE; EPIGALLOCATECHIN-3-GALLATE; INACTIVATION
 AB Imatinib, a selective tyrosine kinase inhibitor, has been used as a
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    understood. The serious clinical problems of imatinib-resistance demand
    alternative treatment strategy. (-)-Epigallocatechin- 3-gallate (EGCG),
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    anti-tumor effects on various types of cancer cells. Here, we report
    for the first time that EGCG has shown anti-tumor effects on
    gastrointestinal stromal tumor cell line GIST-T1 by suppressing cell
    proliferation and eventually inducing cell death via caspase-dependent
    pathways. GIST-T1 and imatinib resistant GIST-T1 (GIST-T1 IR) cells
    were used to assess the effects of EGCG. In both cell types, KIT
    activity was completely inhibited after 4 h treatment with 60 mu M
    EGCG. EGCG specifically inhibited activated KIT, which was demonstrated
    by using Ba/F3 cells transfected with human wild-type KIT construct. At
    a dose of 30 mu M EGCG, the KIT activity remains but at more than 40 mu
    M EGCG, the KIT activity was abolished in these transfected-Ba/F3
    cells. Our results suggest that EGCG has a promising potential as a
    natural KIT inhibitor and therefore it could be used as a novel
    therapeutic or preventive reagent for GISTs including the
    imatinib-resistant cases.
 C1 [Chi, Hoang Thanh; Vu, Hoang Anh; Iwasaki, Reo; Thao, Le Ba; Sato, Yuko] Res Inst Int Med Ctr Japan, Div Ultrafine Struct, Dept Pathol, Tokyo, Japan.
    [Chi, Hoang Thanh; Iwasaki, Reo; Thao, Le Ba; Watanabe, Toshiki] Univ Tokyo, Dept Med Genome Sci, Grad Sch Frontier Sci, Tokyo, Japan.
    [Hara, Yukihiko] Hara Off Inc, Tea Solut, Sumida Ku, Tokyo, Japan.
    [Taguchi, Takahiro] Kochi Univ, Grad Sch Integrated Arts & Sci, Doctoral Course, Kochi, Japan.
 RP Sato, Y, Res Inst Int Med Ctr Japan, Div Ultrafine Struct, Dept Pathol,
    Tokyo, Japan.
 EM ysato@ri.imcj.go.jp
 FU Japan Foundation for Promotion of International Medical Research
    Co-operation (JF-PIMRC) 
 FX This work was supported by the Japan Foundation for Promotion of
    International Medical Research Co-operation (JF-PIMRC).
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 NR 34
 TC 1
 PU LANDES BIOSCIENCE
 PI AUSTIN
 PA 1002 WEST AVENUE, 2ND FLOOR, AUSTIN, TX 78701 USA
 SN 1538-4047
 J9 CANCER BIOL THER
 JI Cancer Biol. Ther.
 PD OCT 15
 PY 2009
 VL 8
 IS 20
 BP 1934
 EP 1939
 PG 6
 SC Oncology
 GA 533BB
 UT ISI:000272795800009
 ER
 
 PT J
 AU Yang, C
    Zhu, XY
    Yi, L
    Shi, ZY
    Wang, H
    Hu, YL
    Wang, YP
 AF Yang, Chi
    Zhu, Xiangyu
    Yi, Long
    Shi, Zhiyang
    Wang, Hua
    Hu, Yali
    Wang, Yaping
 TI Comparative Study of Three PCR-Based Copy Number Variant Approaches,
    CFMSA, M-PCR, and MLPA, in 22q11.2 Deletion Syndrome
 SO GENETIC TESTING AND MOLECULAR BIOMARKERS
 LA English
 DT Article
 ID SUBTELOMERIC REARRANGEMENTS; ABNORMALITIES; DISEASE
 AB Small submicroscopic DNA copy number variants represent an important
    source of variation in the human genome, human phenotypic diversity,
    and disease susceptibility. Consequently, there is a pressing need for
    the development of methods allowing the efficient, accurate, and cheap
    measurement of genomic copy number polymorphisms in clinical cohorts.
    The PCR-based strategies, being cost-effective and sensitive, are
    considered important in the development of screening techniques.
    PCR-based techniques such as multiplex PCR; multiplex
    ligation-dependent probe amplification; and a new single-tube assay
    technique, the competitive fluorescent multiplex STRP assay, have been
    applied to 22q11.2 detection, a typical example of deletion syndromes.
    In this study, we compared the reliability and application of these
    three techniques in a cohort of 17 patients affected with 22q11.2
    deletion and 300 normal controls. All three techniques shared 100%
    sensitivity; however, the competitive fluorescent multiplex STRP assay
    had the lowest possibility of concurrent false-positive signals from
    two adjoining probes in a genomic region. Moreover, it is a relatively
    fast and low-cost procedure to detect the deletion of 22q11.2 in
    numerous patients with several minor symptoms of deletion syndromes.
    Multiplex PCR, a rapidly developing and cheap technique, allows
    detection of atypical deletions.
 C1 [Zhu, Xiangyu; Hu, Yali] Nanjing Univ, Sch Med, Affiliated Drum Tower Hosp, Dept Obstet & Gynecol, Nanjing 210008, Peoples R China.
    [Yang, Chi; Wang, Yaping] Nanjing Univ, Dept Med Genet, Nanjing 210008, Peoples R China.
    [Yang, Chi; Yi, Long] Nanjing Univ, Dept Pathol, Nanjing 210008, Peoples R China.
    [Yang, Chi; Yi, Long; Hu, Yali; Wang, Yaping] Nanjing Univ, Sch Med, Jiangsu Key Lab Mol Med, Nanjing 210008, Peoples R China.
    [Shi, Zhiyang; Wang, Hua] Jiangsu Prov Ctr Dis Prevent & Control, Nanjing, Peoples R China.
 RP Hu, YL, Nanjing Univ, Sch Med, Affiliated Drum Tower Hosp, Dept Obstet
    & Gynecol, Nanjing 210008, Peoples R China.
 EM yali_hu@hotmail.com
    wangyap@nju.edu.cn
 FU Health Foundation of Jiangsu Province [H2006]; Jiangsu Foundation for
    Development [BS2006012]; Medical Science and Technology Development
    Foundation ; Nanjing Department of Health [ZKX06018]
 FX This work was supported by the Health Foundation of Jiangsu Province
    (grant number: H2006) and the Jiangsu Foundation for Development (grant
    number: BS2006012), the key project of the Medical Science and
    Technology Development Foundation, Nanjing Department of Health (grant
    number: ZKX06018), and the Foundation for the Jiangsu's Outstanding
    Fellow in Medical Science (grant number: LJ200628).
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    10.1002/ajmg.c.30114
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 NR 14
 TC 0
 PU MARY ANN LIEBERT INC
 PI NEW ROCHELLE
 PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
 SN 1945-0265
 J9 GENET TEST MOL BIOMARK
 JI Genet. Test. Mol. Biomark.
 PD DEC
 PY 2009
 VL 13
 IS 6
 BP 803
 EP 808
 DI 10.1089/gtmb.2009.0058
 PG 6
 SC Biochemistry & Molecular Biology; Genetics & Heredity
 GA 531AC
 UT ISI:000272633800017
 ER
 
 PT J
 AU Mills, DR
    Haskell, MD
    Callanan, HM
    Flanagan, DL
    Brilliant, KE
    Yang, DQ
    Hixson, DC
 AF Mills, David R.
    Haskell, Michelle D.
    Callanan, Helen M.
    Flanagan, Donna L.
    Brilliant, Kate E.
    Yang, DongQin
    Hixson, Douglas C.
 TI Monoclonal antibody to novel cell surface epitope on Hsc70 promotes
    morphogenesis of bile ducts in newborn rat liver
 SO CELL STRESS & CHAPERONES
 LA English
 DT Article
 DE Hsc70; Epitope mapping; Cell surface; Cholangiocyte; Bile duct
 ID SHOCK COGNATE PROTEIN; NATURAL-KILLER-CELLS; HUMAN TUMOR-CELLS;
    PROGENITOR CELLS; PLASMA-MEMBRANES; UNCOATING ATPASE; EPITHELIAL-CELLS;
    HSP70; EXPRESSION; DIFFERENTIATION
 AB We previously described a cell surface reactive monoclonal antibody,
    MAb OC.10, which recognizes an epitope shared by rat fetal liver ductal
    cells, hepatic progenitor cells, mature cholangiocytes, and
    hepatocellular carcinomas (HCC). Here, intrasplenic injection of MAb
    OC.10 into newborn rats was shown by immunofluorescence microscopy to
    strongly label intrahepatic bile ducts. Furthermore, the in situ
    labeling of intrahepatic cholangiocytes by injecting MAb OC.10
    increased the number of intraportal and intralobular bile ducts with
    well-defined lumens when compared to IgM-injected control animals. The
    antigen for MAb OC.10 was identified by mass spectrometry as Hsc70, a
    constitutively expressed heat shock protein belonging to the HSP70
    family. Immunoblot analysis demonstrated that MAb OC.10 reacted with
    recombinant bovine Hsc70 protein, with protein immunoprecipitated from
    rat bile duct epithelial (BDE) cell lysates with monoclonal anti-Hsc70
    antibody, and with Hsc70-FLAG protein over-expressed in human 293T
    cells. In addition, Hsc70-specific small interfering RNA reduced the
    amount of OC.10 antigen expressed in nucleofected BDE cells. Consistent
    with the specificity of MAb OC.10 for Hsc70, heat shock did not induce
    OC.10 expression in BDE cells, a characteristic of Hsp70.
    Immunofluorescence with BDE cells further suggested that MAb OC.10
    binds a novel cell surface epitope of Hsc70. This was in contrast to a
    commercially available monoclonal anti-Hsc70 antibody that showed
    strong cytosolic reactivity. These findings demonstrate that
    presentation of the OC.10 epitope differs between cytosolic and surface
    forms of Hsc70 and may suggest distinct differences in protein
    conformation or epitope availability determined in part by
    protein-protein or protein-lipid interactions. Phage display and
    pepscan analysis mapped the epitope for MAb OC.10 to the N-terminal
    340-384 amino acids of the ATPase domain of rat Hsc70. These findings
    suggest that MAb OC.10 recognizes an epitope on rat Hsc70 when
    presented on the cell surface that promotes morphogenic maturation of
    bile ducts in newborn rat liver. Furthermore, since we have shown
    previously that the OC.10 antigen is expressed on HCC subpopulations
    with oval cell characteristics, our current results indicate that Hsc70
    has the potential to be expressed on the surface of certain tumor cells.
 C1 [Mills, David R.] Rhode Isl Hosp, Providence, RI 02903 USA.
    [Mills, David R.; Haskell, Michelle D.; Callanan, Helen M.; Flanagan, Donna L.; Brilliant, Kate E.; Yang, DongQin; Hixson, Douglas C.] Brown Univ, Rhode Isl Hosp, Dept Med, Div Hematol & Oncol,Warren Alpert Med Sch, Providence, RI 02903 USA.
 RP Mills, DR, Rhode Isl Hosp, George Bldg Room 362,593 Eddy St,
    Providence, RI 02903 USA.
 EM David_Mills@Brown.edu
    Douglas_Hixson@Brown.edu
 FU National Institutes of Health [CA93840, CA42715, RRP20RR017695];
    National Center for Research Resources (NCRR) [P20RR016457]; National
    Institutes of Health (NIH) 
 FX We wish to thank Laura Bangs and Sandy DeAngelis for clerical
    assistance and Dr. James G. Clifton for technical assistance with the
    QSTAR XL mass spectrometry studies. This work was supported by grants
    CA93840, CA42715, and RRP20RR017695 (to D. C. H.) from the National
    Institutes of Health and RI-INBRE Grant P20RR016457 (to D. R. M.) from
    the National Center for Research Resources (NCRR), a component of the
    National Institutes of Health (NIH). Its contents are solely the
    responsibility of the authors and do not necessarily represent the
    official views of NCRR or NIH.
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 NR 58
 TC 1
 PU SPRINGER
 PI DORDRECHT
 PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
 SN 1355-8145
 J9 CELL STRESS CHAPERONES
 JI Cell Stress Chaperones
 PD JAN
 PY 2010
 VL 15
 IS 1
 BP 39
 EP 53
 DI 10.1007/s12192-009-0120-2
 PG 15
 SC Cell Biology
 GA 530CU
 UT ISI:000272567300004
 ER
 
 PT J
 AU Lin, CR
    Yang, LQ
    Tanasa, B
    Hutt, K
    Ju, BG
    Ohgi, K
    Zhang, J
    Rose, DW
    Fu, XD
    Glass, CK
    Rosenfeld, MG
 AF Lin, Chunru
    Yang, Liuqing
    Tanasa, Bogdan
    Hutt, Kasey
    Ju, Bong-gun
    Ohgi, Kenny
    Zhang, Jie
    Rose, David W.
    Fu, Xiang-Dong
    Glass, Christopher K.
    Rosenfeld, Michael G.
 TI Nuclear Receptor-Induced Chromosomal Proximity and DNA Breaks Underlie
    Specific Translocations in Cancer
 SO CELL
 LA English
 DT Article
 ID CLASS-SWITCH RECOMBINATION; DOUBLE-STRAND BREAKS; PROSTATE-CANCER;
    REGULATED TRANSCRIPTION; L1 RETROTRANSPOSITION; HOMOLOGOUS
    RECOMBINATION; GENOME INSTABILITY; ANDROGEN RECEPTOR; HISTONE H3; GENE
 AB Chromosomal translocations are a hallmark of leukemia/lymphoma and also
    appear in solid tumors, but the underlying mechanism remains elusive.
    By establishing a cellular model that mimics the relative frequency of
    authentic translocation events without proliferation selection, we
    report mechanisms of nuclear receptor-dependent tumor translocations.
    Intronic binding of liganded androgen receptor (AR) first juxtaposes
    translocation loci by triggering intra-and interchromosomal
    interactions. AR then promotes site-specific DNA double-stranded breaks
    (DSBs) at translocation loci by recruiting two types of enzymatic
    activities induced by genotoxic stress and liganded AR, including
    activation-induced cytidine deaminase and the LINE-1 repeat-encoded
    ORF2 endonuclease. These enzymes synergistically generate
    site-selective DSBs at juxtaposed translocation loci that are ligated
    by nonhomologous end joining pathway for specific translocations. Our
    data suggest that the confluence of two parallel pathways initiated by
    liganded nuclear receptor and genotoxic stress underlies nonrandom
    tumor translocations, which may function in many types of tumors and
    pathological processes.
 C1 [Lin, Chunru; Yang, Liuqing; Tanasa, Bogdan; Ju, Bong-gun; Ohgi, Kenny; Zhang, Jie; Rosenfeld, Michael G.] Univ Calif San Diego, Sch Med, Howard Hughes Med Inst, La Jolla, CA 92093 USA.
    [Hutt, Kasey] Univ Calif San Diego, Sch Med, Bioinformat Grad Program, La Jolla, CA 92093 USA.
    [Rose, David W.; Rosenfeld, Michael G.] Univ Calif San Diego, Sch Med, Dept Med, Div Endocrinol & Metab, La Jolla, CA 92093 USA.
    [Fu, Xiang-Dong; Glass, Christopher K.] Univ Calif San Diego, Sch Med, Dept Cellular & Mol Med, La Jolla, CA 92093 USA.
    [Ju, Bong-gun] Sogang Univ, Dept Life Sci, Seoul 121742, South Korea.
 RP Rosenfeld, MG, Univ Calif San Diego, Sch Med, Howard Hughes Med Inst,
    9500 Gilman Dr, La Jolla, CA 92093 USA.
 EM mrosenfeld@ucsd.edu
 FU National Institutes of Health (NIH) [DK39949, DK18477, CA97134,
    NS34934]; Department of Defense (DoD) [00325108]; Prostate Cancer
    Foundation 
 FX We thank C. Nelson for various cell culture assistance, J. Hightower
    for artwork, D. Benson for assistance with the manuscript, V. Lunyak
    and X. Zhu for critical comments, M. Schwartz and E. Nunez for
    assistance with fluorescence microscopy and FISH technology, Y. Zhang
    for providing the FLAG-DOT1L construct, M. B. Kastan for providing the
    HA-ER-I-PpoI construct, J. L. Goodier for providing LINE-1 ORF1, ORF2
    constructs, Ankara vaccinia virus that expresses T7 polymerase, and
    polyclonal antibody against ORF2, S. Heinz for providing PIWIL1 and
    PIWIL2 expression constructs, and AstraZeneca for providing Casodex. M.
    G. R. is a Howard Hughes Medical Institute Investigator. This study was
    funded by grants from The National Institutes of Health (NIH; DK39949,
    DK18477, CA97134, NS34934), the Department of Defense (DoD), and
    Prostate Cancer Foundation to M. G. R., and X. D. F., and NIH grants to
    X. D. F. and C. K. G. C. L. is a fellow of Susan G. Komen for the Cure
    (KG080247), and L. Yang is an awardee of Era of Hope Postdoctoral Award
    supported by the DoD (grant 00325108).
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 NR 55
 TC 51
 PU CELL PRESS
 PI CAMBRIDGE
 PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
 SN 0092-8674
 J9 CELL
 JI Cell
 PD DEC 11
 PY 2009
 VL 139
 IS 6
 BP 1069
 EP 1083
 DI 10.1016/j.cell.2009.11.030
 PG 15
 SC Biochemistry & Molecular Biology; Cell Biology
 GA 530WK
 UT ISI:000272622800010
 ER
 
 PT J
 AU Yang, IV
    Wade, CM
    Kang, HM
    Alper, S
    Rutledge, H
    Lackford, B
    Eskin, E
    Daly, MJ
    Schwartz, DA
 AF Yang, Ivana V.
    Wade, Claire M.
    Kang, Hyun Min
    Alper, Scott
    Rutledge, Holly
    Lackford, Brad
    Eskin, Eleazar
    Daly, Mark J.
    Schwartz, David A.
 TI Identification of Novel Genes That Mediate Innate Immunity Using Inbred
    Mice
 SO GENETICS
 LA English
 DT Article
 ID WHOLE-GENOME ASSOCIATION; TOLL-LIKE RECEPTORS; SALMONELLA-ENTERITIDIS;
    INFLAMMATORY RESPONSE; POPULATION-STRUCTURE; CONGENIC STRAINS;
    HUMAN-DISEASE; LOCI; LIPOPOLYSACCHARIDE; PERSISTENCE
 AB Innate immunity is the first line of defense against microbial
    infections. Although polymorphisms in toll-like receptors (TLRs) and
    downstream signaling molecules (CD14, TLR2, TLR4, TLR5, and IRAK4)
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    portion of the ability of the host to respond to bacteria, fungi, and
    viruses. To identify other genes involved in the innate immune
    response, we challenged 16 inbred murine strains with
    lipopolysaccharide (LPS) systemically and measured serum concentrations
    of pro-inflammatory cytokines IL-1 beta, IL-6, and TNF alpha, and the
    chemokine KC 6 hr post-treatment. Loci that segregate with strain
    phenotypes were identified by whole genome association (WGA) mapping of
    cytokine concentrations. Published gene expression profiles and
    quantitative trait loci (QTL) were then utilized to prioritize loci and
    genes that potentially regulate the host response to LPS. Sixteen loci
    were selected for further investigation by combining WGA analysis with
    previously published QTL for murine response to LPS or gram negative
    bacteria. Thirty-eight genes within these loci were then selected for
    further investigation on the basis of the significance of the
    identified locus, transcriptional response to LPS, and biological
    plausibility. RNA interference-mediated inhibition of 4 of 38 candidate
    genes was shown to block the production of IL-6 in J774A.1 macrophages.
    In summary, our analysis identified 4 genes that have not previously
    been implicated in innate immunity, namely, 1110058L19Rik,
    4933415F23Rik, Fbxo9, and Ipo7. These genes could represent potential
    sepsis biomarkers or therapeutic targets that should be further
    investigated in human populations.
 C1 [Yang, Ivana V.; Schwartz, David A.] Natl Jewish Hlth, Dept Med, Denver, CO 80206 USA.
    [Yang, Ivana V.; Alper, Scott; Schwartz, David A.] Natl Jewish Hlth, Ctr Genes Environm & Hlth, Denver, CO 80206 USA.
    [Alper, Scott] Natl Jewish Hlth, Dept Immunol, Denver, CO 80206 USA.
    [Wade, Claire M.; Daly, Mark J.] Massachusetts Gen Hosp, Ctr Human Genet Res, Boston, MA 02114 USA.
    [Wade, Claire M.; Daly, Mark J.] MIT, Cambridge, MA 02142 USA.
    [Wade, Claire M.; Daly, Mark J.] Harvard Univ, Broad Inst, Cambridge, MA 02142 USA.
    [Kang, Hyun Min] Univ Calif San Diego, Dept Comp Sci & Engn, La Jolla, CA 92093 USA.
    [Rutledge, Holly; Lackford, Brad] Natl Inst Environm Hlth Sci, Res Triangle Pk, NC 27709 USA.
    [Eskin, Eleazar] Univ Calif Los Angeles, Dept Comp Sci, Los Angeles, CA 90095 USA.
    [Eskin, Eleazar] Univ Calif Los Angeles, Dept Human Genet, Los Angeles, CA 90095 USA.
 RP Yang, IV, Natl Jewish Hlth, Dept Med, 1400 Jackson St,A630, Denver, CO
    80206 USA.
 EM yangi@njhealth.org
 FU Department of Veterans Affairs ; National Institute of Environmental
    Health Sciences [ES11375, ES011961]; National Institutes of Health,
    National Institute of the Environmental Health Sciences, and National
    Heart, Lung, and Blood Institute 
 FX This study was funded by the Department of Veterans Affairs (merit
    review), the National Institute of Environmental Health Sciences
    (ES11375 and ES011961), and the Intramural Research Program of the
    National Institutes of Health, National Institute of the Environmental
    Health Sciences, and National Heart, Lung, and Blood Institute.
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 NR 29
 TC 1
 PU GENETICS SOC AM
 PI BETHESDA
 PA 9650 ROCKVILLE AVE, BETHESDA, MD 20814 USA
 SN 0016-6731
 J9 GENETICS
 JI Genetics
 PD DEC
 PY 2009
 VL 183
 IS 4
 BP 1535
 EP 1544
 DI 10.1534/genetics.109.107540
 PG 10
 SC Genetics & Heredity
 GA 528HV
 UT ISI:000272435000026
 ER
 
 PT J
 AU Oyama, T
    Yasui, Y
    Sugie, S
    Koketsu, M
    Watanabe, K
    Tanaka, T
 AF Oyama, Takeru
    Yasui, Yumiko
    Sugie, Shigeyuki
    Koketsu, Mamoru
    Watanabe, Kunitomo
    Tanaka, Takuji
 TI Dietary Tricin Suppresses Inflammation-Related Colon Carcinogenesis in
    Male Crj: CD-1 Mice
 SO CANCER PREVENTION RESEARCH
 LA English
 DT Article
 ID DEXTRAN SODIUM-SULFATE; BRAN CONSTITUENT TRICIN; CANCER
    CHEMOPREVENTION; RICE BRAN; COLORECTAL-CANCER; FLAVONE TRICIN;
    AZOXYMETHANE; PLASMA; PREVENTION; EXTRACTS
 AB The flavone 4',5,7-trihydroxy-3',5'-dimethoxyflavone (tricin) present
    in rice, oats, barley, and wheat exhibits antigrowth activity in
    several human cancer cell lines and anti-inflammatory potential.
    However, the chemopreventive activity has not yet been elucidated in
    preclinical animal models of colorectal cancer. This study was designed
    to determine whether dietary tricin exerts inflammation-associated
    colon carcinogenesis induced by azoxymethane and dextran sulfate sodium
    in mice. Male Crj: CD-1 mice were initiated with a single i.p.
    injection of azoxymethane (10 mg/kg body weight) and followed by a
    1-week exposure to dextran sulfate sodium (1.5%, w/v) in drinking water
    to induce colonic neoplasms. They were then given the experimental diet
    containing 50 or 250 ppm tricin. The experiment was terminated at week
    18 to determine the chemopreventive efficacy of tricin. In addition,
    the effects of dietary tricin on the expression of several inflammatory
    cytokines, including tumor necrosis factor (TNF)-alpha, were assayed.
    The development of colonic adenomas and adenocarcinomas was
    significantly reduced by feeding with 50 and 250 ppm tricin,
    respectively. Dietary tricin also significantly reduced the
    proliferation of adenocarcinoma cells as well as the numbers of
    mitoses/anaphase bridging in adenocarcinoma cells. The dietary
    administration with tricin significantly inhibited the expression of
    TNF-alpha in the nonlesional cypts. Our findings that dietary tricin
    inhibits inflammation-related mouse colon carcinogenesis by suppressing
    the expression of TNF-alpha in the nonlesional cyrpts and the
    proliferation of adenocarcinomas suggest a potential use of tricin for
    clinical trials of colorectal cancer chemoprevention.
 C1 [Oyama, Takeru; Yasui, Yumiko; Sugie, Shigeyuki; Tanaka, Takuji] Kanazawa Med Univ, Dept Oncol Pathol, Uchinada, Ishikawa 9200293, Japan.
    [Koketsu, Mamoru] Gifu Univ, Life Sci Res Ctr, Div Instrumental Anal, Gifu, Japan.
    [Watanabe, Kunitomo] Gifu Univ, Life Sci Res Ctr, Div Anaerobe Res, Gifu, Japan.
    [Tanaka, Takuji] Tohkai Cytopathol Inst Canc Res & Prevent, Gifu, Japan.
 RP Tanaka, T, Kanazawa Med Univ, Dept Oncol Pathol, 1-1 Daigaku, Uchinada,
    Ishikawa 9200293, Japan.
 EM takutt@kanazawa-med.ac.jp
 FU Ministry of Health, Labour and Welfare of Japan [18592076, 17015016,
    18880030]; Ministry of Education, Culture, Sports, Science and
    Technology of Japan [H2008-12]
 FX Grant-in-Aid for Cancer Research, for the Third-Term Comprehensive
    10-Year Strategy for Cancer Control from the Ministry of Health, Labour
    and Welfare of Japan; Grants-in-Aid grant nos. 18592076 (T. Tanaka),
    17015016 (T. Tanaka), and 18880030 (Y. Yasui) for Scientific Research
    from the Ministry of Education, Culture, Sports, Science and Technology
    of Japan; and grant H2008-12 (T. Tanaka) for the Project Research from
    the High-Technology Center of Kanazawa Medical University.
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 NR 43
 TC 1
 PU AMER ASSOC CANCER RESEARCH
 PI PHILADELPHIA
 PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
 SN 1940-6207
 J9 CANCER PREV RES
 JI Cancer Prev. Res.
 PD DEC
 PY 2009
 VL 2
 IS 12
 BP 1031
 EP 1038
 DI 10.1158/1940-6207.CAPR-09-0061
 PG 8
 SC Oncology
 GA 528TM
 UT ISI:000272469900006
 ER
 
 PT J
 AU Kambe, A
    Yoshioka, H
    Kamitani, H
    Watanabe, T
    Baek, SJ
    Eling, TE
 AF Kambe, Atsushi
    Yoshioka, Hiroki
    Kamitani, Hideki
    Watanabe, Takashi
    Baek, Seung Joon
    Eling, Thomas E.
 TI The Cyclooxygenase Inhibitor Sulindac Sulfide Inhibits EP4 Expression
    and Suppresses the Growth of Glioblastoma Cells
 SO CANCER PREVENTION RESEARCH
 LA English
 DT Article
 ID ACTIVATING TRANSCRIPTION FACTOR-3; BETA SUPERFAMILY MEMBER;
    GENE-EXPRESSION; PROGNOSTIC-SIGNIFICANCE; SP1 PHOSPHORYLATION;
    COLORECTAL-CANCER; INDUCED APOPTOSIS; PROTEIN-KINASE; BREAST-CANCER;
    RECEPTOR
 AB EP4 expression in human glioblastoma cells correlates with growth on
    soft agar. The cyclooxygenase inhibitor sulindac sulfide first altered
    specificity protein-1 (Sp-1) and early growth response gene-1
    expression, then increased the expression of nonsteroidal
    anti-inflammatory drug-activated gene 1 and activating transcription
    factor 3, and then decreased EP4 expression. EP4 suppression was
    dependent on blocking the Sp-1 binding sites in the human EP4 promoter.
    Mutation in the Sp-1 sites in EP4 altered the promoter activity and
    abolished sulindac sulfide effects. The inhibitory effect of sulindac
    sulfide on EP4 expression was reversed by PD98059, a mitogen-activated
    protein/extracellular signal-regulated kinase kinase-1/extracellular
    signal-regulated kinase inhibitor. Sp-1 phosphorylation was dependent
    on sulindac sulfide-induced Erk activation. Chromatin
    immunoprecipitation assay confirmed that Sp-1 phosphorylation decreases
    Sp-1 binding to DNA and leads to the suppression of EP4. Inhibition of
    cell growth on soft agar assay was found to be a highly complex process
    and seems to require not only the inhibition of cyclooxygenase activity
    but also increased expression of nonsteroidal anti-inflammatory
    drug-activated gene 1 and activating transcription factor 3 and
    suppression of EP4 expression. Our data suggest that the suppression of
    EP4 expression by sulindac sulfide represents a new mechanism for
    understanding the tumor suppressor activity.
 C1 [Kambe, Atsushi; Yoshioka, Hiroki; Eling, Thomas E.] Natl Inst Environm Hlth Sci, Mol Carcinogenesis Lab, NIH, Res Triangle Pk, NC 27709 USA.
    [Kambe, Atsushi; Yoshioka, Hiroki; Kamitani, Hideki; Watanabe, Takashi] Tottori Univ, Fac Med, Inst Neurol Sci, Div Neurosurg, Tottori 680, Japan.
    [Baek, Seung Joon] Univ Tennessee, Coll Vet Med, Dept Pathobiol, Knoxville, TN 37901 USA.
 RP Eling, TE, Natl Inst Environm Hlth Sci, Mol Carcinogenesis Lab, NIH,
    111 TW Alexander Dr, Res Triangle Pk, NC 27709 USA.
 EM Eling@niehs.nih.gov
 FU NIH, National Institute of Environmental Health Sciences Intramural
    Research Program 
 FX NIH, National Institute of Environmental Health Sciences Intramural
    Research Program.
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 NR 37
 TC 0
 PU AMER ASSOC CANCER RESEARCH
 PI PHILADELPHIA
 PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
 SN 1940-6207
 J9 CANCER PREV RES
 JI Cancer Prev. Res.
 PD DEC
 PY 2009
 VL 2
 IS 12
 BP 1088
 EP 1099
 DI 10.1158/1940-6207.CAPR-09-0140
 PG 12
 SC Oncology
 GA 528TM
 UT ISI:000272469900012
 ER
 
 PT J
 AU Guo, QY
    Wang, YN
    Yang, X
    Mao, HP
    Yu, XQ
 AF Guo Qunying
    Wang Yaning
    Yang Xiao
    Mao Haiping
    Yu Xueqing
 TI Effects of High Glucose on the Expression of VEGF and Its Receptors in
    Rat Peritoneal Mesothelial Cells
 SO BLOOD PURIFICATION
 LA English
 DT Meeting Abstract
 C1 [Guo Qunying; Wang Yaning; Yang Xiao; Mao Haiping; Yu Xueqing] Sun Yat Sen Univ, Guangzhou 510275, Guangdong, Peoples R China.
 NR 0
 TC 0
 PU KARGER
 PI BASEL
 PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND
 SN 0253-5068
 J9 BLOOD PURIFICAT
 JI Blood Purif.
 PY 2009
 VL 28
 IS 4
 BP 302
 EP 302
 PG 1
 SC Hematology; Urology & Nephrology
 GA 527AP
 UT ISI:000272338500021
 ER
 
 PT J
 AU Wang, XF
    Jin, X
    Wang, XY
    Liu, J
    Feng, JJ
    Yang, QQ
    Mu, WL
    Shi, XJ
    Lu, ZJ
 AF Wang, Xiu-Fang
    Jin, Xia
    Wang, Xiaoyan
    Liu, Jing
    Feng, Jingjing
    Yang, QinQing
    Mu, Wenli
    Shi, Xiaojuan
    Lu, Zhanjun
 TI Effects of L1-ORF2 fragments on green fluorescent protein gene
    expression
 SO GENETICS AND MOLECULAR BIOLOGY
 LA English
 DT Article
 DE gene expression; green fluorescent protein gene; L1-ORF2; transcription
    termination; orientation
 ID X-CHROMOSOME INACTIVATION; LINE-1 RETROTRANSPOSON; HUMAN GENOME; L1
    RETROTRANSPOSON; CHAPERONE ACTIVITY; MOBILE ELEMENTS; ORF1 PROTEIN;
    EVOLUTION; MOUSE; CELLS
 AB The retrotransposon known as long interspersed nuclear element-1 (L1)
    is 6 kb long, although most L1s in mammalian and other eukaryotic cells
    are truncated. L1 contains two open reading frames, ORF1 and ORF2, that
    code for an RNA-binding protein and a protein with endonuclease and
    reverse transcriptase activities, respectively. In this work, we
    examined the effects of full length L1-ORF2 and ORF2 fragments on green
    fluorescent protein gene (GFP) expression when inserted into the
    pEGFP-C1 vector downstream of GFP. All of the ORF2 fragments in sense
    orientation inhibited GFP expression more than when in antisense
    orientation, which suggests that small ORF2 fragments contribute to the
    distinct inhibitory effects of this ORF on gene expression. These
    results provide the first evidence that different 280-bp fragments have
    distinct effects on the termination of gene transcription, and that
    when inserted in the antisense direction, fragment 280-9 (the 3' end
    fragment of ORF2) induces premature termination of transcription that
    is consistent with the effect of ORF2.
 C1 [Wang, Xiu-Fang; Jin, Xia; Wang, Xiaoyan; Liu, Jing; Feng, Jingjing; Yang, QinQing; Mu, Wenli; Shi, Xiaojuan; Lu, Zhanjun] Hebei Med Univ, Dept Genet, Hebei Key Lab Lab Anim, Shijiazhuang 050017, Hebei Province, Peoples R China.
 RP Lu, ZJ, Hebei Med Univ, Dept Genet, Hebei Key Lab Lab Anim, 361
    Zhongshan E Rd, Shijiazhuang 050017, Hebei Province, Peoples R China.
 EM lslab@hebmu.edu.cn
 FU Hebei Province Natural Science Foundation of China [C2008001065]
 FX This study was supported by grant C2008001065 from the Hebei Province
    Natural Science Foundation of China.
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 NR 35
 TC 0
 PU SOC BRASIL GENETICA
 PI RIBEIRAO PRET
 PA RUA CAP ADELMIO NORBET DA SILVA, 736, ALTO DA BOA VISTA, 14025-670
    RIBEIRAO PRET, BRAZIL
 SN 1415-4757
 J9 GENET MOL BIOL
 JI Genet. Mol. Biol.
 PY 2009
 VL 32
 IS 4
 BP 688
 EP 696
 PG 9
 SC Biochemistry & Molecular Biology; Genetics & Heredity
 GA 524ZK
 UT ISI:000272182700003
 ER
 
 PT J
 AU Dai, RY
    Chen, Y
    Fu, J
    Dong, LW
    Ren, YB
    Yang, GZ
    Qian, YW
    Cao, J
    Tang, SH
    Yang, SL
    Wang, HY
 AF Dai, Rong-Yang
    Chen, Yao
    Fu, Jing
    Dong, Li-Wei
    Ren, Yi-Bin
    Yang, Guang-Zhen
    Qian, You-Wen
    Cao, Jie
    Tang, Shan-Hua
    Yang, Sheng-Li
    Wang, Hong-Yang
 TI p28(GANK) inhibits endoplasmic reticulum stress-induced cell death via
    enhancement of the endoplasmic reticulum adaptive capacity
 SO CELL RESEARCH
 LA English
 DT Article
 DE p28(GANK); ER stress; UPR; GRP78; apoptosis
 ID UNFOLDED PROTEIN RESPONSE; NF-KAPPA-B; HUMAN HEPATOCELLULAR-CARCINOMA;
    INDUCED PHOSPHORYLATION; ONCOPROTEIN P28(GANK); REGULATOR GRP78/BIP;
    SIGNALING PATHWAY; TUMOR-DEVELOPMENT; ER CHAPERONE; KINASE
 AB It has been shown that oncoprotein p28(GANK), which is consistently
    overexpressed in human hepatocellular carcinoma (HCC), plays a critical
    role in tumorigenesis of HCC. However, the underlying mechanism remains
    unclear. Here, we demonstrated that p28(GANK) inhibits apoptosis in HCC
    cells induced by the endoplasmic reticulum (ER) stress. During ER
    stress, p28(GANK) enhances the unfolded protein response, promotes ER
    recovery from translational repression, and thereby facilitates cell's
    ability to cope with the stress conditions. Furthermore, p28(GANK)
    upregulates glucose-regulated protein 78 (GRP78), a key ER chaperone
    protein, which subsequently enhances the ER folding capacity and
    promotes recovery from ER stress. We also demonstrated that p28(GANK)
    increases p38 mitogen-activated protein kinase and Akt phosphorylation,
    and inhibits nuclear factor kappa B (NF-kappa B) activation under ER
    stress, which in turn contributes to GRP78 upregulation. Taken
    together, our results indicate that p28(GANK) inhibits ER
    stress-induced apoptosis in HCC cells, at least in part, by enhancing
    the adaptive response and GRP78 expression. We propose that p28(GANK)
    has potential implications for HCC progression under the ER stress
    conditions.
 C1 [Dai, Rong-Yang; Yang, Sheng-Li; Wang, Hong-Yang] Shanghai Jiao Tong Univ, Shanghai Canc Inst, State Key Lab Oncogenes & Related Genes, Shanghai 200032, Peoples R China.
    [Dai, Rong-Yang; Yang, Sheng-Li; Wang, Hong-Yang] Shanghai Jiao Tong Univ, Inst Canc, Shanghai 200032, Peoples R China.
    [Dai, Rong-Yang; Chen, Yao; Fu, Jing; Dong, Li-Wei; Ren, Yi-Bin; Yang, Guang-Zhen; Qian, You-Wen; Cao, Jie; Tang, Shan-Hua; Wang, Hong-Yang] Eastern Hepatobiliary Surg Inst, Int Cooperat Lab Signal Transduct, Shanghai 200438, Peoples R China.
 RP Wang, HY, Shanghai Jiao Tong Univ, Shanghai Canc Inst, State Key Lab
    Oncogenes & Related Genes, Shanghai 200032, Peoples R China.
 EM hywangk@vip.sina.com
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 NR 47
 TC 4
 PU INST BIOCHEMISTRY & CELL BIOLOGY
 PI SHANGHAI
 PA SIBS, CAS, 319 YUEYAND ROAD, SHANGHAI, 200031, PEOPLES R CHINA
 SN 1001-0602
 J9 CELL RES
 JI Cell Res.
 PD NOV
 PY 2009
 VL 19
 IS 11
 BP 1243
 EP 1257
 DI 10.1038/cr.2009.104
 PG 15
 SC Cell Biology
 GA 524LU
 UT ISI:000272145600005
 ER
 
 PT J
 AU Wu, YR
    Deng, ZY
    Lai, JB
    Zhang, YY
    Yang, CP
    Yin, BJ
    Zhao, QZ
    Zhang, L
    Li, Y
    Yang, CW
    Xie, Q
 AF Wu, Yaorong
    Deng, Zhiyong
    Lai, Jianbin
    Zhang, Yiyue
    Yang, Cuiping
    Yin, Bojiao
    Zhao, Qingzhen
    Zhang, Ling
    Li, Yin
    Yang, Chengwei
    Xie, Qi
 TI Dual function of Arabidopsis ATAF1 in abiotic and biotic stress
    responses
 SO CELL RESEARCH
 LA English
 DT Article
 DE abiotic stress; Arabidopsis; ATAF1; biotic stress
 ID NAC TRANSCRIPTION FACTORS; LATERAL ROOT DEVELOPMENT; ABSCISIC-ACID;
    DEFENSE RESPONSES; REACTIVE OXYGEN; OXIDATIVE STRESS; CELL-DEATH; E3
    LIGASE; GENE; PROTEIN
 AB NAC family genes encode plant-specific transcription factors involved
    in diverse biological processes. In this study, the Arabidopsis NAC
    gene ATAF1 was found to be induced by drought, high-salinity, abscisic
    acid (ABA), methyl jasmonate, mechanical wounding, and Botrytis cinerea
    infection. Significant induction of ATAF1 was found in an ABA-deficient
    mutant aba2 subjected to drought or high salinity, revealing an
    ABA-independent mechanism of expression. Arabidopsis
    ATAF1-overexpression lines displayed many altered phenotypes, including
    dwarfism and short primary roots. Furthermore, in vivo experiments
    indicate that ATAF1 is a bona fide regulator modulating plant responses
    to many abiotic stresses and necrotrophic-pathogen infection.
    Overexpression of ATAF1 in Arabidopsis increased plant sensitivity to
    ABA, salt, and oxidative stresses. Especially, ATAF1 overexpression
    plants, but not mutant lines, showed remarkably enhanced plant
    tolerance to drought. Additionally, ATAF1 overexpression enhanced plant
    susceptibility to the necrotrophic pathogen B. cinerea, but did not
    alter disease symptoms caused by avirulent or virulent strains of P.
    syringae pv tomato DC3000. Transgenic plants overexpressing ATAF1 were
    hypersensitive to oxidative stress, suggesting that reactive oxygen
    intermediates may be related to ATAF1-mediated signaling in response to
    both pathogen and abiotic stresses.
 C1 [Wu, Yaorong; Lai, Jianbin; Zhang, Yiyue; Yin, Bojiao; Zhao, Qingzhen; Xie, Qi] Chinese Acad Sci, Inst Genet & Dev Biol, Natl Ctr Plant Gene Res, State Key Lab Plant Genom, Beijing 100101, Peoples R China.
    [Deng, Zhiyong; Lai, Jianbin; Zhang, Yiyue; Yang, Cuiping; Yin, Bojiao; Zhang, Ling; Li, Yin; Yang, Chengwei; Xie, Qi] Sun Yat Sen Zhongshan Univ, Sch Life Sci, State Key Lab Biocontrol, Guangzhou 510275, Guangdong, Peoples R China.
 RP Xie, Q, Chinese Acad Sci, Inst Genet & Dev Biol, Natl Ctr Plant Gene
    Res, State Key Lab Plant Genom, Datun Rd, Beijing 100101, Peoples R
    China.
 EM qxie@genetics.ac.cn
 FU National Natural Science Foundation of China
    [30530400/90717006/30670195]; Chinese Academy of Science
    [KSCX2-YW-N-010, CXTD-S2005-2]; Guangdong Natural Science Foundation,
    China [5300648]
 FX We would like to thank Dr Nam-Hai Chua (Rockefeller University) for
    kindly providing the pBA002Myc vector and the Arabidopsis Biological
    Resource Center (ABRC), Ohio State University for providing T-DNA
    insertion lines. This work was supported by grants from National
    Natural Science Foundation of China (No. 30530400/90717006/30670195) to
    Q Xie and Y Wu, the Chinese Academy of Science (KSCX2-YW-N-010 and
    CXTD-S2005-2), and the Guangdong Natural Science Foundation, China (No.
    5300648) to Z Deng.
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 NR 45
 TC 6
 PU INST BIOCHEMISTRY & CELL BIOLOGY
 PI SHANGHAI
 PA SIBS, CAS, 319 YUEYAND ROAD, SHANGHAI, 200031, PEOPLES R CHINA
 SN 1001-0602
 J9 CELL RES
 JI Cell Res.
 PD NOV
 PY 2009
 VL 19
 IS 11
 BP 1279
 EP 1290
 DI 10.1038/cr.2009.108
 PG 12
 SC Cell Biology
 GA 524LU
 UT ISI:000272145600008
 ER
 
 PT J
 AU Cai, YQ
    Yang, YH
    Shen, MH
    Zhou, TH
 AF Cai, Yuqi
    Yang, Yuehong
    Shen, Minhong
    Zhou, Tianhua
 TI Inhibition of cytokinesis by overexpression of NudCL that is localized
    to the centrosome and midbody
 SO CELL RESEARCH
 LA English
 DT Letter
 ID PROTEIN; MICROTUBULES
 C1 [Cai, Yuqi; Yang, Yuehong; Shen, Minhong; Zhou, Tianhua] Zhejiang Univ, Sch Med, Dept Cell Biol, Hangzhou 310058, Zhejiang, Peoples R China.
    [Cai, Yuqi; Yang, Yuehong; Shen, Minhong; Zhou, Tianhua] Zhejiang Univ, Sch Med, Ctr Dis Modeling, Hangzhou 310058, Zhejiang, Peoples R China.
 RP Zhou, TH, Zhejiang Univ, Sch Med, Dept Cell Biol, Hangzhou 310058,
    Zhejiang, Peoples R China.
 EM tzhou@zju.edu.cn
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 NR 11
 TC 1
 PU INST BIOCHEMISTRY & CELL BIOLOGY
 PI SHANGHAI
 PA SIBS, CAS, 319 YUEYAND ROAD, SHANGHAI, 200031, PEOPLES R CHINA
 SN 1001-0602
 J9 CELL RES
 JI Cell Res.
 PD NOV
 PY 2009
 VL 19
 IS 11
 BP 1305
 EP 1308
 DI 10.1038/cr.2009.118
 PG 4
 SC Cell Biology
 GA 524LU
 UT ISI:000272145600010
 ER
 
 PT J
 AU Jasmin, JF
    Yang, M
    Iacovitti, L
    Lisanti, MP
 AF Jasmin, Jean-Francois
    Yang, Ming
    Iacovitti, Lorraine
    Lisanti, Michael P.
 TI Genetic ablation of caveolin-1 increases neural stem cell proliferation
    in the subventricular zone (SVZ) of the adult mouse brain
 SO CELL CYCLE
 LA English
 DT Article
 DE neural stem cells; caveolin gene family; subventricular zone;
    proliferation
 ID DENTATE GYRUS; HUNTINGTONS-DISEASE; RAT HIPPOCAMPUS; GENERATED NEURONS;
    PROTEIN-COMPONENT; MEMBRANE DOMAINS; CHAIN MIGRATION; PLASMA-MEMBRANE;
    SHOW EVIDENCE; IN-VIVO
 AB Adult neural stem cells are self-renewing multipotent cells that have
    the potential to replace dysfunctional and/or dying neuronal cells at
    the site of brain injury or degeneration. Caveolins are well-known
    tumor-suppressor genes that were recently found to be involved in the
    regulation of stem cell proliferation. For instance, ablation of the
    caveolin-1 (Cav-1) gene in mice markedly increases the proliferation of
    intestinal and mammary stem cells. However, the roles of caveolins in
    the proliferation of adult neural stem cells still remain unknown. In
    this study, dual-label immunofluorescence analysis of the proliferation
    marker, Ki67, and the stem cell markers, nestin and Sox2, was performed
    on brains of 8 week-old wild-type (WT) and Cav-1 knockout (KO) mice.
    Our results demonstrate an increased number of Ki67-positive nuclei in
    the subventricular zone (SVZ) of Cav-1 KO brains. Importantly, our
    dual-label immunofluorescence analyses demonstrate increased
    co-localization of Ki67 with both nestin and Sox2 in the SVZ of Cav-1
    KO brains. Remarkably similar results were also obtained with Cav-2 and
    Cav-3 KO mouse brains as well, with increased proliferation of adult
    neural stem cells. Thus, the SVZ of caveolin KO mouse brains displays
    an increased proliferation of adult neural stem cells. Caveolin
    proteins might represent new crucial regulators of adult neural stem
    cell proliferation.
 C1 [Jasmin, Jean-Francois; Lisanti, Michael P.] Thomas Jefferson Univ, Dept Stem Cell Biol & Regenerat Med, Philadelphia, PA 19107 USA.
    [Jasmin, Jean-Francois; Lisanti, Michael P.] Thomas Jefferson Univ, Dept Canc Biol, Philadelphia, PA 19107 USA.
    [Lisanti, Michael P.] Thomas Jefferson Univ, Dept Med Oncol, Kimmel Canc Ctr, Philadelphia, PA 19107 USA.
    [Jasmin, Jean-Francois; Iacovitti, Lorraine; Lisanti, Michael P.] Thomas Jefferson Univ, Jefferson Stem Cell Biol & Regenerat Med Ctr, Philadelphia, PA 19107 USA.
    [Yang, Ming; Iacovitti, Lorraine] Thomas Jefferson Univ, Dept Neurol, Philadelphia, PA 19107 USA.
    [Iacovitti, Lorraine] Thomas Jefferson Univ, Farber Inst Neurosci, Philadelphia, PA 19107 USA.
 RP Jasmin, JF, Thomas Jefferson Univ, Dept Stem Cell Biol & Regenerat Med,
    Philadelphia, PA 19107 USA.
 EM jeanfrancois.jasmin@jefferson.edu
    mlisanti@mail.jci.tju.edu
 FU NIH [R01-CA098779, R01-CA120876]
 FX This work was supported by NIH grants (R01-CA098779 and R01-CA120876)
    to M.P.L. and a Hassel Foundation Award to L.I.
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 PI AUSTIN
 PA 1002 WEST AVENUE, 2ND FLOOR, AUSTIN, TX 78701 USA
 SN 1538-4101
 J9 CELL CYCLE
 JI Cell Cycle
 PD DEC 1
 PY 2009
 VL 8
 IS 23
 BP 3978
 EP 3983
 PG 6
 SC Cell Biology
 GA 525MD
 UT ISI:000272219200037
 ER
 
 PT J
 AU Visser, S
    Yang, XL
 AF Visser, Stacy
    Yang, Xiaolong
 TI Identification of LATS transcriptional targets in HeLa cells using
    whole human genome oligonucleotide microarray
 SO GENE
 LA English
 DT Article
 DE LATS1; LATS2; Microarray; Tumor suppressor; Cell proliferation;
    Apoptosis; Cell migration
 ID ACUTE LYMPHOBLASTIC-LEUKEMIA; DROSOPHILA TUMOR-SUPPRESSOR;
    DOWN-REGULATION; HIPPO PATHWAY; PROMOTER HYPERMETHYLATION; HUMAN
    HOMOLOG; CONTACT INHIBITION; NEGATIVE REGULATOR; PROTEIN-KINASE;
    GROWTH-CONTROL
 AB Human LATS1 and LATS2) (LATS1/2) are tumor suppressors that have been
    shown to be mutated or downregulated in several human cancers including
    leukemia, lung, prostate and breast cancers. However, the precise
    mechanisms and the proteins modulated by LATS1/2 that are responsible
    for these events remain largely unknown. To elucidate potential
    signaling pathways, the current study investigated the expression
    profile in HeLa cells with reduced expression of LATS1/2. Using
    RNA-mediated interference, both LATS1 and LATS2 were substantially
    knocked-down, and accordingly, this lead to an increase in multiple
    phenotypes associated with tumor progression, including enhanced cell
    proliferation, resistance to drug-induced cell death, and increased
    cell migration. Using whole human genome Oligo (60-met) arrays
    (Agilent), genes modulated by loss of LATS1/2 were identified and
    functionally grouped into categories including cell proliferation, cell
    death, cell adhesion and motility, as well as cell communication.
    Selected genes, including known tumor suppressor genes and oncogenes
    such as CDKN1A, WISP2, SLIT2, TP53INP1, BIRC4BP, SPRY2, SPRY4, SPRED1,
    FAT4, and CYR61 were confirmed by qRT-PCR to be significantly
    differentially expressed. Importantly, the collection of genes
    identified suggests that LATS1/2 function through diverse mechanisms
    and multiple signaling pathways including the Hippo signaling pathway,
    as well as the p53. Ras-ERK, or WNT networks, to inhibit tumor
    progression. (C) 2009 Elsevier B.V. All rights reserved.
 C1 [Visser, Stacy; Yang, Xiaolong] Queens Univ, Dept Pathol & Mol Med, Kingston, ON K7L 3N6, Canada.
 RP Yang, XL, Queens Univ, Dept Pathol & Mol Med, Kingston, ON K7L 3N6,
    Canada.
 EM yang@cliff.path.queensu.ca
 FU Canadian Institute of Health Research (CIHR) [77726]; Ontario Ministry
    of Research and Innovation, Canada ; Queen's University, Canada 
 FX We would like to thank Yawei Hao for technical support, Dr. Harriet
    Feilotter for microarray design, Hong Guo for performing the microarray
    experiments, Dr. David Lillicrap for use of ABI Prism 7700 Sequence
    Detection System, and Babak Rashidi for aiding with analysis of the
    microarray experiments. This work was supported by Canadian Institute
    of Health Research (CIHR #77726), a New Investigator Award from
    Canadian Institute of Health Research (CIHR), and an Early Researcher
    Award from Ontario Ministry of Research and Innovation, Canada, to
    Xiaolong Yang, as well as the Dr. Robert John Wilson Fellowship from
    Queen's University, Canada, to Stacy Visser.
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 NR 54
 TC 4
 PU ELSEVIER SCIENCE BV
 PI AMSTERDAM
 PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
 SN 0378-1119
 J9 GENE
 JI Gene
 PD JAN 1
 PY 2010
 VL 449
 IS 1-2
 BP 22
 EP 29
 DI 10.1016/j.gene.2009.09.008
 PG 8
 SC Genetics & Heredity
 GA 523JA
 UT ISI:000272067900003
 ER
 
 PT J
 AU Wang, N
    Sang, XC
    Li, YF
    Ling, YH
    Zhao, FM
    Yang, ZL
    He, GH
 AF Wang, Nan
    Sang, Xian-Chun
    Li, Yun-Feng
    Ling, Ying-Hua
    Zhao, Fang-Ming
    Yang, Zheng-Lin
    He, Guang-Hua
 TI Gene Mapping and Expression Analysis of a Novel Mutant reproduce organs
    absent (roa) in Rice
 SO GENES & GENOMICS
 LA English
 DT Article
 DE rice (Oryza sativa L.); flower mutant; gene mapping; ABCE model
 ID MADS-BOX GENES; FLORAL ORGAN; FLOWER DEVELOPMENT; ORYZA-SATIVA;
    IDENTITY; ARABIDOPSIS; CONSERVATION; OSMADS1
 AB Mutant plays an important role in function analysis in plant. A rice
    flower mutant reproduce organs absent (roa), showing a stable
    inheritance during several years of study, was identified in rice
    (Oryza sativa L. ssp. Indica) cultivar Jinhui10 treated with EMS and
    used in this study. This mutant showed following: elongated palea and
    pedicle; absence of inner three whorls of floral organs; multi-whorls
    glume like organs inside the lemma/palea; spikelet meristem like organ
    upon the pedicle. These phenotypes suggested that ROA is a key gene in
    rice spikelet development. Genetic analysis confirmed that the mutant
    traits were controlled by a single recessive nuclear gene. By gene
    mapping, ROA was restricted between two SSR markers RM221 and RM1342 on
    the chromosome 2. It concluded that ROA was a novel gene involving in
    flower development in rice. Besides, the mutation of ROA influenced the
    transcription level of floral homeotic genes; the expression of floral
    homeotic genes decreased in roa panicle compared with wild-type, and it
    suggested that ROA affected flower development by influencing the
    expression of floral homeotic genes.
 C1 [Wang, Nan; Sang, Xian-Chun; Li, Yun-Feng; Ling, Ying-Hua; Zhao, Fang-Ming; Yang, Zheng-Lin; He, Guang-Hua] Southwest Univ, Rice Res Inst, Minist Agr, Key Lab Biotechnol & Crop Qual Improvement, Chongqing 400715, Peoples R China.
 RP He, GH, Southwest Univ, Rice Res Inst, Minist Agr, Key Lab Biotechnol &
    Crop Qual Improvement, Chongqing 400715, Peoples R China.
 EM hegh1968@yahoo.com.cn
 FU National Natural Sciences Foundation [30800598]; Excellent Youth
    Foundation Project of Chongqing (CSTC) [2008BA1033]; Natural Sciences
    Foundation Project of Chongqing [2008BB1258]; Fine Animals and Plants
    Breeding Project of Chongqing (CSTC) [2007AA1019]
 FX This research was supported by the National Natural Sciences Foundation
    (30800598), the Excellent Youth Foundation Project of Chongqing (CSTC,
    2008BA1033), the Natural Sciences Foundation Project of Chongqing
    (CSTC, 2008BB1258) and the Fine Animals and Plants Breeding Project of
    Chongqing (CSTC, 2007AA1019).
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 NR 23
 TC 0
 PU KOREAN SOC GENETICS
 PI SEOUL
 PA KOREAN SCIENCE & TECHNOLOGY CENTER, RM 1002, 635-4 YEOKSAM-DONG,
    KANGNAM, SEOUL, 135-703, SOUTH KOREA
 SN 1976-9571
 J9 GENES GENOM
 JI Genes Genom.
 PD OCT
 PY 2009
 VL 31
 IS 5
 BP 361
 EP 368
 PG 8
 SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology;
    Genetics & Heredity
 GA 521PI
 UT ISI:000271933800004
 ER
 
 PT J
 AU Chang, YS
    Oh, W
    Choi, SJ
    Sung, DK
    Kim, SY
    Choi, EY
    Kang, S
    Jin, HJ
    Yang, YS
    Park, WS
 AF Chang, Yun Sil
    Oh, Wonil
    Choi, Soo Jin
    Sung, Dong Kyung
    Kim, Soo Yoon
    Choi, Eun Yang
    Kang, Saem
    Jin, Hye Jin
    Yang, Yoon Sun
    Park, Won Soon
 TI Human Umbilical Cord Blood-Derived Mesenchymal Stem Cells Attenuate
    Hyperoxia-Induced Lung Injury in Neonatal Rats
 SO CELL TRANSPLANTATION
 LA English
 DT Article
 DE Hyperoxic lung injury; Transplantation; Animal; Newborn; Inflammation;
    Cell differentiation
 ID BRONCHOPULMONARY DYSPLASIA; BONE-MARROW; PROGENITOR CELLS; RETINOIC
    ACID; STROMAL CELLS; MICE; GROWTH; TRANSPLANTATION; EXPRESSION;
    DIFFERENTIATION
 AB Recent evidence suggests mesenchymal stem cells (MSCs) can downmodulate
    bleomycin-induced lung injury, and umbilical cord blood (UCB) is a
    promising source for human MSCs. This study examined whether
    intratracheal or intraperitoneal transplantation of human UCB-derived
    MSCs can attenuate hyperoxia-induced lung injury in immunocompetent
    newborn rats. Wild-type Sprague-Dawley rats were randomly exposed to
    95% oxygen or air from birth. In the transplantation groups, a single
    dose of PKH26-labeled human UCB-derived MSCs was administered either
    intratracheally (2 x 10(6) cells) or intraperitoneally (5 x 105 cells)
    at postnatal day (P) 5. At P14, the harvested lungs were examined for
    morphometric analyses of alveolarization and TUNEL staining, as well as
    the myeoloperoxidase activity, the level of tumor necrosis factor
    (TNF)-alpha, interleukin (IL)-6, and transforming growth factor
    (TGF)-beta mRNA, a-smooth muscle actin (SMA) protein, and collagen
    levels. Differentiation of MSCs to the respiratory epithelium was also
    evaluated both in vitro before transplantation and in vivo after
    transplantation. Despite one fourth dosage of MSCs, significantly more
    PKB26-labeled donor cells were recovered with intratracheal
    administration than with intraperitoneal administration both during
    normoxia and hyperoxia. The hyperoxia-induced increase in the number of
    TUNEL-positive cells, myeloperoixdase activity, and the level of IL-6
    mRNA were significantly attenuated with both intratracheal and
    intraperitoneal MSCs transplantation. However, the hyperoxia-induced
    impaired alveolarization and increased the level of TNF-alpha and
    TGF-beta mRNA, alpha-SMA protein, and collagen were significantly
    attenuated only with intratracheal MSCs transplantation. MSCs
    differentiated into respiratory epithelium in vitro and a few
    PKH26-positive donor cells were colocalized with pro surfactant protein
    C in the damaged lungs. In conclusion, intratracheal transplantation of
    human UCB-derived MSCs is more effective than intraperitoneal
    transplantation in attenuating the hyperoxia-induced lung injury in
    neonatal rats.
 C1 [Chang, Yun Sil; Park, Won Soon] Samsung Med Ctr, Dept Pediat, Seoul 135710, South Korea.
    [Chang, Yun Sil; Sung, Dong Kyung; Kim, Soo Yoon; Choi, Eun Yang; Kang, Saem; Park, Won Soon] Sungkyunkwan Univ, Sch Med, Samsung Biomed Res Inst, Seoul, South Korea.
    [Oh, Wonil; Choi, Soo Jin; Jin, Hye Jin; Yang, Yoon Sun] MEDIPOST Co Ltd, Biomed Res Inst, Seoul, South Korea.
 RP Park, WS, Samsung Med Ctr, Dept Pediat, 50 Irwon Dong, Seoul 135710,
    South Korea.
 EM wonspark@skku.edu
 FU Korea Research Foundation ; Korean Government (MOEHRD)
    [KRF-2005-041-EO0219]; Medipost Research Institute 
 FX The authors wish to thank to Dr. Su Jin Cho for her advice on the
    morphometric analysis of the lung. This work was supported by the Korea
    Research Foundation Grant funded by the Korean Government (MOEHRD)
    (KRF-2005-041-EO0219) and a grant funded by Medipost Research Institute.
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 NR 45
 TC 11
 PU COGNIZANT COMMUNICATION CORP
 PI ELMSFORD
 PA 3 HARTSDALE ROAD, ELMSFORD, NY 10523-3701 USA
 SN 0963-6897
 J9 CELL TRANSPLANT
 JI Cell Transplant.
 PY 2009
 VL 18
 IS 8
 BP 869
 EP 886
 DI 10.3727/096368909X471189
 PG 18
 SC Cell & Tissue Engineering; Medicine, Research & Experimental;
    Transplantation
 GA 521PE
 UT ISI:000271933400005
 ER
 
 PT J
 AU Wang, SC
    Lu, MC
    Chen, HL
    Tseng, HI
    Ke, YY
    Wu, YC
    Yang, PY
 AF Wang, Shih-Chung
    Lu, Mei-Chin
    Chen, Hsiu-Lin
    Tseng, Hsing-I
    Ke, Yu-Yuan
    Wu, Yang-Chang
    Yang, Pei-Yu
 TI Cytotoxicity of calotropin is through caspase activation and
    downregulation of anti-apoptotic proteins in K562 cells
 SO CELL BIOLOGY INTERNATIONAL
 LA English
 DT Article
 DE Apoptosis; Calotropin; Caspase; Cell cycle
 ID CYCLE ARREST; G2/M ARREST; CANCER; INHIBITOR; INDUCTION; PATHWAYS; AKT
 AB Calotropin is one of cardenolides isolated from milkweed used for
    medicinal purposes in many Asian countries. Whereas calotropin
    possesses cytotoxicity against several cancer cells, the mechanisms of
    action remain unclear. We set out to evaluate the cytotoxic mechanism
    of calotropin on human chronic myeloid leukemia K562 cells. Calotropin
    inhibited the growth of K562 cells in a time- and dose-dependent manner
    by G(2)/M phase arrest. It upregulated the expression of p27 leading to
    this arrest by downregulating the G2/M regulatory proteins, cyclins A
    and B, and by upregulating the cdk inhibitor, p27. Furthermore, it
    downregulated anti-apoptotic signaling (XIAP and survivin) and survival
    pathways (p-Akt and NF kappa B), leading to caspase-3 activation which
    resulted in the induction of apoptosis. In all, calotropin exerted its
    anticancer activity on K562 cells by modulating the pro-survival
    signaling that leads to induction of apoptosis. (C) 2009 International
    Federation for Cell Biology. Published by Elsevier Ltd. All rights
    reserved.
 C1 [Lu, Mei-Chin; Wu, Yang-Chang; Yang, Pei-Yu] Kaohsiung Med Univ, Grad Inst Nat Prod, Kaohsiung 807, Taiwan.
    [Wu, Yang-Chang] Kaohsiung Med Univ, Ctr Excellence Environm Med, Kaohsiung 807, Taiwan.
    [Wang, Shih-Chung; Ke, Yu-Yuan] Changhua Christian Hosp, Dept Pediat, Changhua 500, Taiwan.
    [Chen, Hsiu-Lin; Tseng, Hsing-I] Kaohsiung Med Univ Hosp, Dept Pediat, Kaohsiung 807, Taiwan.
    [Yang, Pei-Yu] Show Chwan Mem Hosp, Dept Med Res, Changhua, Taiwan.
 RP Wu, YC, Kaohsiung Med Univ, Grad Inst Nat Prod, Kaohsiung 807, Taiwan.
 EM yachwu@kmu.edu.tw
    yachwu@kmu.edu.tw
 FU Changhua Christian Hospital [95-CCH-KMU-11, 12]; [NSC-952314-B-037-051]
 FX This work was supported in part by a grant from Changhua Christian
    Hospital (95-CCH-KMU-11 and 12) and NSC-952314-B-037-051.
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 NR 20
 TC 1
 PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
 PI LONDON
 PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
 SN 1065-6995
 J9 CELL BIOL INT
 JI Cell Biol. Int.
 PD DEC
 PY 2009
 VL 33
 IS 12
 BP 1230
 EP 1236
 DI 10.1016/j.cellbi.2009.08.013
 PG 7
 SC Cell Biology
 GA 521EI
 UT ISI:000271902600004
 ER
 
 PT J
 AU Lin, SH
    Liu, CM
    Liu, YL
    Fann, CSJ
    Hsiao, PC
    Wu, JY
    Hung, SI
    Chen, CH
    Wu, HM
    Jou, YS
    Liu, SK
    Hwang, TJ
    Hsieh, MH
    Chang, CC
    Yang, WC
    Lin, JJ
    Chou, FHC
    Faraone, SV
    Tsuang, MT
    Hwu, HG
    Chen, WJ
 AF Lin, S. -H.
    Liu, C. -M.
    Liu, Y. -L.
    Fann, C. Shen-Jang
    Hsiao, P. -C.
    Wu, J. -Y.
    Hung, S. -I.
    Chen, C. -H.
    Wu, H. -M.
    Jou, Y. -S.
    Liu, S. K.
    Hwang, T. J.
    Hsieh, M. H.
    Chang, C. -C.
    Yang, W. -C.
    Lin, J. -J.
    Chou, F. H. -C.
    Faraone, S. V.
    Tsuang, M. T.
    Hwu, H. -G.
    Chen, W. J.
 TI Clustering by neurocognition for fine mapping of the schizophrenia
    susceptibility loci on chromosome 6p
 SO GENES BRAIN AND BEHAVIOR
 LA English
 DT Article
 DE Candidate gene; cluster analysis; endophenotype; executive dysfunction;
    schizophrenia; sustained attention deficit
 ID CARD SORTING TEST; SUSTAINED ATTENTION DEFICITS; MINOR PHYSICAL
    ANOMALIES; DYSBINDIN GENE DTNBP1; BONE MORPHOGENETIC PROTEIN-6;
    CONTINUOUS PERFORMANCE-TEST; FAMILY-BASED TESTS; NONPSYCHOTIC
    RELATIVES; TAIWANESE FAMILIES; LINKAGE ANALYSIS
 AB Chromosome 6p is one of the most commonly implicated regions in the
    genome-wide linkage scans of schizophrenia, whereas further association
    studies for markers in this region were inconsistent likely due to
    heterogeneity. This study aimed to identify more homogeneous subgroups
    of families for fine mapping on regions around markers D6S296 and
    D6S309 (both in 6p24.3) as well as D6S274 (in 6p22.3) by means of
    similarity in neurocognitive functioning. A total of 160 families of
    patients with schizophrenia comprising at least two affected siblings
    who had data for eight neurocognitive test variables of the continuous
    performance test (CPT) and the Wisconsin card sorting test (WCST) were
    subjected to cluster analysis with data visualization using the test
    scores of both affected siblings. Family clusters derived were then
    used separately in family-based association tests for 64 single
    nucleotide polymorphisms (SNPs) covering the region of 6p24.3 and
    6p22.3. Three clusters were derived from the family-based clustering,
    with deficit cluster 1 representing deficit on the CPT, deficit cluster
    2 representing deficit on both the CPT and the WCST, and a third
    cluster of nondeficit. After adjustment using false discovery rate for
    multiple testing, SNP rs13873 and haplotype rs1225934-rs13873 on
    BMP6-TXNDC5 genes were significantly associated with schizophrenia for
    the deficit cluster 1 but not for the deficit cluster 2 or nondeficit
    cluster. Our results provide further evidence that the BMP6-TXNDC5
    locus on 6p24.3 may play a role in the selective impairments on
    sustained attention of schizophrenia.
 C1 [Lin, S. -H.; Hsiao, P. -C.; Hwu, H. -G.; Chen, W. J.] Natl Taiwan Univ, Coll Publ Hlth, Inst Epidemiol, Taipei 100, Taiwan.
    [Lin, S. -H.; Hsiao, P. -C.; Chen, W. J.] Natl Taiwan Univ, Genet Epidemiol Core Lab, Div Genom Med, Res Ctr Med Excellence, Taipei 100, Taiwan.
    [Liu, C. -M.; Liu, S. K.; Hwang, T. J.; Hsieh, M. H.; Hwu, H. -G.; Chen, W. J.] Natl Taiwan Univ Hosp, Dept Psychiat, Taipei, Taiwan.
    [Liu, C. -M.; Liu, S. K.; Hwang, T. J.; Hsieh, M. H.; Hwu, H. -G.; Chen, W. J.] Natl Taiwan Univ, Coll Med, Taipei 100, Taiwan.
    [Liu, Y. -L.] Natl Hlth Res Inst, Div Mental Hlth & Subst Abuse Res, Zhunan, Taiwan.
    [Wu, J. -Y.; Hung, S. -I.] Acad Sinica, Inst Biomed Sci, Natl Genotyping Ctr, Taipei, Taiwan.
    [Chen, C. -H.] Acad Sinica, Inst Stat Sci, Taipei 11529, Taiwan.
    [Wu, J. -Y.] Tamkang Univ, Dept Math, Taipei, Taiwan.
    [Yang, W. -C.] Acad Sinica, Taiwan Int Grad Program, Program Mol Med, Taipei 115, Taiwan.
    [Liu, S. K.] Far Eastern Mem Hosp, Taipei, Taiwan.
    [Yang, W. -C.] Natl Yang Ming Univ, Inst Biochem & Mol Biol, Taipei 112, Taiwan.
    [Lin, J. -J.] Chimei Med Ctr, Dept Psychiat, Tainan, Taiwan.
    [Chou, F. H. -C.] Kai Suan Psychiat Hosp, Kaohsiung, Taiwan.
    [Faraone, S. V.] SUNY Upstate Med Univ, Dept Psychiat, Syracuse, NY USA.
    [Faraone, S. V.] SUNY Upstate Med Univ, Dept Neurosci & Physiol, Syracuse, NY USA.
    [Tsuang, M. T.] Harvard Univ, Harvard Inst Psychiat Epidemiol & Genet, Boston, MA 02115 USA.
    [Tsuang, M. T.] Harvard Univ, Sch Med, Dept Epidemiol, Boston, MA 02115 USA.
    [Tsuang, M. T.] Harvard Univ, Sch Med, Dept Psychiat, Boston, MA 02115 USA.
    [Tsuang, M. T.] Univ Calif San Diego, Dept Psychiat, Ctr Behav Genom, San Diego, CA 92103 USA.
    [Hwu, H. -G.] Natl Taiwan Univ, Coll Sci, Dept Psychol, Taipei 10764, Taiwan.
 RP Chen, WJ, Natl Taiwan Univ, Coll Publ Hlth, Inst Epidemiol, 17 Xuzhou
    Rd, Taipei 100, Taiwan.
 EM wjchen@ntu.edu.tw
 FU National Research Program for Genomic Medicine (NRPGM) ; National
    Science Council (NSC), Taiwan [NSC-91-3112-B-002-011,
    NSC-92-3112-B-002-019, NSC-93-3112-B-002-012, NSC-94-3112-B-002];
    National Health Research Institute (NHRI), Taiwan [NHRI-90-8825PP,
    NHRI-EX91, 92, 93, 94-9113PP, NHRI-EX98-9511PP]; Neurobiology and
    Cognitive Science Center ; National Taiwan University [96R0506];
    Department of Health, Taiwan [DOH94-TD-G-111-035]; National Institute
    of Mental Health (NIMH), USA [1R01 MH59624-01, 1R01 MH59624-02];
    Department of Medical Research ; National Taiwan University Hospital 
 FX This study was supported in part by the grants from National Research
    Program for Genomic Medicine (NRPGM), National Science Council (NSC),
    Taiwan (NSC-91-3112-B-002-011; NSC-92-3112-B-002-019;
    NSC-93-3112-B-002-012; NSC-94-3112-B-002); National Health Research
    Institute (NHRI), Taiwan (NHRI-90-8825PP; NHRI-EX91, 92, 93, 94-9113PP;
    NHRI-EX98-9511PP); Neurobiology and Cognitive Science Center, National
    Taiwan University (96R0506); Department of Health, Taiwan
    (DOH94-TD-G-111-035); and National Institute of Mental Health (NIMH),
    USA (1R01 MH59624-01, 1R01 MH59624-02). We acknowledge the SNP
    genotyping work done by the National Genotyping Center (NGC), NSC,
    Taiwan and the support from the Department of Medical Research,
    National Taiwan University Hospital.
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 NR 68
 TC 1
 PU WILEY-BLACKWELL PUBLISHING, INC
 PI MALDEN
 PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
 SN 1601-1848
 J9 GENES BRAIN BEHAV
 JI Genes Brain Behav.
 PD NOV
 PY 2009
 VL 8
 IS 8
 BP 785
 EP 794
 DI 10.1111/j.1601-183X.2009.00523.x
 PG 10
 SC Behavioral Sciences; Neurosciences
 GA 517QY
 UT ISI:000271633300006
 ER
 
 PT J
 AU Aravindaram, K
    Yu, HH
    Lan, CW
    Wang, PH
    Chen, YH
    Chen, HM
    Yagita, H
    Yang, NS
 AF Aravindaram, K.
    Yu, H-H
    Lan, C-W
    Wang, P-H
    Chen, Y-H
    Chen, H-M
    Yagita, H.
    Yang, N-S
 TI Transgenic expression of human gp100 and RANTES at specific time points
    for suppression of melanoma
 SO GENE THERAPY
 LA English
 DT Article
 DE prime-boost; melanoma; chemokine; vaccinia virus; migration; death
    receptors
 ID APOPTOSIS-INDUCING LIGAND; VACCINIA VIRUS ANKARA; MURINE RENAL-CANCER;
    DENDRITIC CELLS; IN-VIVO; TUMOR REJECTION; NK CELLS; IMMUNE-RESPONSE;
    CC-CHEMOKINE; T-CELLS
 AB The induction of strong cell-mediated immunity against targeted cancer
    cells is difficult, and often requires specific vaccination schema and
    the appropriate adjuvants to be effective. The chemokine RANTES has
    been studied as a vaccine adjuvant in cancer therapy, but specific
    applications remain to be determined. For gene-based vaccination
    against B16 melanoma in C57BL/6JNarl mice, initial priming with mouse
    RANTES cDNA followed 24 h later by human gp100 DNA vaccination, and
    later boosting with a viral vector expressing mRANTES and hgp100
    strongly suppressed B16/hgp100 primary tumors and lung metastasis. The
    inclusion of mRANTES in this vaccination regimen gave significantly
    better suppression of tumor growth, substantially enhanced mouse
    survival, and led to greater cytotoxic activity of splenocytes against
    B16/hgp100 cells than vaccination against hgp100 alone. B16/hgp100
    melanoma cells were resistant to the ligands TRAIL and FasL in vitro
    but sensitized to them in vivo owing to the priming effect of cytokines
    in response to vaccination. Our data demonstrate that co-vaccination
    with chemokine (mRANTES) and tumor-specific (hgp100) genes in a
    specific time sequence is more effective at suppressing tumor growth
    and metastasis than hgp100 alone, and this effect may be mediated by
    sensitization of tumor cells to death ligands. Gene Therapy (2009) 16,
    1329-1339; doi:10.1038/gt.2009.90; published online 23 July 2009
 C1 [Aravindaram, K.; Yu, H-H; Lan, C-W; Wang, P-H; Chen, Y-H; Chen, H-M; Yang, N-S] Acad Sinica, Agr Biotechnol Res Ctr, Taipei 115, Taiwan.
    [Yagita, H.] Juntendo Univ, Sch Med, Dept Immunol, Tokyo 113, Japan.
 RP Yang, NS, Acad Sinica, Agr Biotechnol Res Ctr, 128 Sect 2,Acad Rd,
    Taipei 115, Taiwan.
 EM nsyang@gate.sinica.edu.tw
 FU National Science Council, Taiwan [94-2320-B-001-044]
 FX This work was supported by a Grant (94-2320-B-001-044) from the
    National Science Council, Taiwan.
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 NR 48
 TC 1
 PU NATURE PUBLISHING GROUP
 PI LONDON
 PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
 SN 0969-7128
 J9 GENE THERAPY
 JI Gene Ther.
 PD NOV
 PY 2009
 VL 16
 IS 11
 BP 1329
 EP 1339
 DI 10.1038/gt.2009.90
 PG 11
 SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology;
    Genetics & Heredity; Medicine, Research & Experimental
 GA 518CB
 UT ISI:000271666600007
 ER
 
 PT J
 AU Yang, K
    Sun, K
    Srinivasan, KN
    Salmon, J
    Marques, ET
    Xu, J
    August, JT
 AF Yang, K.
    Sun, K.
    Srinivasan, K. N.
    Salmon, J.
    Marques, E. T.
    Xu, J.
    August, J. T.
 TI Immune responses to T-cell epitopes of SARS CoV-N protein are enhanced
    by N immunization with a chimera of lysosome-associated membrane protein
 SO GENE THERAPY
 LA English
 DT Article
 DE SARS CoV; N; LAMP; cluster of dominant T-cell epitopes; DNA vaccine;
    ELISpot
 ID NEUTRALIZING ANTIBODY-RESPONSE; MHC CLASS-I; TARGETING ANTIGEN;
    DENDRITIC CELLS; DNA VACCINE; ENDOSOMAL/LYSOSOMAL COMPARTMENTS;
    GENE-PRODUCT; MEMORY; CD4(+); TRAFFICKING
 AB In our previous study by Gupta et al, dominant T-cell epitopes of SARS
    CoV-N(N) protein were predicted by software. The spectrum of interferon
    (IFN)-gamma responses of Balb/c mice immunized against two different
    forms of SARS CoV-N plasmid was then analyzed. A cluster of dominant
    T-cell epitopes of SARS CoV-N protein was found in the N-terminus
    (amino acids 76-114). On the basis of this study, four different
    plasmids were constructed: (i) DNA encoding the unmodified N (p-N) or
    N70-122 (p-N70-122) as an endogenous cytoplasmic protein or (ii) DNA
    encoding a lysosome-associated membrane protein (LAMP) chimera with N
    (p-LAMP/N) or N70-122 (p-LAMP/N70-122). The immune responses of mice to
    these four constructs were evaluated. The results showed marked
    differences in the responses of the immunized mice. A single priming
    immunization with the p-LAMP/N construct was sufficient to elicit an
    antibody response. Enzyme-linked immunospot (ELISpot) assay indicated
    that p-LAMP/N70-122 and p-LAMP/N plasmids both elicited a greater
    IFN-gamma response than p-N. p-N and p-N70-122 constructs induced low
    or undetectable levels of cytokine secretion. We also found that the
    p-LAMP/N70-122 construct promoted a long-lasting T-cell memory response
    without an additional boost 6 months after three immunizations. These
    findings show that DNA vaccines, even epitope-based DNA vaccines using
    LAMP as chimera, can elicit both humoral and cellular immune responses.
    Gene Therapy (2009) 16, 1353-1362; doi:10.1038/gt.2009.92; published
    online 3 September 2009
 C1 [Yang, K.] Fourth Mil Med Univ, Dept Immunol, Xian 710032, Shaanxi Prov, Peoples R China.
    [Yang, K.; Srinivasan, K. N.; Salmon, J.; Marques, E. T.; August, J. T.] Johns Hopkins Univ, Sch Med, Dept Pharmacol & Mol Sci, Baltimore, MD 21205 USA.
    [Sun, K.] Div Biomed Sci, Singapore, Singapore.
    [Srinivasan, K. N.] Hlth Sci Author, Ctr Drug Adm, Prod Evaluat & Registrat Div, Singapore, Singapore.
    [Marques, E. T.] Johns Hopkins Univ, Sch Med, Dept Med, Div Infect Dis, Baltimore, MD 21205 USA.
    [Xu, J.] Fourth Mil Med Univ, Tangdu Hosp, Dept Neurol, Xian 710032, Shaanxi Prov, Peoples R China.
 RP Yang, K, Fourth Mil Med Univ, Dept Immunol, 17 Changle W Rd, Xian
    710032, Shaanxi Prov, Peoples R China.
 EM yangkunkun@fmmu.edu.cn
    taugust@jhmi.edu
 FU National Institute of Allergy and Infectious Diseases ; National
    Institutes of Health ; Department of Health and Human Services of USA
    [HHSN266200400085C]; National High-tech R&D Program of China
    [2006AA02A237]
 FX This study was supported by grants from the National Institute of
    Allergy and Infectious Diseases, the National Institutes of Health,
    Department of Health and Human Services, contract no. HHSN266200400085C
    of USA, and the National High-tech R&D Program (863 Program) of China
    (No. 2006AA02A237). We thank Chikhlikar PR, Paul Tan, Vladimir Perovic,
    Keun OK Jung, Garg S, Milton Maciel Jr, Betty Hart and Delores Henson
    for their excellent technical assistance. The support of the NIH AIDS
    Research and Reference Reagent Program in providing the SARS-N peptides
    and purified SARS-N protein is gratefully acknowledged.
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 NR 41
 TC 0
 PU NATURE PUBLISHING GROUP
 PI LONDON
 PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
 SN 0969-7128
 J9 GENE THERAPY
 JI Gene Ther.
 PD NOV
 PY 2009
 VL 16
 IS 11
 BP 1353
 EP 1362
 DI 10.1038/gt.2009.92
 PG 10
 SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology;
    Genetics & Heredity; Medicine, Research & Experimental
 GA 518CB
 UT ISI:000271666600009
 ER
 
 PT J
 AU Cui, J
    Le, GW
    Yang, RL
    Shi, YH
 AF Cui, Jue
    Le, Guowei
    Yang, Ruili
    Shi, Yonghui
 TI Lipoic acid attenuates high fat diet-induced chronic oxidative stress
    and immunosuppression in mice jejunum: A microarray analysis
 SO CELLULAR IMMUNOLOGY
 LA English
 DT Article
 DE High fat diet; Chronic oxidative stress; Lipoic acid; Jejunum; DNA
    microarray; B cell receptor signaling pathway; T cell differentiation;
    Free radical scavenger
 ID TYROSINE PHOSPHORYLATION; LIPID-PEROXIDATION; MUCOSAL IMMUNITY;
    T-LYMPHOCYTES; ACTIVATION; CELLS; RESPONSES; TRANSCRIPTION;
    ANTIOXIDANTS; METABOLISM
 AB A high fat diet (HFD) has long been linked to immune dysfunction,
    including diminished numbers or reactivity of lymphocytes, increased
    susceptibility to infection, inhibited lymphocytes function during
    antigen-specific responses and developed oxidative stress. Whereas the
    molecular mechanistic events associated with immune deficiency remain
    to be fully determined. Using the DNA microarray system, we analyzed
    the gene expression patterns of lymphocyte related signal transduction
    proteins in jejunum of C57BL/6 mice in order to gain insight on the
    possible molecular mechanism by which HFD induced oxidative stress
    effects on signal transduction of lymphocytes. Results of present study
    showed that HFD induced oxidative stress and immunosuppression in
    jejunum. Antioxidant lipoic acid (LA) supplement ameliorated that HFD
    induced oxidative stress and immunosuppression by recovering
    transcriptional levels of the gene involved in B cell receptor, T cell
    differentiation signaling pathway, and free radical scavengers. The
    present study indicates that a HFD can induce chronic oxidative stress,
    suppress signal transduction of gut-associated lymphocytes, and lead to
    an inhibition of mucosal immunity. (C) 2009 Published by Elsevier Inc.
 C1 [Cui, Jue; Le, Guowei; Yang, Ruili; Shi, Yonghui] Jiangnan Univ, State Key Lab Food Sci & Technol, Wuxi, Jiangsu, Peoples R China.
 RP Le, GW, Jiangnan Univ, State Key Lab Food Sci & Technol, Wuxi, Jiangsu,
    Peoples R China.
 EM cuijue1980@hotmail.com
    lgw@jiangnan.edu.cn
 FU National Natural Science Foundation of China [30571347]
 FX This work was supported by the National Natural Science Foundation of
    China (Grant 30571347).
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 NR 39
 TC 3
 PU ACADEMIC PRESS INC ELSEVIER SCIENCE
 PI SAN DIEGO
 PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
 SN 0008-8749
 J9 CELL IMMUNOL
 JI Cell. Immunol.
 PY 2009
 VL 260
 IS 1
 BP 44
 EP 50
 DI 10.1016/j.cellimm.2009.08.001
 PG 7
 SC Cell Biology; Immunology
 GA 519RF
 UT ISI:000271784500008
 ER
 
 PT J
 AU Coutandin, D
    Lohr, F
    Niesen, FH
    Ikeya, T
    Weber, TA
    Schafer, B
    Zielonka, EM
    Bullock, AN
    Yang, A
    Guntert, P
    Knapp, S
    McKeon, F
    Ou, HD
    Dotsch, V
 AF Coutandin, D.
    Loehr, F.
    Niesen, F. H.
    Ikeya, T.
    Weber, T. A.
    Schaefer, B.
    Zielonka, E. M.
    Bullock, A. N.
    Yang, A.
    Guentert, P.
    Knapp, S.
    McKeon, F.
    Ou, H. D.
    Doetsch, V.
 TI Conformational stability and activity of p73 require a second helix in
    the tetramerization domain
 SO CELL DEATH AND DIFFERENTIATION
 LA English
 DT Article
 DE p73; p63; p53 family; heterooligomerization; tetramerization;
    transcriptional activity
 ID TRIPLE-RESONANCE EXPERIMENTS; SQUAMOUS-CELL CARCINOMAS; P53
    TUMOR-SUPPRESSOR; TRANSFORMING DOMAIN; LARGE PROTEINS; LI-FRAUMENI;
    DNA-BINDING; P63; FAMILY; EXPRESSION
 AB p73 and p63, the two ancestral members of the p53 family, are involved
    in neurogenesis, epithelial stem cell maintenance and quality control
    of female germ cells. The highly conserved oligomerization domain ( OD)
    of tumor suppressor p53 is essential for its biological functions, and
    its structure was believed to be the prototype for all three proteins.
    However, we report that the ODs of p73 and p63 differ from the OD of
    p53 by containing an additional alpha-helix that is not present in the
    structure of the p53 OD. Deletion of this helix causes a dissociation
    of the OD into dimers; it also causes conformational instability and
    reduces the transcriptional activity of p73. Moreover, we show that ODs
    of p73 and p63 strongly interact and that a large number of different
    heterotetramers are supported by the additional helix. Detailed
    analysis shows that the heterotetramer consisting of two homodimers is
    thermodynamically more stable than the two homotetramers. No
    heterooligomerization between p53 and the p73/p63 subfamily was
    observed, supporting the notion of functional orthogonality within the
    p53 family. Cell Death and Differentiation (2009) 16, 1582-1589; doi:
    10.1038/cdd.2009.139; published online 18 September 2009
 C1 [Ou, H. D.] Goethe Univ Frankfurt, Ctr Biomol Magnet Resonance, Inst Biophys Chem, D-60438 Frankfurt, Hessen, Germany.
    [Coutandin, D.; Loehr, F.; Ikeya, T.; Weber, T. A.; Schaefer, B.; Zielonka, E. M.; Guentert, P.; Ou, H. D.; Doetsch, V.] Goethe Univ Frankfurt, Cluster Excellence Macromol Complexes CEF, D-60438 Frankfurt, Hessen, Germany.
    [Niesen, F. H.; Bullock, A. N.; Knapp, S.] Univ Oxford, Struct Genom Consortium, Nuffield Dept Med, Oxford OX3 7DQ, England.
    [Yang, A.; McKeon, F.] Harvard Univ, Dept Cell Biol, Sch Med, Boston, MA USA.
    [Guentert, P.] Frankfurt Inst Adv Studies, Frankfurt, Germany.
    [Knapp, S.] Univ Oxford, Struct Genom Consortium, Dept Clin Pharmacol, Oxford OX3 7DQ, England.
    [Zielonka, E. M.; McKeon, F.] Genome Inst Singapore, Singapore 138672, Singapore.
 RP Ou, HD, Goethe Univ Frankfurt, Ctr Biomol Magnet Resonance, Inst
    Biophys Chem, Max von Laue Str 9, D-60438 Frankfurt, Hessen, Germany.
 EM hou@salk.edu
    vdoetsch@em.uni-frankfurt.de
 FU Deutsche Forschungsgemeinschaft [DO 545/2-1]; EU [LSHB-CT-019067];
    Centre for Biomolecular Magnetic Resonance at the University of
    Frankfurt (BMRZ) ; Cluster of Excellence Frankfurt ; Volkswagen
    Foundation ; Canadian Institutes for Health Research [1097737];
    Canadian Foundation for Innovation ; Genome Canada through the Ontario
    Genomics Institute ; GlaxoSmithKline ; Karolinska Institutet ; Knut and
    Alice Wallenberg Foundation ; Ontario Innovation Trust ; Ontario
    Ministry for Research and Innovation ; Merck Co., Inc. ; Novartis
    Research Foundation ; Swedish Agency for Innovation Systems ; Swedish
    Foundation for Strategic Research ; Wellcome Trust 
 FX We thank Benjamin Bardiaux (Institut Pasteur) for providing a modified
    version of ARIA2.2 capable of handling tetramers with a D2 symmetry,
    and Hongmei Mou for help with immunohistochemistry. The research was
    funded by the Deutsche Forschungsgemeinschaft (DO 545/2-1), by the
    EU-Grant EPISTEM (LSHB-CT-019067), by the Centre for Biomolecular
    Magnetic Resonance at the University of Frankfurt (BMRZ), by the
    Cluster of Excellence Frankfurt (Macromolecular Complexes) and by the
    Volkswagen Foundation (PG). The Structural Genomics Consortium is a
    registered charity (number 1097737) that receives funds from the
    Canadian Institutes for Health Research, the Canadian Foundation for
    Innovation, Genome Canada through the Ontario Genomics Institute, from
    GlaxoSmithKline, Karolinska Institutet, the Knut and Alice Wallenberg
    Foundation, the Ontario Innovation Trust, the Ontario Ministry for
    Research and Innovation, Merck & Co., Inc., the Novartis Research
    Foundation, the Swedish Agency for Innovation Systems, the Swedish
    Foundation for Strategic Research and from the Wellcome Trust.
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 NR 40
 TC 9
 PU NATURE PUBLISHING GROUP
 PI LONDON
 PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
 SN 1350-9047
 J9 CELL DEATH DIFFERENTIATION
 JI Cell Death Differ.
 PD DEC
 PY 2009
 VL 16
 IS 12
 BP 1582
 EP 1589
 DI 10.1038/cdd.2009.139
 PG 8
 SC Biochemistry & Molecular Biology; Cell Biology
 GA 519QY
 UT ISI:000271783600003
 ER
 
 PT J
 AU Yang, L
    Stephens, GJ
 AF Yang, Li
    Stephens, Gary J.
 TI Effects of neuropathy on high-voltage-activated Ca2+ current in sensory
    neurones
 SO CELL CALCIUM
 LA English
 DT Article
 DE Calcium channel; R-type channel; Neuropathy; DRG; SNX-482
 ID DEPENDENT CALCIUM-CHANNEL; ROOT GANGLION NEURONS; SCIATIC-NERVE INJURY;
    N-TYPE; DORSAL-HORN; MICE LACKING; NEUROTRANSMITTER RELEASE;
    SYNAPTIC-TRANSMISSION; DENDRITIC SPINES; MOLECULAR-BASIS
 AB Voltage-dependent Ca2+ channels (VDCCs) have emerged as targets to
    treat neuropathic pain; however, amongst VDCCs, the precise role of the
    Ca(V)2.3 subtype in nociception remains unproven. Here, we investigate
    the effects of partial sciatic nerve ligation (PSNL) on Ca2+ currents
    in small/medium diameter dorsal root ganglia (DRG) neurones isolated
    from Ca(V)2.3(-/-) knock-out and wild-type (WT) mice. DRG neurones from
    Ca(V)2.3(-/-) mice had significantly reduced sensitivity to SNX-482
    versus WT mice. DRGs from Ca(V)2.3(-/-) mice also had increased
    sensitivity to the Ca(V)2.2 VDCC blocker omega-conotoxin. In WT mice,
    PSNL caused a significant increase in omega-conotoxin-sensitivity and a
    reduction in SNX-482-sensitivity. In Ca(V)2.3(-/-) mice, PSNL caused a
    significant reduction in w-conotoxin-sensitivity and an increase in
    nifedipine sensitivity. PSNL-induced changes in Ca2+ current were not
    accompanied by effects on voltage-dependence of activation in either
    Ca(V)2.3(-/-) or WT mice. These data suggest that Ca(V)2.3 subunits
    contribute, but do not fully underlie, drug-resistant (R-type) Ca2+
    current in these cells. In WT mice, PSNL caused adaptive changes in
    Ca(V)2.2- and Ca(V)2.3-mediated Ca2+ currents, supporting roles for
    these VDCCs in nociception during neuropathy. In Ca(V)2.3(-/-) mice,
    PSNL-induced changes in Ca(V)1 and Ca(V)2.2 Ca2+ current, consistent
    with alternative adaptive mechanisms occurring in the absence of
    Ca(V)2.3 subunits. (c) 2009 Elsevier Ltd. All rights reserved.
 C1 [Yang, Li; Stephens, Gary J.] Univ Reading, Sch Pharm, Reading RG6 6AJ, Berks, England.
 RP Stephens, GJ, Univ Reading, Sch Pharm, POB 228, Reading RG6 6AJ, Berks,
    England.
 EM g.j.stephens@reading.ac.uk
 FU BBSRC 
 FX We wish to thank Alomone Labs, Israel for kind gifts of SNX-482 and
    Ca<INF>V</INF>2.3 antibody, and in particular the support of Dr. Alon
    Meir. We also wish to thank Prof. Toni Schneider, University of Koln,
    Germany for original supply of breeding pairs of C57B1/6 WT and
    Ca<INF>V</INF>2.3(-/-) mice. The authors declare no conflicts of
    interest. Work funded by BBSRC.
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 NR 58
 TC 1
 PU CHURCHILL LIVINGSTONE
 PI EDINBURGH
 PA JOURNAL PRODUCTION DEPT, ROBERT STEVENSON HOUSE, 1-3 BAXTERS PLACE,
    LEITH WALK, EDINBURGH EH1 3AF, MIDLOTHIAN, SCOTLAND
 SN 0143-4160
 J9 CELL CALCIUM
 JI Cell Calcium
 PD OCT
 PY 2009
 VL 46
 IS 4
 BP 248
 EP 256
 DI 10.1016/j.ceca.2009.08.001
 PG 9
 SC Cell Biology
 GA 518KK
 UT ISI:000271690100004
 ER
 
 PT J
 AU Byeon, IJL
    Meng, X
    Jung, JW
    Zhao, GP
    Yang, RF
    Ahn, JW
    Shi, J
    Concel, J
    Aiken, C
    Zhang, PJ
    Gronenborn, AM
 AF Byeon, In-Ja L.
    Meng, Xin
    Jung, Jinwon
    Zhao, Gongpu
    Yang, Ruifeng
    Ahn, Jinwoo
    Shi, Jiong
    Concel, Jason
    Aiken, Christopher
    Zhang, Peijun
    Gronenborn, Angela M.
 TI Structural Convergence between Cryo-EM and NMR Reveals Intersubunit
    Interactions Critical for HIV-1 Capsid Function
 SO CELL
 LA English
 DT Article
 ID C-TERMINAL DOMAIN; DIMERIZATION DOMAIN; CRYSTAL-STRUCTURES;
    MEMBRANE-PROTEINS; TUBULAR CRYSTALS; GAG POLYPROTEIN; VIRUS;
    RESOLUTION; ALIGNMENT; RECONSTRUCTIONS
 AB Mature HIV-1 particles contain conical-shaped capsids that enclose the
    viral RNA genome and perform essential functions in the virus life
    cycle. Previous structural analysis of two-and three-dimensional arrays
    of the capsid protein (CA) hexamer revealed three interfaces. Here, we
    present a cryoEM study of a tubular assembly of CA and a
    high-resolution NMR structure of the CA C-terminal domain (CTD) dimer.
    In the solution dimer structure, the monomers exhibit different
    relative orientations compared to previous X-ray structures. The
    solution structure fits well into the EM density map, suggesting that
    the dimer interface is retained in the assembled CA. We also identified
    a CTD-CTD interface at the local three-fold axis in the cryoEM map and
    confirmed its functional importance by mutagenesis. In the tubular
    assembly, CA intermolecular interfaces vary slightly, accommodating the
    asymmetry present in tubes. This provides the necessary plasticity to
    allow for controlled virus capsid dis/assembly.
 C1 [Byeon, In-Ja L.; Meng, Xin; Jung, Jinwon; Zhao, Gongpu; Ahn, Jinwoo; Concel, Jason; Zhang, Peijun; Gronenborn, Angela M.] Univ Pittsburgh, Sch Med, Dept Biol Struct, Pittsburgh, PA 15260 USA.
    [Yang, Ruifeng; Shi, Jiong; Aiken, Christopher] Vanderbilt Univ, Sch Med, Dept Microbiol & Immunol, Nashville, TN 37232 USA.
 RP Zhang, PJ, Univ Pittsburgh, Sch Med, Dept Biol Struct, Pittsburgh, PA
    15260 USA.
 EM pez7@pitt.edu
    amg100@pitt.edu
 FU National Institutes of Health [GM082251, AI076121, GM085043]
 FX We thank Dr. Joanne Yeh for useful discussions and Dr. Teresa
    Brosenitsch for critical reading of the manuscript. We thank Drs. Koji
    Yonekura, Edward Egelman, and Niko Grigorieff for sharing their image
    processing software and Dr. Jing Zhou for technical assistance. This
    work is a contribution from the Pittsburgh Center for HIV Protein
    Interactions and was supported by the National Institutes of Health
    (GM082251, AI076121, and GM085043).
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 NR 56
 TC 19
 PU CELL PRESS
 PI CAMBRIDGE
 PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
 SN 0092-8674
 J9 CELL
 JI Cell
 PD NOV 13
 PY 2009
 VL 139
 IS 4
 BP 780
 EP 790
 DI 10.1016/j.cell.2009.10.010
 PG 11
 SC Biochemistry & Molecular Biology; Cell Biology
 GA 519EG
 UT ISI:000271747200021
 ER
 
 PT J
 AU Jin, MJ
    Kawakami, K
    Fukui, Y
    Tsukioka, S
    Oda, M
    Watanabe, G
    Takechi, T
    Oka, T
    Minamoto, T
 AF Jin, MingJi
    Kawakami, Kazuyuki
    Fukui, Yousuke
    Tsukioka, Sayaka
    Oda, Makoto
    Watanabe, Go
    Takechi, Teiji
    Oka, Toshinori
    Minamoto, Toshinari
 TI Different histological types of non-small cell lung cancer have
    distinct folate and DNA methylation levels
 SO CANCER SCIENCE
 LA English
 DT Article
 ID TUMOR-SUPPRESSOR GENES; COLORECTAL CANCERS; ESOPHAGEAL ADENOCARCINOMA;
    COLON-CANCER; RISK-FACTORS; SMOKING; PHENOTYPE; HYPERMETHYLATION;
    HYDROLASE; PROFILES
 AB Aberrant DNA methylation is a commonly observed epigenetic change in
    lung cancer. Folate has been suggested to play a role in the
    homeostasis of DNA methylation and has also been implicated in cancer
    chemotherapy. We investigated a possible role for folate in DNA
    methylation by measuring folate concentrations in tumors and adjacent
    normal tissues from 72 non-small cell lung cancer (NSCLC) patients.
    These were compared to DNA methylation levels and to
    clinicopathological features. Folate concentrations were determined as
    the sum of 5,10-methylenetetrahydrofolate and tetrahydrofolate. The
    MethyLight assay was used to quantitate methylation in promoter regions
    of P16(CDKN2A), APC, CDH13, RARB, RASSF1, RUNX3, and MYOD1. Methylation
    of LINE-1 repeats was used as a surrogate for global methylation.
    Folate levels in tumors correlated positively with LINE-1, CDH13, and
    RUNX3 methylation. Folate concentrations and methylation of LINE-1,
    RASSF1, and RUNX3 were significantly higher in adenocarcinoma compared
    to squamous cell carcinoma (SCC). Two sets of array-based data
    retrieved from the Gene Expression Omnibus consistently showed that
    expression of FOLR1, a folate transport enzyme, and GGH, an enzyme that
    prevents folate retention, were higher and lower, respectively, in
    adenocarcinomas compared to SCC. This was independently validated by
    quantitative RT-PCR in 26 adenocarcinomas and 13 SCC. Our results
    suggest that folate metabolism plays a role in aberrant DNA methylation
    in NSCLC. The histological subtype differences in folate concentration
    and DNA methylation observed here were associated with distinct
    expression patterns for folate metabolizing enzymes. These findings may
    have clinical applications for histology-directed chemotherapy with
    fluoropyrimidine and anti-folates in NSCLC. (Cancer Sci 2009l; 100:
    2325-2330).
 C1 [Jin, MingJi; Kawakami, Kazuyuki; Minamoto, Toshinari] Kanazawa Univ, Canc Res Inst, Mol & Cellular Targeting Translat Oncol Ctr, Div Translat & Clin Oncol, Kanazawa, Ishikawa 920, Japan.
    [Fukui, Yousuke; Tsukioka, Sayaka; Oka, Toshinori] Taiho Pharmaceut Co, Tokushima Res Ctr, Tokushima, Japan.
    [Oda, Makoto; Watanabe, Go] Kanazawa Univ, Grad Sch Med Sci, Dept Gen & Cardiothorac Surg, Kanazawa, Ishikawa 920, Japan.
    [Takechi, Teiji] Taiho Pharmaceut Co, Prod Planning & Lifecycle Management Dept, Tokyo, Japan.
 RP Kawakami, K, Kanazawa Univ, Canc Res Inst, Mol & Cellular Targeting
    Translat Oncol Ctr, Div Translat & Clin Oncol, Kanazawa, Ishikawa 920,
    Japan.
 EM kawakami@med.kanazawa-u.ac.jp
 FU Japanese Society for the Promotion of Science 
 FX This work was supported in part by Grants-in-Aid for Scientific
    Research from the Japanese Society for the Promotion of Science.
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 NR 35
 TC 3
 PU WILEY-BLACKWELL PUBLISHING, INC
 PI MALDEN
 PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
 SN 1347-9032
 J9 CANCER SCI
 JI Cancer Sci.
 PD DEC
 PY 2009
 VL 100
 IS 12
 BP 2325
 EP 2330
 DI 10.1111/j.1349-7006.2009.01321.x
 PG 6
 SC Oncology
 GA 518QX
 UT ISI:000271709300013
 ER
 
 PT J
 AU Watanabe, G
    Kato, S
    Nakata, H
    Ishida, T
    Ohuchi, N
    Ishioka, C
 AF Watanabe, Gou
    Kato, Shunsuke
    Nakata, Hideyuki
    Ishida, Takanori
    Ohuchi, Noriaki
    Ishioka, Chikashi
 TI alpha B-crystallin: A novel p53-target gene required for p53-dependent
    apoptosis
 SO CANCER SCIENCE
 LA English
 DT Article
 ID TUMOR-SUPPRESSOR PROTEIN; NON-LENTICULAR TISSUES; TRANSCRIPTIONAL
    ACTIVITY; MUTATION ANALYSIS; TP53 DATABASE; P53; ACTIVATION;
    EXPRESSION; LENS; CASPASE-3
 AB The p53 protein is a transcription factor that trans-activates various
    genes in response to DNA-damaging stress. To search for new p53-target
    genes, we applied a cDNA microarray system using two independent
    p53-inducible cell lines, followed by in silico analysis to detect p53
    response elements. Here, we report on crystallin alpha B gene (CRYAB),
    which encodes alpha B-crystallin, and is one of the genes directly
    trans-activated by p53. We confirmed it is directly transcribed by p53
    using promoter analysis, deletion reporter assay, ChIP assay and EMSA.
    alpha B-crystallin is also upregulated in a p53-dependent manner and
    binds to the DNA-binding domain of p53. Overexpression of alpha
    B-crystallin increased p53 protein and, in contrast, repression of
    alpha B-crystallin decreased p53 protein. Interestingly, both
    overexpression and repression of alpha B-crystallin reduced
    p53-dependent apoptosis. In conclusion, we identified that alpha
    B-crystallin was a novel p53-target gene and required for p53-dependent
    apoptosis using two independent p53-inducible cell lines. This is the
    first report associating p53 directly with a heat shock protein through
    trans-activation and physical interaction. (Cancer Sci 2009; 100:
    2368-2375).
 C1 [Watanabe, Gou; Kato, Shunsuke; Nakata, Hideyuki; Ishioka, Chikashi] Tohoku Univ, Res Inst Dev Aging & Canc, Dept Clin Oncol, Sendai, Miyagi 980, Japan.
    [Watanabe, Gou; Ishida, Takanori; Ohuchi, Noriaki] Tohoku Univ, Sch Med, Div Surg Oncol, Sendai, Miyagi 980, Japan.
 RP Ishioka, C, Tohoku Univ, Res Inst Dev Aging & Canc, Dept Clin Oncol,
    Sendai, Miyagi 980, Japan.
 EM chikashi@idac.tohoku.ac.jp
 FU Ministry of Education, Sciences, Sports, and Culture [12217010,
    17015002]; Gonryo Medical Foundation 
 FX We thank Shin Takahashi, Satsuki Mashiko, and Atsuko Sato for their
    technical assistance. This study was supported by grants-in-aid from
    the Ministry of Education, Sciences, Sports, and Culture (12217010 and
    17015002), and the Gonryo Medical Foundation to C.I.
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 NR 44
 TC 4
 PU WILEY-BLACKWELL PUBLISHING, INC
 PI MALDEN
 PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
 SN 1347-9032
 J9 CANCER SCI
 JI Cancer Sci.
 PD DEC
 PY 2009
 VL 100
 IS 12
 BP 2368
 EP 2375
 DI 10.1111/j.1349-7006.2009.01316.x
 PG 8
 SC Oncology
 GA 518QX
 UT ISI:000271709300020
 ER
 
 PT S
 AU Mann, DL
    Celluzzi, CM
    Hankey, KG
    Harris, KM
    Watanabe, R
    Hasumi, K
 AF Mann, Dean L.
    Celluzzi, Christina M.
    Hankey, Kim G.
    Harris, Kristina M.
    Watanabe, Ryuko
    Hasumi, Kenichiro
 ED Steinman, R; Banchereau, J; Finn, OJ
 TI Combining Conventional Therapies with Intratumoral Injection of
    Autologous Dendritic Cells and Activated T Cells to Treat Patients with
    Advanced Cancers
 SO CANCER VACCINES
 SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES
 LA English
 DT Proceedings Paper
 CT 6th International Cancer Vaccine Symposium
 CY OCT 28-30, 2008
 CL New York, NY
 SP New York Acad Sci
 DE dendritic cells; activated T cells; combination immunotherapy;
    intratumoral injection; cancer vaccine
 ID PERIPHERAL-BLOOD LYMPHOCYTES; ADOPTIVE TRANSFER; TUMOR-CELLS; IN-VIVO;
    ESTABLISHED TUMORS; IMMUNOTHERAPY; CYCLOPHOSPHAMIDE; IMMUNITY;
    RADIATION; APOPTOSIS
 AB Dendritic cells (DCs) are potent antigen-presenting cells that have
    been used in cancer immunotherapy. To take advantage of the ability of
    DCs to acquire antigenic materials from their environment and generate
    primary as well as recall immune responses, 37 patients with advanced
    cancers were enrolled in a series of protocols based on direct
    intratumoral injection of immature DCs. To augment antigen uptake and
    antitumor immune response, DC injection was combined with radiotherapy
    or chemotherapy and/or injection of activated T cells. Treatments were
    well tolerated with no adverse reactions. Clinical responses were based
    on Response Evaluation Criteria in Solid Tumors, with the majority of
    patients showing stable disease. One of two patients who also received
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 RP Mann, DL, Univ Maryland, Sch Med, Dept Pathol, Baltimore, MD 21201 USA.
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 NR 44
 TC 1
 PU BLACKWELL PUBLISHING
 PI OXFORD
 PA 9600 GARSINGTON RD, OXFORD OX4 2DQ, OXEN, ENGLAND
 SN 0077-8923
 BN 978-1-57331-759-7
 J9 ANN N Y ACAD SCI
 JI Ann.NY Acad.Sci.
 PY 2009
 VL 1174
 BP 41
 EP 50
 DI 10.1111/j.1749-6632.2009.04934.x
 PG 10
 SC Multidisciplinary Sciences
 GA BMC20
 UT ISI:000271828500006
 ER
 
 PT J
 AU Yang, SS
    Huang, HC
 AF Yang, Sharon S.
    Huang, Hong-Chih
 TI The Impact of Longevity Risk on the Optimal Contribution Rate and Asset
    Allocation for Defined Contribution Pension Plans
 SO GENEVA PAPERS ON RISK AND INSURANCE-ISSUES AND PRACTICE
 LA English
 DT Article
 DE longevity risk; asset allocation; income replacement ratio
 ID GUARANTEED ANNUITY OPTIONS; MORTALITY; ACCUMULATION; MANAGEMENT;
    VALUATION; SCHEMES; DESIGN; PHASE
 AB This research studies the interaction between longevity risk and asset
    allocation for a defined contribution pension plan. We investigate the
    investment strategy during the accumulation phase to deal with
    longevity risk during the decumulation phase. The longevity risk is
    demonstrated using the U. K. mortality experience for pensioners. We
    experiment with three patterns of mortality: base, projection and
    stochastic mortality rates. The optimal asset allocation and
    contribution rate are determined by minimizing the variance of the
    error between the value of pension fund and required pension fund plus
    the square of the expected value of the error. The required pension
    fund is decided by the pension fund target, measured using the income
    replacement ratio. We consider four assets in the asset allocation and
    observe four types of changes to the rebalancing investment strategies.
    The results show a life cycle investment strategy and indicate that
    longevity risk can be hedged by either raising the contribution rate or
    setting a more aggressive asset allocation. The Geneva Papers (2009)
    34, 660-681. doi: 10.1057/gpp.2009.18
 C1 [Yang, Sharon S.] Natl Cent Univ, Dept Finance, Tao Yuan, Taiwan.
    [Huang, Hong-Chih] Natl Chengchi Univ, Dept Risk Management & Insurance, Taipei, Taiwan.
 RP Yang, SS, Natl Cent Univ, Dept Finance, 300 Rd, Tao Yuan, Taiwan.
 EM syang@ncu.edu.tw
    jerry2@nccu.edu.tw
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 NR 38
 TC 2
 PU PALGRAVE MACMILLAN LTD
 PI BASINGSTOKE
 PA BRUNEL RD BLDG, HOUNDMILLS, BASINGSTOKE RG21 6XS, HANTS, ENGLAND
 SN 1018-5895
 J9 GENEVA PAP RISK INSUR-ISS PR
 JI Geneva Pap. Risk Insur.-Issues Pract.
 PD OCT
 PY 2009
 VL 34
 IS 4
 BP 660
 EP 681
 DI 10.1057/gpp.2009.18
 PG 22
 SC Business, Finance
 GA 515ME
 UT ISI:000271474800013
 ER
 
 PT J
 AU Zhao, ZM
    Sun, YX
    Hou, N
    Teng, Y
    Wang, YL
    Yang, X
 AF Zhao, Zengming
    Sun, Yanxun
    Hou, Ning
    Teng, Yan
    Wang, Youliang
    Yang, Xiao
 TI Capn8 Promoter Directs the Expression of Cre Recombinase in Gastric Pit
    Cells of Transgenic Mice
 SO GENESIS
 LA English
 DT Article
 DE gastric pit cell; gastric epithelium; Cre recombinase; transgenic
    mouse; calpain-8
 ID MOUSE STOMACH; EPITHELIAL-CELLS; PROGENITOR; SECRETION; DYNAMICS;
    CORPUS; LIVER; MODEL; CIS
 AB Gastric Pit cells are high-turnover epithelial cells of the gastric
    mucosa. They secrete mucus to protect the gastric epithelium from acid
    and pepsin. To investigate the genetic mechanisms underlying the
    physiological functions of gastric pit cells, we generated a transgenic
    mouse line, namely, Capn8-Cre, in which the expression of Cre
    recombinase was controlled by the promoter of the intracellular
    Ca2+-regulated cysteine protease calpain-8. To test the tissue
    distribution and excision activity of Cre recombinase, the Capn8-Cre
    transgenic mice were bred with the ROSA26 reporter strain and a mouse
    strain that carries Smad4 conditional alleles (Smad4(Co/Co)).
    Multiple-tissue PCR and LacZ staining demonstrated that Capn8-Cre
    transgenic mouse expressed Cre recombinase in the gastric pit cells.
    Cre recombinase activity was also detected in the liver and skin
    tissues. These data suggest that the Capn8-Cre mouse line described
    here could be used to dissect gene function in gastric pit cells.
    genesis 47:674-679, 2009. (C) 2009 Wiley-Liss, Inc.
 C1 [Zhao, Zengming; Sun, Yanxun; Hou, Ning; Teng, Yan; Wang, Youliang; Yang, Xiao] Inst Biotechnol, Genet Lab Dev & Dis, State Key Lab Prote, Beijing 100071, Peoples R China.
    [Yang, Xiao] Shanghai Jiao Tong Univ, Model Organism Div, E Inst, Shanghai Univ, Shanghai 200030, Peoples R China.
 RP Yang, X, Inst Biotechnol, Genet Lab Dev & Dis, State Key Lab Prote, 20
    Dongdajie, Beijing 100071, Peoples R China.
 EM yangx@nic.bmi.ac.cn
 FU Chinese National Key Program on Basic Research [2005CB522506,
    2006CB943501, 2006BA123B01-3]; Key Project for Drug Discoven and
    Development in China [20019ZX09501]; Key Project for Infections
    Diseases in China [2008ZX10002-016]; National Natural Science
    Foundation of China [30671077, 30430350]; Beijing Municipal Project
    [Z0006303041231]; E-Institutes of Shanghai Municipal Education
    Commission [F03003]
 FX Contract grant sponsor: Chinese National Key Program on Basic Research,
    Contract grant numbers: 2005CB522506, 2006CB943501, 2oo6BA123B01-3;
    Contract grant sponsor: Key Project for Drug Discoven and Development
    in China; Contract grant number: 20019ZX09501-027; Contract grant
    sponsor: Key Project for Infections Diseases in China, Contract grant
    number: 2008ZX10002-016; Contract giant sponsor: National Natural
    Science Foundation of China, Contract grant numbers: 30671077,
    30430350; Contract grant sponsor: Beijing Municipal Project, Contract
    grant number: Z0006303041231; Contract grant sponsor: E-Institutes of
    Shanghai Municipal Education Commission, Contract grant nurnher: F03003
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 NR 27
 TC 1
 PU WILEY-LISS
 PI HOBOKEN
 PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA
 SN 1526-954X
 J9 GENESIS
 JI Genesis
 PD OCT
 PY 2009
 VL 47
 IS 10
 BP 674
 EP 679
 DI 10.1002/dvg.20552
 PG 6
 SC Developmental Biology; Genetics & Heredity
 GA 516SM
 UT ISI:000271562900004
 ER
 
 PT J
 AU Huh, YH
    Ryu, JH
    Shin, S
    Lee, DU
    Yang, S
    Oh, KS
    Chun, CH
    Choi, JK
    Song, WK
    Chun, JS
 AF Huh, Yun Hyun
    Ryu, Je-Hwang
    Shin, Sun
    Lee, Dong-Uk
    Yang, Siyoung
    Oh, Kyung-Shin
    Chun, Churl-Hong
    Choi, Jeong-Keun
    Song, Woo Keun
    Chun, Jang-Soo
 TI Esophageal cancer related gene 4 (ECRG4) is a marker of articular
    chondrocyte differentiation and cartilage destruction
 SO GENE
 LA English
 DT Article
 DE Articular cartilage; Chondrocytes; Collagen II; ECRG4; Osteoarthritis
 ID II COLLAGEN EXPRESSION; GROWTH-FACTOR-I; MESENCHYMAL CELLS;
    CHONDROGENESIS; LIMB; OSTEOARTHRITIS; VITRO
 AB With the aim of identifying novel genes regulating cartilage
    development and degeneration, we screened a cartilage-specific
    expressed sequence tag database. Esophageal cancer related gene 4
    (ECRG4) was selected, based on the criteria of chondrocyte-specific'
    and 'unknown function.' ECRG4 expression was particularly abundant in
    chondrocytes and cartilage, compared to various other mouse tissues.
    ECRG4 is a secreted protein that undergoes cleavage after secretion.
    The protein is specifically expressed in chondrocytes in a manner
    dependent on differentiation status. The expression is very low in
    mesenchymal cells, and dramatically increased during chondrogenic
    differentiation. The ECRG4 level in differentiated chondrocytes is
    decreased during hypertrophic maturation, both in vitro and in vivo,
    and additionally in dedifferentiating chondrocytes induced by
    interleukin-1 beta or serial subculture, chondrocytes of human
    osteoarthritic cartilage and experimental mouse osteoarthritic
    cartilage. However, ectopic expression or exogenous ECRG4 treatment in
    a primary culture cell system does not affect chondrogenesis of
    mesenchymal cells, hypertrophic maturation of chondrocytes or
    dedifferentiation of differentiated chondrocytes. Additionally,
    cartilage development and organization of extracellular matrix are not
    affected in transgenic mice overexpressing ECRG4 in cartilage tissue.
    However, ectopic expression of ECRG4 reduced proliferation of primary
    culture chondrocytes. While the underlying mechanisms of ECRG4
    expression and specific roles remain to be elucidated in more detail,
    our results support its function as a marker of differentiated
    articular chondrocytes and cartilage destruction. (C) 2009 Elsevier
    B.V. All rights reserved.
 C1 [Huh, Yun Hyun; Ryu, Je-Hwang; Shin, Sun; Lee, Dong-Uk; Yang, Siyoung; Oh, Kyung-Shin; Choi, Jeong-Keun; Song, Woo Keun; Chun, Jang-Soo] Gwangju Inst Sci & Technol, Cell Dynam Res Ctr, Kwangju 500712, South Korea.
    [Huh, Yun Hyun; Ryu, Je-Hwang; Shin, Sun; Lee, Dong-Uk; Yang, Siyoung; Oh, Kyung-Shin; Choi, Jeong-Keun; Song, Woo Keun; Chun, Jang-Soo] Gwangju Inst Sci & Technol, BioImaging Res Ctr, Dept Life Sci, Kwangju 500712, South Korea.
    [Chun, Churl-Hong] Wonkwang Univ, Sch Med, Dept Orthopaed Surg, Iksan 570711, South Korea.
 RP Chun, JS, Gwangju Inst Sci & Technol, Cell Dynam Res Ctr, Kwangju
    500712, South Korea.
 EM jschun@gist.ac.kr
 FU Cell Dynamics Research Center, Korea Science and Engineering Foundation
    (KOSEF) [R11-2007-007-01001-0]; Korea Research Foundation
    [KRF-2006-312-C00611]
 FX This work was supported by grants from Cell Dynamics Research Center,
    Korea Science and Engineering Foundation (KOSEF R11-2007-007-01001-0)
    and Korea Research Foundation (KRF-2006-312-C00611).
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 TC 3
 PU ELSEVIER SCIENCE BV
 PI AMSTERDAM
 PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
 SN 0378-1119
 J9 GENE
 JI Gene
 PD DEC 1
 PY 2009
 VL 448
 IS 1
 BP 7
 EP 15
 DI 10.1016/j.gene.2009.08.015
 PG 9
 SC Genetics & Heredity
 GA 516SG
 UT ISI:000271562300002
 ER
 
 PT J
 AU Lai, RH
    Wang, MJ
    Yang, SH
    Chen, JY
 AF Lai, Rai-Hua
    Wang, Mei-Jung
    Yang, Shung-Haur
    Chen, Jeou-Yuan
 TI Genomic organization and functional characterization of the promoter
    for the human suppressor of cytokine signaling 6 gene
 SO GENE
 LA English
 DT Article
 DE SOCS6; Genomic structure; Promoter analysis; Promoter hypermethylation
 ID SQUAMOUS-CELL CARCINOMA; CYTOKINE SIGNALING-1; NEGATIVE REGULATOR;
    ABERRANT METHYLATION; COLORECTAL-CANCER; JAK/STAT PATHWAY;
    INSULIN-RECEPTOR; CHROMOSOME 18Q; GASTRIC-CANCER; OVARIAN-CANCER
 AB In this study, we report the expression and genomic structure of the
    gene encoding human suppressor of cytokine signaling 6 (SOCS5), and the
    characterization of the functional promoter region. The human SOCS6
    gene, spanning 40 kb on chromosome 18q22.2, is composed of two exons
    separated by an intron of 35 kb. Two transcripts are ubiquitously
    expressed, and both encode the full-length open reading frame of SOCS6.
    A primer extension assay revealed that the major transcription
    initiation site is located 469 bp upstream the ATG codon. Luciferase
    promoter analysis demonstrated that the 5'-flanking region is able to
    drive transcription, and the CpG-rich sequences near the transcription
    initiation site are important for the TATA-less SOCS6 promoter
    activity. Analogous to SOCS1 and SOCS3, which are down-regulated in
    several human cancers, SOCS6 is expressed at lower levels in carcinomas
    of stomach and colon. We demonstrated that hypermethylation of the
    SOCS6 promoter is one of the mechanisms for the epigenetic regulation
    of SOCS6 expression. Firstly, in vitro methylation of the reporter
    promoter plasmid significantly suppressed the promoter activity.
    Secondly, SOCS6 expression in vivo was enhanced by treating cells with
    a methyltransferase inhibitor. The SOCS6 gene from various species
    shares significant homology in amino acid sequences, transcription
    factor binding motifs in promoter regions and the two-exon genomic
    structure, suggesting that the SOCS6 gene is highly conserved. (C) 2009
    Elsevier B.V. All rights reserved.
 C1 [Lai, Rai-Hua] Natl Yang Ming Univ, Inst Pharmacol, Taipei 112, Taiwan.
    [Wang, Mei-Jung; Chen, Jeou-Yuan] Acad Sinica, Inst Biomed Sci, Taipei, Taiwan.
    [Yang, Shung-Haur] Taipei Vet Gen Hosp, Dept Surg, Taipei, Taiwan.
    [Chen, Jeou-Yuan] Natl Yang Ming Univ, Inst Genome Sci, Taipei 112, Taiwan.
 RP Chen, JY, 128 Sect,2 Acad Rd, Taipei 11529, Taiwan.
 EM bmchen@ibms.sinica.edu.tw
 FU National Science Council, Taiwan [95-2320-B-001-043-MY3]
 FX We thank Dr. C.-W. Wu (Department of Surgery, Taipei Veterans General
    Hospital, Taiwan) for providing primary gastric tumorous and
    non-tumorous tissues. This work was supported by a research grant
    (95-2320-B-001-043-MY3) to J.Y.C. from the National Science Council,
    Taiwan. We thank Dr. Y.-J. Chen (Institute of Genome Sciences, National
    Yang-Ming University) for providing the RP11-1461316 BAC clone.
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 NR 52
 TC 0
 PU ELSEVIER SCIENCE BV
 PI AMSTERDAM
 PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
 SN 0378-1119
 J9 GENE
 JI Gene
 PD DEC 1
 PY 2009
 VL 448
 IS 1
 BP 64
 EP 73
 DI 10.1016/j.gene.2009.07.022
 PG 10
 SC Genetics & Heredity
 GA 516SG
 UT ISI:000271562300008
 ER
 
 PT J
 AU Mizuno, S
    Kobayashi, M
    Tomita, S
    Miki, I
    Masuda, A
    Onoyama, M
    Habu, Y
    Inokuchi, H
    Watanabe, Y
 AF Mizuno, Shigeto
    Kobayashi, Masao
    Tomita, Shohken
    Miki, Ikuya
    Masuda, Atsuhiro
    Onoyama, Mitsuko
    Habu, Yasuki
    Inokuchi, Hideto
    Watanabe, Yoshiyuki
 TI Validation of the pepsinogen test method for gastric cancer screening
    using a follow-up study
 SO GASTRIC CANCER
 LA English
 DT Article
 DE Pepsinogen; Gastric cancer; Screening; Follow-up study
 ID SERUM PEPSINOGEN; STOMACH-CANCER; CELLULAR LOCALIZATION; ATROPHIC
    GASTRITIS; JAPAN; RISK; IMMUNOFLUORESCENCE; POPULATION; PROGRAM
 AB Serum pepsinogen (PG) measurement has been used for gastric cancer
    screening since the 1990s. However, there are no reports comparing the
    screening validity of the PG test method with that of conventional
    X-ray examination directly in the same population, using a follow-up
    study.
    From April 2000 to March 2001, 12 120 residents of Osaka Prefecture,
    who underwent opportunistic screening at a medical checkup organization
    in Osaka city (hereafter, "the organization"), were enrolled. They
    received both a barium meal examination and PG test simultaneously. All
    the participants were followed up for a 1-year period after the
    screening. For the participants advised to undergo endoscopic
    examination, the results of those who were examined at the organization
    were tallied. The other participants were checked using the Osaka
    Cancer Registry (hereafter, "the registry").
    Of the 12 120 participants, 493 (4.1%) were positive with the PG method
    and 728 (6.0%) were positive with the X-ray method. Fifty-four (0.4%)
    were positive for both methods. Thirteen gastric cancer cases were
    diagnosed by successive esophagogastroduodenoscopies at the
    organization. Six additional gastric cancer cases were identified by
    record linkage with the registry. The sensitivity, specificity, and
    positive predictive values of the PG method with a PGI cutoff level of
    a parts per thousand currency sign30 ng/ml and PGI/PGII ratio of a
    parts per thousand currency sign2.0 were 36.8%, 96.0%, and 1.4%,
    respectively. These values for the direct X-ray examination were 68.4%,
    94.1%, and 1.8%, respectively.
    The PG test method alone with a PGI cutoff level of a parts per
    thousand currency sign30 ng/ml and PGI/PGII a parts per thousand
    currency sign 2.0 is not appropriate for gastric cancer screening.
 C1 [Watanabe, Yoshiyuki] Kyoto Prefectural Univ Med, Grad Sch Med Sci, Dept Epidemiol Community Hlth & Med, Kamigyo Ku, Kyoto 6028566, Japan.
    [Mizuno, Shigeto; Miki, Ikuya; Masuda, Atsuhiro; Onoyama, Mitsuko] Kobe Pharmaceut Univ, Dept Med Pharmaceut, Kobe, Hyogo 658, Japan.
    [Kobayashi, Masao] Kyoto Second Red Cross Hosp, Dept Hlth Care, Kyoto, Japan.
    [Tomita, Shohken] Kansai Occupat Hlth Assoc, Osaka, Japan.
    [Habu, Yasuki] Saiseikai Noe Hosp, Dept Gastroenterol, Osaka, Japan.
    [Inokuchi, Hideto] Hyogo Canc Ctr, Dept Gastroenterol, Akashi, Hyogo, Japan.
 RP Watanabe, Y, Kyoto Prefectural Univ Med, Grad Sch Med Sci, Dept
    Epidemiol Community Hlth & Med, Kamigyo Ku, 465 Kajii Cho, Kyoto
    6028566, Japan.
 FU Ministry of Health, Labour and Welfare, Japan [H16-025]
 FX This work was supported in part by a Grant-in-Aid for Research from the
    Ministry of Health, Labour and Welfare, Japan (H16-025).
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 NR 30
 TC 1
 PU SPRINGER
 PI NEW YORK
 PA 233 SPRING ST, NEW YORK, NY 10013 USA
 SN 1436-3291
 J9 GASTRIC CANCER
 JI Gastric Cancer
 PD OCT
 PY 2009
 VL 12
 IS 3
 BP 158
 EP 163
 DI 10.1007/s10120-009-0522-y
 PG 6
 SC Oncology; Gastroenterology & Hepatology
 GA 515VX
 UT ISI:000271502100007
 ER
 
 PT J
 AU Krueger, B
    Haerteis, S
    Yang, LM
    Hartner, A
    Rauh, R
    Korbmacher, C
    Diakov, A
 AF Krueger, Bettina
    Haerteis, Silke
    Yang, Limin
    Hartner, Andrea
    Rauh, Robert
    Korbmacher, Christoph
    Diakov, Alexei
 TI Cholesterol Depletion of the Plasma Membrane Prevents Activation of the
    Epithelial Sodium Channel (ENaC) by SGK1
 SO CELLULAR PHYSIOLOGY AND BIOCHEMISTRY
 LA English
 DT Article
 DE Epithelial sodium channel (ENaC); Serum- and glucocorticoid-induced
    kinase isoform 1; Lipid raft; Methyl-beta-cyclodextrin; Cholesterol;
    Xenopus laevis oocytes
 ID TRANSMEMBRANE CONDUCTANCE REGULATOR; CELL-SURFACE EXPRESSION; LIPID
    RAFTS; CYSTIC-FIBROSIS; ION CHANNELS; NEDD4-2-DEPENDENT MECHANISM; OPEN
    PROBABILITY; APICAL MEMBRANE; XENOPUS-OOCYTES; SLIT DIAPHRAGM
 AB The lipid environment of the epithelial sodium channel (ENaC) and its
    possible association with so-called lipid rafts may be relevant to its
    function. The aim of our study was to confirm the association of ENaC
    with lipid rafts and to analyze the effect of cholesterol depletion of
    the plasma membrane by methyl-beta-cyclodextrin (M beta CD) on channel
    function and regulation. Using sucrose density gradient centrifugation
    we demonstrated that a significant portion of ENaC protein distributes
    to low density fractions thought to be typical lipid raft fractions.
    Importantly, cholesterol depletion of cell lysate by M beta CD shifted
    ENaC to non-raft fractions of higher density. Live cell imaging
    demonstrated that treatment with M beta CD largely reduced filipin
    staining over time, confirming cholesterol depletion of the plasma
    membrane. For electrophysiological studies intact oocytes were exposed
    to 20 mM M beta CD for three hours. M beta CD treatment had no
    consistent effect on baseline whole-cell ENaC currents. In addition to
    the typical single channel conductance of about 5 pS, subconductance
    states of ENaC were occasionally observed in patches from M beta CD
    treated but not from control oocytes. Importantly, in outside-out patch
    clamp recordings the stimulatory effect of recombinant SGK1 in the
    pipette solution was essentially abolished in oocytes pretreated with M
    beta CD. These results indicate that ENaC activation by cytosolic SGK1
    is compromised by removing cholesterol from the plasma membrane. Thus,
    ENaC activation by SGK1 may require the presence of an intact lipid
    environment and/or of lipid rafts as signalling platform. Copyright (C)
    2009 S. Karger AG, Basel
 C1 [Krueger, Bettina; Haerteis, Silke; Yang, Limin; Rauh, Robert; Korbmacher, Christoph; Diakov, Alexei] Univ Erlangen Nurnberg, Inst Zellulare & Mol Physiol, D-91054 Erlangen, Germany.
    [Hartner, Andrea] Univ Erlangen Nurnberg, Kinder & Jugendklin Univ Klinikums Erlangen, D-91054 Erlangen, Germany.
 RP Korbmacher, C, Univ Erlangen Nurnberg, Inst Zellulare & Mol Physiol,
    Waldstr 6, D-91054 Erlangen, Germany.
 EM christoph.korbmacher@physiologie2.med.uni-erlangen.de
 FU Deutsche Forschungsgemeinschaft [SFB423]; Johannes and Frieda Marohn
    Stiftung ; Elitenetwork Bavaria ; BioMedTec International Graduate
    School (BIGSS) ; Fritz Thyssen Foundation 
 FX The expert technical assistance of Ralf Rinke, Jessica Ott and Celine
    Harlay is gratefully acknowledged. We thank Johannes Loffing for his
    help with the characterization of the antibodies. This study was
    supported by grants of the Deutsche Forschungsgemeinschaft (SFB423:
    Kidney injury: Pathogenesis and Regenerative Mechanisms; project A12;
    C. K.), the Johannes and Frieda Marohn Stiftung (C. K.), an
    Elitenetwork Bavaria (ENB) fellowship (S. H.), and the BioMedTec
    International Graduate School (BIGSS) 'Lead Structures of Cell
    Function' of the ENB (S. H.), and by a travel grant to B. K. from the
    Fritz Thyssen Foundation.
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 NR 66
 TC 10
 PU KARGER
 PI BASEL
 PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND
 SN 1015-8987
 J9 CELL PHYSIOL BIOCHEM
 JI Cell. Physiol. Biochem.
 PY 2009
 VL 24
 IS 5-6
 BP 605
 EP 618
 DI 10.1159/000257516
 PG 14
 SC Cell Biology; Physiology
 GA 516IP
 UT ISI:000271535900029
 ER
 
 PT J
 AU Nishiyama, A
    Xin, L
    Sharov, AA
    Thomas, M
    Mowrer, G
    Meyers, E
    Piao, YL
    Mehta, S
    Yee, S
    Nakatake, Y
    Stagg, C
    Sharova, L
    Correa-Cerro, LS
    Bassey, U
    Hoang, H
    Kim, E
    Tapnio, R
    Qian, Y
    Dudekula, D
    Zalzman, M
    Li, MX
    Falco, G
    Yang, HT
    Lee, SL
    Monti, M
    Stanghellini, I
    Islam, MN
    Nagaraja, R
    Goldberg, I
    Wang, WD
    Longo, DL
    Schlessinger, D
    Ko, MSH
 AF Nishiyama, Akira
    Xin, Li
    Sharov, Alexei A.
    Thomas, Marshall
    Mowrer, Gregory
    Meyers, Emily
    Piao, Yulan
    Mehta, Samir
    Yee, Sarah
    Nakatake, Yuhki
    Stagg, Carole
    Sharova, Lioudmila
    Correa-Cerro, Lina S.
    Bassey, Uwem
    Hoang, Hien
    Kim, Eugene
    Tapnio, Richard
    Qian, Yong
    Dudekula, Dawood
    Zalzman, Michal
    Li, Manxiang
    Falco, Geppino
    Yang, Hsih-Te
    Lee, Sung-Lim
    Monti, Manuela
    Stanghellini, Ilaria
    Islam, Md. Nurul
    Nagaraja, Ramaiah
    Goldberg, Ilya
    Wang, Weidong
    Longo, Dan L.
    Schlessinger, David
    Ko, Minoru S. H.
 TI Uncovering Early Response of Gene Regulatory Networks in ESCs by
    Systematic Induction of Transcription Factors
 SO CELL STEM CELL
 LA English
 DT Article
 ID EMBRYONIC STEM-CELLS; GENOME-WIDE; DEVELOPMENTAL REGULATORS; SIGNALING
    PATHWAYS; MOUSE EMBRYOS; SELF-RENEWAL; PLURIPOTENCY; EXPRESSION;
    DIFFERENTIATION; CHROMATIN
 AB To examine transcription factor (TF) network(s), we created mouse ESC
    lines, in each of which 1 of 50 TFs tagged with a FLAG moiety is
    inserted into a ubiquitously controllable tetracycline-repressible
    locus. Of the 50 TFs, Cdx2 provoked the most extensive transcriptome
    perturbation in ESCs, followed by Esx1, Sox9, Tcf3, KIN, and Gata3.
    ChIP-Seq revealed that CDX2 binds to promoters of upregulated target
    genes. By contrast, genes downregulated by CDX2 did not show CDX2
    binding but were enriched with binding sites for POU5F1, SOX2, and
    NANOG. Genes with binding sites for these core TFs were also
    downregulated by the induction of at least 15 other TFs, suggesting a
    common initial step for ESC differentiation mediated by interference
    with the binding of core TFs to their target genes. These ESC lines
    provide a fundamental resource to study biological networks in ESCs and
    mice.
 C1 [Nishiyama, Akira; Xin, Li; Sharov, Alexei A.; Thomas, Marshall; Mowrer, Gregory; Meyers, Emily; Piao, Yulan; Mehta, Samir; Yee, Sarah; Nakatake, Yuhki; Stagg, Carole; Sharova, Lioudmila; Correa-Cerro, Lina S.; Bassey, Uwem; Hoang, Hien; Kim, Eugene; Tapnio, Richard; Qian, Yong; Dudekula, Dawood; Zalzman, Michal; Li, Manxiang; Falco, Geppino; Yang, Hsih-Te; Lee, Sung-Lim; Monti, Manuela; Stanghellini, Ilaria; Islam, Md. Nurul; Nagaraja, Ramaiah; Goldberg, Ilya; Wang, Weidong; Longo, Dan L.; Schlessinger, David; Ko, Minoru S. H.] NIA, NIH, Baltimore, MD 21224 USA.
 RP Ko, MSH, NIA, NIH, Baltimore, MD 21224 USA.
 EM kom@mail.nih.gov
 FU Intramural Research Program of the NIH, National Institute on Aging 
 FX We thank Dr. Hitoshi Niwa for providing the Tet-inducible vector system
    and some cDNA clones and for discussion. This research was supported
    entirely by the Intramural Research Program of the NIH, National
    Institute on Aging.
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 GA 514NP
 UT ISI:000271401900013
 ER
 
 PT J
 AU Oze, I
    Matsuo, K
    Suzuki, T
    Kawase, T
    Watanabe, M
    Hiraki, A
    Ito, H
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 AF Oze, Isao
    Matsuo, Keitaro
    Suzuki, Takeshi
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    Ozawa, Taijiro
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    Hasegawa, Yasuhisa
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    Tajima, Kazuo
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    Tanaka, Hideo
 TI Impact of Multiple Alcohol Dehydrogenase Gene Polymorphisms on Risk of
    Upper Aerodigestive Tract Cancers in a Japanese Population
 SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION
 LA English
 DT Article
 ID SQUAMOUS-CELL CARCINOMA; ALDEHYDE DEHYDROGENASES;
    ENVIRONMENTAL-FACTORS; ESOPHAGEAL CANCER; POOLED ANALYSIS; HEAVY
    DRINKERS; NECK-CANCER; ADH GENES; DRINKING; SMOKING
 AB Alcohol intake is positively associated with the risk of upper
    aerodigestive tract (UAT) cancer. The genes that encode
    alcohol-metabolizing enzymes, primarily alcohol dehydrogenases (ADH)
    and aldehyde dehydrogenases (ALDH), are polymorphic. In Caucasians,
    significant associations between polymorphisms in ADH1B (rs1229984) and
    ADH1C (rs698 and rs1693482), and UAT cancer have been observed, despite
    strong linkage disequilibrium among them. Moreover, UAT cancer was
    significantly associated with rs1573496 in ADH7, and not with rs1984362
    in ADH4. However, little evidence is available concerning ADH4 or ADH7
    polymorphisms in Asian populations. We conducted a matched case-control
    study to clarify the role of ADH polymorphisms in a Japanese
    population. Cases and controls were 585 patients with UAT cancer and
    1,170 noncancer outpatients. Geno-typing for ADHs and ALDH2 was done
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    were assessed by odds ratios and 95% confidence intervals using
    conditional logistic regression models that adjusted for age, sex,
    smoking, drinking, and ALDH2. Adjusted odds ratios were significant for
    rs4148887 and rs3805322 in ADH4, rs1229984 in ADH1B, rs698 and
    rs1693482 in ADH1C, and rs284787, rs1154460, and rs3737482 in ADH7. We
    also observed that ADH7 rs3737482 and ADH4 rs4148887 had independently
    and statistically significant effects on UAT cancer. The magnitude of
    effect of these ADH polymorphisms was greater in subjects who were
    heavy drinkers, heavy smokers, and had esophageal cancer. These
    findings show that multiple ADH gene polymorphisms were associated with
    UAT cancer in this Japanese population. Further studies in various
    ethnicities are required. (Cancer Epidemiol Biomarkers Prev
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 C1 [Matsuo, Keitaro] Aichi Canc Ctr, Div Epidemiol & Prevent, Res Inst, Chikusa Ku, Nagoya, Aichi 4648681, Japan.
    [Ozawa, Taijiro; Hasegawa, Yasuhisa] Cent Hosp, Aichi Canc Ctr, Dept Head Neck Surg, Nagoya, Aichi, Japan.
    [Hatooka, Shunzo; Shinoda, Masayuki] Cent Hosp, Aichi Canc Ctr, Dept Thorac Surg, Nagoya, Aichi, Japan.
    [Yatabe, Yasuhi] Cent Hosp, Aichi Canc Ctr, Dept Pathol & Mol Diagnost, Nagoya, Aichi, Japan.
    [Suzuki, Takeshi] Nagoya City Univ, Grad Sch Med Sci, Dept Med Oncol & Immunol, Nagoya, Aichi, Japan.
    [Hiraki, Akio] Okayama Univ, Ctr Hlth, Okayama, Japan.
    [Oze, Isao; Kiura, Katsuyuki; Tanimoto, Mitsune] Okayama Univ, Dept Hematol Oncol & Resp Med, Grad Sch Med Dent & Pharmaceut Sci, Okayama, Japan.
    [Matsuo, Keitaro; Tanaka, Hideo] Nagoya Univ, Dept Epidemiol, Grad Sch Med, Nagoya, Aichi 4648601, Japan.
 RP Matsuo, K, Aichi Canc Ctr, Div Epidemiol & Prevent, Res Inst, Chikusa
    Ku, 1-1 Kanokoden, Nagoya, Aichi 4648681, Japan.
 EM kmatsuo@aichi-cc.jp
 FU Ministry of Education, Science, Sports, Culture and Technology of Japan
    ; Ministry of Health, Labour and Welfare of Japan ; Foundation for
    Promotion of Cancer Research in Japan ; Uehara Memorial Foundation 
 FX Grant support: Grants-in-Aid for Scientific Research from the Ministry
    of Education, Science, Sports, Culture and Technology of Japan, for
    Cancer Research from the Ministry of Health, Labour and Welfare of
    Japan, and for the Third Term Comprehensive 10-year Strategy for Cancer
    Control from the Ministry of Health, Labour and Welfare of Japan, This
    study was also Supported in part by the Foundation for Promotion of
    Cancer Research in Japan and by a research grant from the Uehara
    Memorial Foundation. These grantors were not Involved in the study
    design, subject enrollment, study analysis or interpretation, or
    submission of the manuscript for this study
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 TC 4
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 PI PHILADELPHIA
 PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
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 PY 2009
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 UT ISI:000271562600043
 ER
 
 PT J
 AU Lorenzo, VF
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    Simonson, TS
    Nussenzveig, R
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    Prchal, JT
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 AF Lorenzo, Felipe, V
    Yang, Yingzhong
    Simonson, Tatum S.
    Nussenzveig, Roberto
    Jorde, Lynn B.
    Prchal, Josef T.
    Ge, Ri-Li
 TI Genetic adaptation to extreme hypoxia: Study of high-altitude pulmonary
    edema in a three-generation Han Chinese family
 SO BLOOD CELLS MOLECULES AND DISEASES
 LA English
 DT Article
 DE Hypoxia; Erythropoietin; High-altitude pulmonary edema (HAPE);
    Endothelial nitric oxide (eNOS); Hypoxia inducible factor (HIF)
 ID OXIDE SYNTHASE GENE; CHRONIC MOUNTAIN-SICKNESS; ASSOCIATION;
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 AB Organismal response to hypoxia is essential for critical regulation of
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    and cerebral edema. A significant population difference in response to
    hypoxia exist as many highland Tibetan, Ethiopian, and Andean natives
    developed adaptive mechanisms to extreme hypoxia. A proportion of
    non-adapted individuals exposed to high attitude develop pulmonary
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    polycythemia. The isolation of causative gene(s) responsible for HAPE
    and other extreme hypoxia complications would provide a rational basis
    for specific targeted therapy of HAPE, allow its targeted prevention
    for at-risk populations, and clarify the pathophysiology of other
    hypoxic maladaptations. The only suggested genetic linkage among
    unrelated individuals with HAPE has been with endothelial nitric oxide
    synthase (eNOS) gene. Here we describe a family with multiple members
    affected with HAPE in three generations. Families with multiple
    affected members with HAPE have not been described. We first ruled out
    linkage of HAPE with the eNOS gene. We then performed an analysis of
    the whole genome using high-density SNP arrays (Affymetrix v5.0) and,
    assuming a single gene causation of HAPE, ruled out linkage with 34
    other candidate genes. Only the HIF2A haplotype was shared by
    individuals who exhibit the HAPE phenotype, and work on its possible
    causative role in HAPE is in progress. The small size of our family
    does not provide sufficient power for a conclusive analysis of linkage.
    We hope that collaboration with other investigators with access to more
    HAPE patients will lead to the identification of gene(s) responsible
    for HAPE and possibly other maladaptive hypoxic complications. (C) 2009
    Elsevier Inc. All rights reserved.
 C1 [Lorenzo, Felipe, V; Yang, Yingzhong; Prchal, Josef T.] Univ Utah, Sch Med, Div Hematol, Salt Lake City, UT 84132 USA.
    [Yang, Yingzhong; Ge, Ri-Li] Qinghai Univ, Res Ctr High Attitude Med, Xining 810001, Qinghai, Peoples R China.
    [Simonson, Tatum S.; Jorde, Lynn B.] Univ Utah, Sch Med, Dept Human Genet, Salt Lake City, UT 84132 USA.
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 RP Prchal, JT, Univ Utah, Sch Med, Div Hematol, SOM 5C210,30 N 1900 E,
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 EM josef.prchal@hsc.utah.edu
    geriligao@hotmail.com
 FU NIH [R01 HL50077-11, GM-59290]
 FX The presented study was supported by R01 HL50077-11, VAH Merit review
    grant (JTP) NIH grant GM-59290 (LJ).
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 PI SAN DIEGO
 PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
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 UT ISI:000271484600001
 ER
 
 PT J
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    Liu, SX
    Yang, PY
    Han, CF
    Wang, JL
    Liu, J
    Han, YM
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 AF Zhang, Ting
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 SO BLOOD
 LA English
 DT Article
 ID REGULATORY DENDRITIC CELLS; BETA-CATENIN; EXTRACELLULAR-MATRIX; STROMAL
    CELLS; I INTERFERON; INTEGRINS; GENE; PHOSPHORYLATION; DIFFERENTIATION;
    MACROPHAGES
 AB Tissue microenvironment and stroma-derived extracellular matrix (ECM)
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    isolated ex vivo. Exogenous cytokines such as interleukin-12 (IL-12)
    and IL-15 are required to maintain the survival and activity of mouse
    NK cells cultured in vitro. Whether and how ECM molecules such as
    fibronectin can support the survival of NK cells remain unknown. We
    demonstrate that fibronectin, just like IL-15, can maintain survival of
    mouse NK cells in vitro. Furthermore, we show that fibronectin binds to
    the CD11b on NK cells, and then CD11b recruits and activates Src. Src
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    extracellular signal-related kinase (ERK) phosphorylation, resulting in
    the increased expression of antiapoptotic protein B-cell leukemia 2
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    NK cells is dramatically decreased in the beta-catenin-deficient mice.
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 C1 [Zhang, Ting; Wang, Jianli; Cao, Xuetao] Zhejiang Univ, Sch Med, Inst Immunol, Hangzhou 310058, Zhejiang, Peoples R China.
    [Zhang, Ting; Liu, Shuxun; Yang, Pengyuan; Han, Chaofeng; Liu, Juan; Han, Yanmei; Yu, Yizhi; Cao, Xuetao] Mil Med Coll 2, Natl Key Lab Med Immunol, Shanghai, Peoples R China.
    [Zhang, Ting; Liu, Shuxun; Yang, Pengyuan; Han, Chaofeng; Liu, Juan; Han, Yanmei; Yu, Yizhi; Cao, Xuetao] Mil Med Coll 2, Inst Immunol, Shanghai, Peoples R China.
 RP Cao, XT, Zhejiang Univ, Sch Med, Inst Immunol, Hangzhou 310058,
    Zhejiang, Peoples R China.
 EM caoxt@public3.sta.net.cn
 FU National Natural Science Foundation of China [30672386, 30572121,
    30721091]; National Key Basic Research Program of China [2007CB512403,
    2009CB522402]
 FX This work was supported by grants from the National Natural Science
    Foundation of China ( 30672386, 30572121, 30721091) and National Key
    Basic Research Program of China ( 2007CB512403, 2009CB522402).
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 NR 42
 TC 3
 PU AMER SOC HEMATOLOGY
 PI WASHINGTON
 PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
 SN 0006-4971
 J9 BLOOD
 JI Blood
 PD NOV 5
 PY 2009
 VL 114
 IS 19
 BP 4081
 EP 4088
 DI 10.1182/blood-2009-05-219881
 PG 8
 SC Hematology
 GA 515TJ
 UT ISI:000271495500020
 ER
 
 PT J
 AU Huang, SC
    Cho, A
    Norton, S
    Liu, ES
    Park, J
    Zhou, AY
    Munagala, ID
    Ou, AC
    Yang, G
    Wickrema, A
    Tang, TK
    Benz, EJ
 AF Huang, Shu-Ching
    Cho, Aeri
    Norton, Stephanie
    Liu, Eva S.
    Park, Jennie
    Zhou, Anyu
    Munagala, Indira D.
    Ou, Alexander C.
    Yang, Guang
    Wickrema, Amittha
    Tang, Tang K.
    Benz, Edward J., Jr.
 TI Coupled transcription-splicing regulation of mutually exclusive
    splicing events at the 5 ' exons of protein 4.1R gene
 SO BLOOD
 LA English
 DT Article
 ID PRE-MESSENGER-RNA; ALTERNATIVE 1ST EXONS; ERYTHROID-DIFFERENTIATION;
    POLYMERASE-II; MAMMALIAN-CELLS; PROMOTER USAGE; SR PROTEINS; SITE AG;
    IN-VIVO; EXPRESSION
 AB The tightly regulated production of distinct erythrocyte protein 4.1R
    isoforms involves differential splicing of 3 mutually exclusive first
    exons (1A, 1B, 1C) to the alternative 3' splice sites (ss) of exon
    2'/2. Here, we demonstrate that exon 1 and 2'/2 splicing diversity is
    regulated by a transcription-coupled splicing mechanism. We also
    implicate distinctive regulatory elements that promote the splicing of
    exon 1A to the distal 3' ss and exon 1B to the proximal 3' ss in murine
    erythroleukemia cells. A hybrid minigene driven by cytomegalovirus
    promoter mimicked 1B-promoter-driven splicing patterns but differed
    from 1A-promoter-driven splicing patterns, suggesting that promoter
    identity affects exon 2'/2 splicing. Furthermore, splicing factor
    SF2/ASF ultraviolet (UV) cross- linked to the exon 2'/2 junction
    CAGAGAA, a sequence that overlaps the distal U2AF35-binding 3'ss.
    Consequently, depletion of SF2/ASF allowed exon 1B to splice to the
    distal 3' ss but had no effect on exon 1A splicing. These findings
    identify for the first time that an SF2/ASF binding site also can serve
    as a 3' ss in a transcript-dependent manner. Taken together, our
    results suggest that 4.1R gene expression involves transcriptional
    regulation coupled with a complex splicing regulatory network. (Blood.
    2009; 114:4233-4242)
 C1 [Huang, Shu-Ching; Cho, Aeri; Norton, Stephanie; Liu, Eva S.; Park, Jennie; Zhou, Anyu; Munagala, Indira D.; Ou, Alexander C.; Yang, Guang; Benz, Edward J., Jr.] Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA.
    [Huang, Shu-Ching; Zhou, Anyu; Yang, Guang; Benz, Edward J., Jr.] Brigham & Womens Hosp, Dept Med, Boston, MA 02115 USA.
    [Wickrema, Amittha] Univ Chicago, Dept Med, Chicago, IL 60637 USA.
    [Tang, Tang K.] Acad Sinica, Inst Biomed Sci, Taipei, Taiwan.
    [Benz, Edward J., Jr.] Dana Farber Harvard Canc Ctr, Boston, MA USA.
    [Benz, Edward J., Jr.] Harvard Univ, Sch Med, Dept Pathol, Boston, MA 02115 USA.
    [Benz, Edward J., Jr.] Childrens Hosp, Dept Pediat, Boston, MA 02115 USA.
 RP Huang, SC, Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA.
 EM shu-ching_huang@dfci.harvard.edu
 FU National Institutes of Health [HL24385]
 FX We thank Shailja Pathania and David Livingston for assistance with the
    ChIP and ChRIP experiments, Karla Neugebauer for using modified Figures
    2A and 2C illustrating the ChIP and ChRIP procedures, and Woan- Yuh
    Tarn for helpful discussion.
    This study was supported by the National Institutes of Health grant
    HL24385 (to E.J.B.) and Claudia BarrAward (to S.C.H.).
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 NR 49
 TC 2
 PU AMER SOC HEMATOLOGY
 PI WASHINGTON
 PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
 SN 0006-4971
 J9 BLOOD
 JI Blood
 PD NOV 5
 PY 2009
 VL 114
 IS 19
 BP 4233
 EP 4242
 DI 10.1182/blood-2009-02-206219
 PG 10
 SC Hematology
 GA 515TJ
 UT ISI:000271495500036
 ER
 
 PT J
 AU Namkung, J
    Elston, RC
    Yang, JM
    Park, T
 AF Namkung, Junghyun
    Elston, Robert C.
    Yang, Jun-Mo
    Park, Taesung
 TI Identification of Gene-Gene Interactions in the Presence of Missing
    Data Using the Multifactor Dimensionality Reduction Method
 SO GENETIC EPIDEMIOLOGY
 LA English
 DT Article
 DE gene-gene interaction; multifactor dimensionality reduction; missing
    genotypes; association study
 ID COMPLEX TRAITS; EM ALGORITHM; SUSCEPTIBILITY; ASSOCIATION; EPISTASIS;
    POLYMORPHISMS; STRATEGIES; CANCER
 AB Gene-gene interaction is believed to play an important role in
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    imputation method that imputes missing genotypes as the most frequent
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    Available, uses all data available for the given loci to increase
    power. In any real data analysis, it is not clear which MDR approach
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 C1 [Park, Taesung] Seoul Natl Univ, Dept Stat, Seoul 151747, South Korea.
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 RP Park, T, Seoul Natl Univ, Dept Stat, Seoul 151747, South Korea.
 EM tspark@stats.snu.ac.kr
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 NR 23
 TC 3
 PU WILEY-LISS
 PI HOBOKEN
 PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA
 SN 0741-0395
 J9 GENET EPIDEMIOL
 JI Genet. Epidemiol.
 PD NOV
 PY 2009
 VL 33
 IS 7
 BP 646
 EP 656
 DI 10.1002/gepi.20416
 PG 11
 SC Genetics & Heredity; Public, Environmental & Occupational Health
 GA 514PB
 UT ISI:000271406100009
 ER
 
 PT J
 AU Yang, H
    Youm, YH
    Vandanmagsar, B
    Rood, J
    Kumar, KG
    Butler, AA
    Dixit, VD
 AF Yang, Hyunwon
    Youm, Yun-Hee
    Vandanmagsar, Bolormaa
    Rood, Jennifer
    Kumar, K. Ganesh
    Butler, Andrew A.
    Dixit, Vishwa Deep
 TI Obesity accelerates thymic aging
 SO BLOOD
 LA English
 DT Article
 ID PROINFLAMMATORY CYTOKINE EXPRESSION; CALORIC RESTRICTION;
    IMMUNE-SYSTEM; MELANOCORTIN-4 RECEPTOR; LIPID-METABOLISM;
    INFLUENZA-VIRUS; T-CELLS; MICE; LEPTIN; AGE
 AB As the expanding obese population grows older, their successful
    immunologic aging will be critical to enhancing the health span.
    Obesity increases risk of infections and cancer, suggesting adverse
    effects on immune surveillance. Here, we report that obesity
    compromises the mechanisms regulating T-cell generation by inducing
    premature thymic involution. Diet-induced obesity reduced thymocyte
    counts and significantly increased apoptosis of developing T-cell
    populations. Obesity accelerated the age-related reduction of T-cell
    receptor (TCR) excision circle bearing peripheral lymphocytes, an index
    of recently generated T cells from thymus. Consistent with reduced
    thymopoiesis, dietary obesity led to reduction in peripheral naive T
    cells with increased frequency of effector-memory cells. Defects in
    thymopoiesis in obese mice were related with decrease in the
    lymphoid-primed multipotent progenitor (Lin(-)Sca1(+)Kit(+) Flt3(+)) as
    well as common lymphoid progenitor (Lin(-)Sca1(+)CD117(lo)CD127(+))
    pools. The TCR spectratyping analysis showed that obesity compromised
    V-beta TCR repertoire diversity. Furthermore, the obesity induced by
    melanocortin 4 receptor deficiency also constricted the T-cell
    repertoire diversity, recapitulating the thymic defects observed with
    diet-induced obesity. In middle-aged humans, progressive adiposity with
    or without type 2 diabetes also compromised thymic output.
    Collectively, these findings establish that obesity constricts T-cell
    diversity by accelerating age-related thymic involution. (Blood. 2009;
    114: 3803-3812)
 C1 [Yang, Hyunwon; Youm, Yun-Hee; Vandanmagsar, Bolormaa; Dixit, Vishwa Deep] Louisiana State Univ Syst, Lab Neuroendocrine Immunol, Pennington Biomed Res Ctr, Baton Rouge, LA 70808 USA.
    [Rood, Jennifer] Louisiana State Univ Syst, Clin Chem Core, Pennington Biomed Res Ctr, Baton Rouge, LA 70808 USA.
    [Kumar, K. Ganesh; Butler, Andrew A.] Louisiana State Univ Syst, Neuropeptide Lab, Pennington Biomed Res Ctr, Baton Rouge, LA 70808 USA.
 RP Dixit, VD, Louisiana State Univ Syst, Lab Neuroendocrine Immunol,
    Pennington Biomed Res Ctr, 6400 Perkins Rd, Baton Rouge, LA 70808 USA.
 EM Vishwa.Dixit@pbrc.edu
 FU Coypu and Pennington Foundation ; National Institutes of Health (NIH)
    [1 P20 RR02/1945]; Pennington Center of Biomedical Research Excellence
    and Clinical Nutrition Research Unit [P30 DK072476]
 FX This work was supported in part by Coypu and Pennington Foundation
    grants (V. D. D.). The present work used the facilities of the Genomics
    and Cell Biology & Cell Imaging Core facilities supported by National
    Institutes of Health (NIH) grant 1 P20 RR02/1945 and Cell Biology and
    Bioimaging Core Facility of the Pennington Center of Biomedical
    Research Excellence and Clinical Nutrition Research Unit (NIH P30
    DK072476).
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 NR 57
 TC 11
 PU AMER SOC HEMATOLOGY
 PI WASHINGTON
 PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
 SN 0006-4971
 J9 BLOOD
 JI Blood
 PD OCT 29
 PY 2009
 VL 114
 IS 18
 BP 3803
 EP 3812
 DI 10.1182/blood-2009-03-213595
 PG 10
 SC Hematology
 GA 512RO
 UT ISI:000271268100015
 ER
 
 PT J
 AU Qian, JF
    Hong, S
    Wang, SQ
    Zhang, L
    Sun, LH
    Wang, M
    Yang, J
    Kwak, LW
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 AF Qian, Jianfei
    Hong, Sungyoul
    Wang, Siqing
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    Yang, Jing
    Kwak, Larry W.
    Hou, Jian
    Yi, Qing
 TI Myeloma cell line-derived, pooled heat shock proteins as a universal
    vaccine for immunotherapy of multiple myeloma
 SO BLOOD
 LA English
 DT Article
 ID METASTATIC MELANOMA PATIENTS; CYTOTOXIC T-LYMPHOCYTES; TUMOR-SPECIFIC
    IMMUNITY; PEPTIDE COMPLEXES; REGULATORY CELLS; IN-VIVO; CPG
    OLIGODEOXYNUCLEOTIDES; CANCER-IMMUNOTHERAPY; CD8-T-CELL MEMORY;
    ADJUVANT ACTIVITY
 AB Tumor cell-derived heat shock proteins are used as vaccines for
    immunotherapy of cancer patients. However, current approaches require
    the generation of custom-made products and are clinically ineffective.
    To improve the applicability of heat shock protein-based immunotherapy
    in cancers and to enhance clinical efficacy, we explored combinational
    treatments in a myeloma setting using pooled heterogeneous or
    allogeneic myeloma cell line-derived glycoprotein 96 (gp96) as
    universal vaccines, and clearly demonstrated that pooled but not single
    gp96 from heterogeneous or allogeneic myeloma cell lines was as
    effective as autologous gp96 in protecting mice from tumor challenge
    and re-challenge and in treating established myeloma. We showed that
    interferon gamma and CD4(+) and CD8(+) T cells were required for
    gp96-induced antimyeloma responses and that pooled gp96 induced broader
    immune responses that protected mice from developing different myeloma.
    Furthermore, pooled gp96 plus CpG in combination with anti-B7H1 or
    anti-interleukin-10 monoclonal anti-bodies were effective in treating
    mice with large tumor burdens. Thus, this study strongly suggests that
    pooled gp96 vaccines from myeloma cell lines can replace gp96 vaccines
    from autologous tumors for immunotherapy and induce immune responses
    against broader tumor antigens that may protect against tumor
    recurrence and development of unrelated tumors in vaccinated myeloma
    patients. (Blood. 2009; 114: 3880-3889)
 C1 [Qian, Jianfei; Hong, Sungyoul; Wang, Siqing; Zhang, Liang; Sun, Luhong; Wang, Michael; Yang, Jing; Kwak, Larry W.; Yi, Qing] Univ Texas MD Anderson Canc Ctr, Div Canc Med, Dept Lymphoma & Myeloma, Houston, TX 77030 USA.
    [Qian, Jianfei; Hong, Sungyoul; Wang, Siqing; Zhang, Liang; Sun, Luhong; Wang, Michael; Yang, Jing; Kwak, Larry W.; Yi, Qing] MD Anderson Canc Ctr, Ctr Canc Immunol Res, Houston, TX 77030 USA.
    [Hou, Jian] Shanghai Chang Zheng Hosp, Dept Hematol, Shanghai, Peoples R China.
 RP Yi, Q, MD Anderson Canc Ctr, Dept Lymphoma & Myeloma, 1515 Holcombe
    Blvd,Unit 0903, Houston, TX 77030 USA.
 EM houjian@medmail.com.cn
    qyi@mdanderson.org
 FU University of Texas M. D. Anderson Cancer Center ; National Cancer
    Institute [R01 CA96569, R01 CA103978, R01 CA138402]; Leukemia &
    Lymphoma Society ; Multiple Myeloma Research Foundation ; Commonwealth
    Foundation for Cancer Research ; National Natural Science Foundation of
    China [30828017]
 FX This work was supported by institutional start-up funds from the
    University of Texas M. D. Anderson Cancer Center, grants from the
    National Cancer Institute (R01 CA96569, R01 CA103978, and R01
    CA138402), the Leukemia & Lymphoma Society, Multiple Myeloma Research
    Foundation, Commonwealth Foundation for Cancer Research, and the
    National Natural Science Foundation of China (no. 30828017).
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 NR 58
 TC 5
 PU AMER SOC HEMATOLOGY
 PI WASHINGTON
 PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
 SN 0006-4971
 J9 BLOOD
 JI Blood
 PD OCT 29
 PY 2009
 VL 114
 IS 18
 BP 3880
 EP 3889
 DI 10.1182/blood-2009-06-227355
 PG 10
 SC Hematology
 GA 512RO
 UT ISI:000271268100023
 ER
 
 PT J
 AU Yang, Y
    Liu, JH
    Mao, HH
    Hu, YA
    Yan, Y
    Zhao, CJ
 AF Yang, Yang
    Liu, Junhua
    Mao, Huihua
    Hu, Yu-An
    Yan, Yan
    Zhao, Chunjie
 TI The expression pattern of Follistatin-like 1 in mouse central nervous
    system development
 SO GENE EXPRESSION PATTERNS
 LA English
 DT Article
 DE Follistatin-like 1; Follistatin; Telencephalon; Cortex; Hippocampus;
    Cortical hem; Diencephalon; Midbrain; Cerebellum; Spinal cord;
    Expression pattern; Mouse
 ID OCC1 MESSENGER-RNA; VISUAL-CORTEX; MACAQUES; PROTEIN; CLONING; GENE;
    LINE
 AB Follistatin-like 1 (Fstl1), also named TSC-36 (TGF-beta-stimulated
    clone 36), was first cloned from the mouse osteoblastic MC3T3-E1 cell
    line and can be up-regulated by TGF-beta. To better study the function
    of Fstl1 during the development of the mouse central nervous system
    (CNS), we examined Fstl1 expression in the developing mouse CNS, in
    detail, by in situ hybridization Our results show that Fstl1 is
    strongly expressed in the telencephalon, diencephalon, brainstem,
    limbic system and spinal cord. In the telencephalon, Fstl1 positive
    cells are mainly located in the ventricular zone (VZ) and the
    subventricular zone (SVZ); a relatively weak signal was observed in
    layers II and III of the neocortex at postnatal stages. Fstl1
    expression is robust in the developing hippocampus and persists to P20.
    In the developing diencephalon and hindbrain. abundant Fstl1 signals
    were also detected in nuclei including the medial habenular nucleus,
    the medial dorsal nucleus, the cochlear nuclei and so on In addition, a
    strong expression of Fstl1 was detected in the thalamencephalic signal
    center, as well as in the olfactory cortex from E14.5 to P0. Meanwhile,
    Fstl1 was expressed in the septal area and the cingulate gyrus of the
    limbic system after birth. A high level of expression was also observed
    in the ventral horn of the spinal cord. These results indicate that
    Fstl1 may play an important role during CNS development in the mouse.
    (C) 2009 Elsevier B.V. All rights reserved.
 C1 [Yang, Yang; Liu, Junhua; Mao, Huihua; Hu, Yu-An; Yan, Yan; Zhao, Chunjie] Southeast Univ, Key Lab Dev Genes & Human Dis, MOE, Sch Med, Nanjing 210009, Jiangsu, Peoples R China.
    [Yang, Yang; Liu, Junhua; Mao, Huihua; Hu, Yu-An; Yan, Yan; Zhao, Chunjie] Southeast Univ, Inst Brain Sci, Sch Med, Nanjing 210009, Jiangsu, Peoples R China.
    [Hu, Yu-An] Jinling Hosp, Inst Lab Med, Nanjing 210002, Peoples R China.
 RP Zhao, CJ, Southeast Univ, Key Lab Dev Genes & Human Dis, MOE, Sch Med,
    87 Dingjiaoqiao Rd, Nanjing 210009, Jiangsu, Peoples R China.
 FU National Nature Science Foundation of China [30525017, 30770696];
    Ministry of Science and Technology of China [2007CB512303]
 FX We thank Yiquan Wei, Li Liu and Xiaoxuan Lu for technical assistance,
    as well as Yiping Li and other members in the laboratory for valuable
    discussions. This work was supported by funds 30525017, 30770696 from
    The National Nature Science Foundation of China and The National Basic
    Research Program of China 2007CB512303 from The Ministry of Science and
    Technology of China to C.Z.
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 NR 10
 TC 1
 PU ELSEVIER SCIENCE BV
 PI AMSTERDAM
 PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
 SN 1567-133X
 J9 GENE EXPR PATTERNS
 JI Gene Expr. Patterns
 PD OCT
 PY 2009
 VL 9
 IS 7
 BP 532
 EP 540
 DI 10.1016/j.gep.2009.07.001
 PG 9
 SC Developmental Biology; Genetics & Heredity
 GA 510NF
 UT ISI:000271094600010
 ER
 
 PT J
 AU Yang, XJ
    Feng, M
    Jiang, X
    Wu, ZL
    Li, ZM
    Aau, MY
    Yu, Q
 AF Yang, Xiaojing
    Feng, Min
    Jiang, Xia
    Wu, Zhenlong
    Li, Zhimei
    Aau, Meiyee
    Yu, Qiang
 TI miR-449a and miR-449b are direct transcriptional targets of E2F1 and
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    targeting CDK6 and CDC25A
 SO GENES & DEVELOPMENT
 LA English
 DT Article
 DE CDC25A; CDK6; DZNep; E2F1; miR-449
 ID EMBRYONIC STEM-CELLS; MICRORNA TARGETS; CANCER; EXPRESSION; APOPTOSIS;
    GENOME; METHYLATION; SIGNATURE; GENES; PLURIPOTENT
 AB The Rb-E2F pathway drives cell cycle progression and cell
    proliferation, and the molecular strategies safeguarding its activity
    are not fully understood. Here we report that E2F1 directly
    transactivates miR-449a/b. miR-449a/b targets and inhibits oncogenic
    CDK6 and CDC25A, resulting in pRb dephosphorylation and cell cycle
    arrest at G1 phase, revealing a negative feedback regulation of the
    pRb-E2F1 pathway. Moreover, miR-449a/b expression in cancer cells is
    epigenetically repressed through histone H3 Lys27 trimethylation, and
    epigenetic drug treatment targeting histone methylation results in
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    function of miR-449a/b through regulating Rb/E2F1 activity, and
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    epigenetic event contributes to E2F1 deregulation and unrestricted
    proliferation in human cancer.
 C1 [Yang, Xiaojing; Feng, Min; Jiang, Xia; Wu, Zhenlong; Li, Zhimei; Aau, Meiyee; Yu, Qiang] ASTAR, Genome Inst Singapore, Singapore 138672, Singapore.
    [Yu, Qiang] Natl Univ Singapore, Dept Physiol, Yong Loo Lin Sch Med, Singapore 117597, Singapore.
 RP Yu, Q, ASTAR, Genome Inst Singapore, Singapore 138672, Singapore.
 EM yuq@gis.a-star.edu.sg
 FU Agency for Science, Technology, and Research (A<SUP>star</SUP>Star) of
    Singapore 
 FX We thank Dr. Kristian Helin for the ER-E2F1 plasmids. This work was
    supported by Agency for Science, Technology, and Research
    (A<SUP>star</SUP>Star) of Singapore.
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 NR 36
 TC 19
 PU COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT
 PI WOODBURY
 PA 500 SUNNYSIDE BLVD, WOODBURY, NY 11797-2924 USA
 SN 0890-9369
 J9 GENE DEVELOP
 JI Genes Dev.
 PD OCT 15
 PY 2009
 VL 23
 IS 20
 BP 2388
 EP 2393
 DI 10.1101/gad.1819009
 PG 6
 SC Cell Biology; Developmental Biology; Genetics & Heredity
 GA 507JP
 UT ISI:000270849700006
 ER
 
 PT J
 AU Tysome, JR
    Briat, A
    Alusi, G
    Cao, F
    Gao, D
    Yu, J
    Wang, P
    Yang, S
    Dong, Z
    Wang, S
    Deng, L
    Francis, J
    Timiryasova, T
    Fodor, I
    Lemoine, NR
    Wang, Y
 AF Tysome, J. R.
    Briat, A.
    Alusi, G.
    Cao, F.
    Gao, D.
    Yu, J.
    Wang, P.
    Yang, S.
    Dong, Z.
    Wang, S.
    Deng, L.
    Francis, J.
    Timiryasova, T.
    Fodor, I.
    Lemoine, N. R.
    Wang, Y.
 TI Lister strain of vaccinia virus armed with endostatin-angiostatin
    fusion gene as a novel therapeutic agent for human pancreatic cancer
 SO GENE THERAPY
 LA English
 DT Article
 DE human pancreatic cancer; adenovirus; vaccinia virus; angiogenesis;
    endostatin; angiostatin
 ID PHASE-II TRIAL; SMALLPOX VACCINATION; THYMIDINE KINASE; BLADDER-CANCER;
    GM-CSF; MICE; TUMORS; ANGIOGENESIS; GEMCITABINE; ADENOVIRUS
 AB Survival after pancreatic cancer remains poor despite incremental
    advances in surgical and adjuvant therapy, and new strategies for
    treatment are needed. Oncolytic virotherapy is an attractive approach
    for cancer treatment. In this study, we have evaluated the
    effectiveness of the Lister vaccine strain of vaccinia virus armed with
    the endostatin-angiostatin fusion gene (VVhEA) as a novel therapeutic
    approach for pancreatic cancer. The Lister vaccine strain of vaccinia
    virus was effective against all human pancreatic carcinoma cells tested
    in vitro, especially those insensitive to oncolytic adenovirus. The
    virus displayed inherently high selectivity for cancer cells, sparing
    normal cells both in vitro and in vivo, with effective infection of
    tumors after both intravenous (i.v.) and intratumoral (i.t.)
    administrations. The expression of the endostatin-angiostatin fusion
    protein was confirmed in a pancreatic cancer model both in vitro and in
    vivo, with evidence of inhibition of angiogenesis. This novel vaccinia
    virus showed significant antitumor potency in vivo against the Suit-2
    model by i.t. administration. This study suggests that the novel Lister
    strain of vaccinia virus armed with the endostatin-angiostatin fusion
    gene is a potential therapeutic agent for pancreatic cancer. Gene
    Therapy (2009) 16, 1223-1233; doi: 10.1038/gt.2009.74; published online
    9 July 2009
 C1 [Tysome, J. R.; Briat, A.; Alusi, G.; Francis, J.; Lemoine, N. R.; Wang, Y.] Barts & London Queen Marys Sch Med & Dent, Inst Canc, Ctr Mol Oncol & Imaging, London EC1 6BQ, England.
    [Cao, F.; Gao, D.; Yu, J.; Wang, P.; Yang, S.; Dong, Z.; Lemoine, N. R.; Wang, Y.] Zhengzhou Univ, Dept Pathol, Sino British Res Ctr Mol Oncol, Zhengzhou, Peoples R China.
    [Wang, S.; Deng, L.] Chinese Acad Sci, Inst Biophys, Ctr Infect & Immun, Natl Lab Biomacromol, Beijing 100080, Peoples R China.
    [Timiryasova, T.; Fodor, I.] Loma Linda Univ, Ctr Hlth Dispar & Mol Med, Loma Linda, CA 92350 USA.
 RP Lemoine, NR, Barts & London Queen Marys Sch Med & Dent, Inst Canc, Ctr
    Mol Oncol & Imaging, Charterhouse Sq, London EC1 6BQ, England.
 EM director@qmcr.qmul.ac.uk
    yaohe.wang@qmul.ac.uk
 FU Cancer Research UK [C633A6253/A6251]; Nature Sciences Foundation of
    China [30530800]; Royal College of Surgeons of England ; Barts and The
    London Research Advisory Board ; US Army/National Medical Technology
    Testbed Inc 
 FX This project is supported by Cancer Research UK (C633A6253/A6251),
    Nature Sciences Foundation of China (30530800) and The Royal College of
    Surgeons of England (JT) and Barts and The London Research Advisory
    Board. IF was sponsored by the US Army/National Medical Technology
    Testbed Inc. We appreciate the critical and insightful comments from Dr
    Gunnel Hallden. We are grateful to Mr John Overton for his pilot
    experiments in vitro. We also appreciate Vipul Bhakta, Keyur Trivedi
    and Mohamed Ikram for IHC staining.
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 NR 56
 TC 8
 PU NATURE PUBLISHING GROUP
 PI LONDON
 PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
 SN 0969-7128
 J9 GENE THERAPY
 JI Gene Ther.
 PD OCT
 PY 2009
 VL 16
 IS 10
 BP 1223
 EP 1233
 DI 10.1038/gt.2009.74
 PG 11
 SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology;
    Genetics & Heredity; Medicine, Research & Experimental
 GA 508LW
 UT ISI:000270933900007
 ER
 
 PT J
 AU Zhou, Y
    Zhang, JY
    Zheng, RQ
    Yu, BG
    Yang, G
 AF Zhou, Yan
    Zhang, Jia-Yong
    Zheng, Rong-Quan
    Yu, Bao-Gen
    Yang, Guang
 TI Complete nucleotide sequence and gene organization of the mitochondrial
    genome of Paa spinosa (Anura: Ranoidae)
 SO GENE
 LA English
 DT Article
 DE Paa spinosa; Mitochondrial genome; Tandem duplication of tRNA-Met gene;
    Phylogenetic tree
 ID TRANSFER-RNA GENES; PHYLOGENETIC-RELATIONSHIPS; EVOLUTIONARY
    IMPLICATIONS; LIVING AMPHIBIANS; RANID FROGS; FAMILY RHACOPHORIDAE;
    LARVAL CHARACTERS; SOUTHERN AFRICA; DNA-SEQUENCES; TREE FROG
 AB The mt genome of Paa spinosa (Anura: Ranoidae) is a circular molecule
    of 18,012 by in length, containing 38 genes (including an extra copy of
    tRNA-Met gene). This mt genome is characterized by three distinctive
    features: a cluster of rearranged tRNA genes (LTPF tRNA gene cluster),
    a tandem duplication of tRNA-Met gene (Met1 and Met2), and distinct
    repeat regions at both 5' and 3'-sides in the control region. Comparing
    the locations and the sequences of all tRNA-Met genes among Ranoidae,
    and constructing NJ tree of the nucleotide of those tRNA-Met genes, we
    suggested a tandem duplication of tRNA-Met gene can be regarded as a
    synapomorphy of Dicroglossinae. To further investigate the phylogenetic
    relationships of anurans. phylogenetic analyses (BI, ML and MP) based
    on the nucleotide dataset and the corresponding amino acid dataset of
    11 protein-coding genes (except ND5 and ATP8) arrived at the similar
    topology. (C) 2009 Elsevier B.V. All rights reserved.
 C1 [Zhou, Yan; Zhang, Jia-Yong; Zheng, Rong-Quan; Yu, Bao-Gen] Zhejiang Normal Univ, Inst Ecol, Jinhua 321004, Zhejiang, Peoples R China.
    [Yang, Guang] Nanjing Normal Univ, Coll Life Sci, Jiangsu Key Lab Biodivers & Biotechnol, Nanjing 210046, Peoples R China.
 RP Zheng, RQ, Zhejiang Normal Univ, Inst Ecol, Jinhua 321004, Zhejiang,
    Peoples R China.
 EM zhengrq@zjnu.cn
 FU Science Technology Commission of Zhejiang Province of China [2006022031]
 FX We thank Xu Shixia and Zhou Yan for their assistance in the laboratory
    work. This research was supported by the Science Technology Commission
    of Zhejiang Province of China (No. 2006022031) to Zheng.
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 NR 79
 TC 2
 PU ELSEVIER SCIENCE BV
 PI AMSTERDAM
 PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
 SN 0378-1119
 J9 GENE
 JI Gene
 PD NOV 15
 PY 2009
 VL 447
 IS 2
 BP 86
 EP 96
 DI 10.1016/j.gene.2009.07.009
 PG 11
 SC Genetics & Heredity
 GA 506LF
 UT ISI:000270775600003
 ER
 
 PT J
 AU Junge, HJ
    Yang, S
    Burton, JB
    Paes, K
    Shu, X
    French, DM
    Costa, M
    Rice, DS
    Ye, WL
 AF Junge, Harald J.
    Yang, Stacey
    Burton, Jeremy B.
    Paes, Kim
    Shu, Xiao
    French, Dorothy M.
    Costa, Mike
    Rice, Dennis S.
    Ye, Weilan
 TI TSPAN12 Regulates Retinal Vascular Development by Promoting Norrin- but
    Not Wnt-Induced FZD4/beta-Catenin Signaling
 SO CELL
 LA English
 DT Article
 ID FAMILIAL EXUDATIVE VITREORETINOPATHY; CATENIN PATHWAY; DISEASE GENE;
    ANGIOGENESIS; MUTATIONS; EXPRESSION; RECEPTORS; EVOLUTION; OLIGOMERS;
    ACTIVATE
 AB Mutations in the genes encoding the Wnt receptor Frizzled-4 (FZD4),
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    expressed in the retinal vasculature, and loss of Tspan12 phenocopies
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    Tspan12 genetically interacts with Norrin or Lrp5. Overexpressed
    TSPAN12 associates with the Norrin-receptor complex and significantly
    increases Norrin/beta-catenin but not Wnt/beta-catenin signaling,
    whereas Tspan12 siRNA abolishes transcriptional responses to Norrin but
    not Wnt3A in retinal endothelial cells. Signaling defects caused by
    Norrin or FZD4 mutations that are predicted to impair receptor
    multimerization are rescued by overexpression of TSPAN12. Our data
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    multimerization of FZD4 and its associated proteins to elicit
    physiological levels of signaling.
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 RP Ye, WL, Genentech Inc, Tumor Biol & Angiogenesis Dept, 1 DNA Way, San
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 EM loni@gene.com
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 NR 33
 TC 24
 PU CELL PRESS
 PI CAMBRIDGE
 PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
 SN 0092-8674
 J9 CELL
 JI Cell
 PD OCT 16
 PY 2009
 VL 139
 IS 2
 BP 299
 EP 311
 DI 10.1016/j.cell.2009.07.048
 PG 13
 SC Biochemistry & Molecular Biology; Cell Biology
 GA 507MI
 UT ISI:000270857500014
 ER
 
 PT J
 AU Zheng, YH
    Cai, Z
    Wang, SQ
    Zhang, X
    Qian, JF
    Hong, S
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 AF Zheng, Yuhuan
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    Wang, Siqing
    Zhang, Xiang
    Qian, Jianfei
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    Li, Haiyan
    Wang, Michael
    Yang, Jing
    Yi, Qing
 TI Macrophages are an abundant component of myeloma microenvironment and
    protect myeloma cells from chemotherapy drug-induced apoptosis
 SO BLOOD
 LA English
 DT Article
 ID MULTIPLE-MYELOMA; DENDRITIC CELLS
 AB Multiple myeloma remains an incurable disease. One of the major
    problems is that myeloma cells develop drug resistance on interaction
    with bone marrow stromal cells. In this study, we examined the effects
    of macrophages (M phi s), a type of stromal cells, on myeloma cell
    survival and response to chemotherapy. We showed that M phi, in
    particular tumor-associated M phi, is a protector of myeloma cells. The
    protective effect was dependent on direct contact between M phi s and
    myeloma cells. M phi s protected both myeloma cell lines and primary
    myeloma cells from spontaneous and chemotherapy drug-induced apoptosis
    by attenuating the activation and cleavage of caspase-dependent
    apoptotic signaling. These findings are clinically relevant because we
    found that CD68(+) M phi s heavily infiltrate the bone marrow of
    patients with myeloma but not the bone marrow of control patients.
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    survival and resistance to chemotherapeutic treatment in vivo. (Blood.
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 C1 [Zheng, Yuhuan; Cai, Zhen; Wang, Siqing; Zhang, Xiang; Qian, Jianfei; Hong, Sungyoul; Li, Haiyan; Wang, Michael; Yang, Jing; Yi, Qing] Univ Texas MD Anderson Canc Ctr, Dept Lymphoma & Myeloma, Div Canc Med, Ctr Canc Immunol Res, Houston, TX 77030 USA.
    [Cai, Zhen] Zhejiang Univ, Dept Hematol, Affiliated Hosp 1, Hangzhou, Zhejiang, Peoples R China.
 RP Zheng, YH, Univ Texas MD Anderson Canc Ctr, Dept Lymphoma & Myeloma,
    Div Canc Med, Ctr Canc Immunol Res, 1515 Holcombe Blvd,Unit 0903,
    Houston, TX 77030 USA.
 EM qyi@mdanderson.org
 FU National Cancer Institute [R01 CA96569, R01 CA103978, CA138402];
    Leukemia & Lymphoma Society Translational Research ; Multiple Myeloma
    Research Foundation ; Commonwealth Foundation for Cancer Research 
 FX This work was supported by the National Cancer Institute (grants R01
    CA96569, R01 CA103978, and CA138402), the Leukemia & Lymphoma Society
    Translational Research Grant, Multiple Myeloma Research Foundation, and
    Commonwealth Foundation for Cancer Research.
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 NR 10
 TC 6
 PU AMER SOC HEMATOLOGY
 PI WASHINGTON
 PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
 SN 0006-4971
 J9 BLOOD
 JI Blood
 PD OCT 22
 PY 2009
 VL 114
 IS 17
 BP 3625
 EP 3628
 DI 10.1182/blood-2009-05-220285
 PG 4
 SC Hematology
 GA 509NK
 UT ISI:000271024500016
 ER
 
 PT J
 AU Zhang, XY
    Meng, ZJ
    Qiu, S
    Xu, Y
    Yang, DL
    Schlaak, JF
    Roggendorf, M
    Lu, MJ
 AF Zhang, Xiaoyong
    Meng, Zhongji
    Qiu, Song
    Xu, Yang
    Yang, Dongliang
    Schlaak, Joerg F.
    Roggendorf, Michael
    Lu, Mengji
 TI Lipopolysaccharide-induced innate immune responses in primary
    hepatocytes downregulates woodchuck hepatitis virus replication via
    interferon-independent pathways
 SO CELLULAR MICROBIOLOGY
 LA English
 DT Article
 ID PERIPHERAL-BLOOD LYMPHOCYTES; TOLL-LIKE RECEPTORS; KAPPA-B ACTIVATION;
    GENE-EXPRESSION; IN-VIVO; SIGNALING PATHWAYS; MONONUCLEAR-CELLS; VIRAL
    CLEARANCE; INFECTION; LIVER
 AB P>Our previous studies have shown that Toll-like receptor (TLR)
    ligands, Poly I:C and lipopolysaccharide (LPS), are able to activate
    non-parenchymal liver cells and trigger the production of interferon
    (IFN) to inhibit hepatitis B virus replication in vivo and in vitro.
    However, little is known about TLR-mediated cellular responses in
    primary hepatocytes. By the model of woodchuck hepatitis virus (WHV)
    infected primary woodchuck hepatocytes (PWHs), Poly I:C and LPS
    stimulation resulted in upregulation of cellular antiviral genes and
    relevant TLRs mRNA expression respectively. LPS stimulation led to a
    pronounced reduction of WHV replicative intermediates without a
    significant IFN induction. Poly I:C transfection resulted in the
    production of IFN and a highly increased expression of antiviral genes
    in PWHs and slight inhibitory effect on WHV replication. LPS could
    activate nuclear factor kappa B, MAPK and PI-3k/Akt pathways in PWHs.
    Further, inhibitors of MAPK-ERK and PI-3k/Akt pathways, but not that of
    IFN signalling pathway, were able to block the antiviral effect of LPS.
    These results indicate that IFN- independent pathways which activated
    by LPS are able to downregulate hepadnaviral replication in hepatocytes.
 C1 [Zhang, Xiaoyong; Meng, Zhongji; Roggendorf, Michael; Lu, Mengji] Univ Hosp Essen, Inst Virol, Essen, Germany.
    [Qiu, Song; Schlaak, Joerg F.] Univ Hosp Essen, Dept Gastroenterol & Hepatol, Essen, Germany.
    [Zhang, Xiaoyong; Qiu, Song; Xu, Yang; Lu, Mengji] Huazhong Univ Sci & Technol, Tongji Med Coll, Tongji Hosp, Dept Microbiol, Wuhan 430074, Peoples R China.
    [Yang, Dongliang] Huazhong Univ Sci & Technol, Tongji Med Coll, Tongji Hosp, Div Clin Immunol, Wuhan 430074, Peoples R China.
    [Meng, Zhongji] Taihe Hosp, Yunyang Med Coll, Dept Infect Dis, Shiyan, Peoples R China.
 RP Lu, MJ, Univ Hosp Essen, Inst Virol, Essen, Germany.
 EM mengji.lu@uni-due.de
 FU Thekla Kemper and Barbara Bleekmann ; Deutsche Forschungsgemeinschaft
    [Lu 669/2-1, GRK1045/1, Lu 669/5-1]; Federal Ministry of Education and
    Research [GU0207]
 FX We are grateful for excellent technical assistance of Thekla Kemper and
    Barbara Bleekmann. This work is partly supported by grants of Deutsche
    Forschungsgemeinschaft (Lu 669/2-1, GRK1045/1, and Lu 669/5-1) and
    Federal Ministry of Education and Research (GU0207).
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 NR 49
 TC 3
 PU WILEY-BLACKWELL PUBLISHING, INC
 PI MALDEN
 PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
 SN 1462-5814
 J9 CELL MICROBIOL
 JI Cell Microbiol.
 PD NOV
 PY 2009
 VL 11
 IS 11
 BP 1624
 EP 1637
 DI 10.1111/j.1462-5822.2009.01353.x
 PG 14
 SC Cell Biology; Microbiology
 GA 504UE
 UT ISI:000270642400008
 ER
 
 PT J
 AU Du, W
    Jiang, P
    Li, N
    Mei, Y
    Wang, X
    Wen, L
    Yang, X
    Wu, M
 AF Du, W.
    Jiang, P.
    Li, N.
    Mei, Y.
    Wang, X.
    Wen, L.
    Yang, X.
    Wu, M.
 TI Suppression of p53 activity by Siva1
 SO CELL DEATH AND DIFFERENTIATION
 LA English
 DT Article
 DE Siva1; p53; Hdm2; ubiquitination
 ID EMBRYONIC LETHALITY; MDM2-DEFICIENT MICE; MDM2; APOPTOSIS; TARGET;
    BINDS; DEGRADATION; PROTEIN; PATHWAY; RESCUE
 AB The tumor suppressor p53 induces potent anti-proliferative responses in
    stressed cells; in unstressed cells this ability of p53 is restrained
    by Hdm2. Expression of Hdm2 is also induced by p53, thereby
    establishing feedback inhibition. Regulation of the p53-Hdm2
    interaction and the feedback inhibition of p53 are not well understood.
    Here, we show that the p53-Hdm2 interaction in unstressed cells is
    promoted by Siva1, which, like Hdm2, is the product of a p53 target
    gene. Siva1 binds to both p53 and Hdm2 through distinct regions and
    enhances Hdm2-mediated p53 ubiquitination and degradation. Siva1
    strongly inhibits p53-mediated gene expression and apoptosis. In
    xenograft mouse models, downregulation of Siva1 markedly inhibits tumor
    formation because of the activation of p53. On DNA damage, the
    interactions of Siva1 with both p53 and Hdm2 are diminished. The
    function of Siva1 seems to be related to its ability to form a
    homo-oligomer as the oligomerization defective splicing variant Siva2
    fails to destabilize p53. These results identify Siva1 as an important
    adaptor promoting p53 degradation through Hdm2. Siva1 may be part of
    the negative feedback loop that inhibits p53 activity at the end of a
    non-lethal stress response. Cell Death and Differentiation (2009) 16,
    1493-1504; doi:10.1038/cdd.2009.89; published online 10 July 2009
 C1 [Wu, M.] Univ Sci & Technol China, Sch Life Sci, Dept Mol & Cell Biol, Hefei 230027, Anhui, Peoples R China.
    [Du, W.; Jiang, P.; Li, N.; Wang, X.; Wen, L.; Wu, M.] Univ Sci & Technol China, Hefei Natl Lab Phys Sci Microscale, Hefei 230027, Anhui, Peoples R China.
    [Mei, Y.; Yang, X.] Univ Penn, Sch Med, Abramson Family Canc Res Inst, Philadelphia, PA 19104 USA.
    [Mei, Y.; Yang, X.] Univ Penn, Sch Med, Dept Canc Biol, Philadelphia, PA 19104 USA.
 RP Wu, M, Univ Sci & Technol China, Sch Life Sci, Dept Mol & Cell Biol,
    Huangshan Rd, Hefei 230027, Anhui, Peoples R China.
 EM xyang@mail.med.upenn.edu
    wumian@ustc.edu.cn
 FU National Natural Science Foundation of China [30530200, 30871290,
    30728003]; Ministry of Science and Technology of China [2006CB933300,
    2006CB910300]; Chinese Academy of Sciences [KSCX1-YW-R-57]; NIH
    [CA088868]
 FX We thank Dr. Serge Benichou (Departement de Maladies Infectieuses,
    Institut Cochin, France) for kindly providing GFP-Siva1. Plasmid
    pcDNA3-Hdm2 was a gift of Dr. Geoffrey M Wahl (The Salk Institute, La
    Jolla, USA). This research was supported by grants from the National
    Natural Science Foundation of China (30530200, 30871290, and 30728003),
    the Ministry of Science and Technology of China (2006CB933300 and
    2006CB910300), the Chinese Academy of Sciences (KSCX1-YW-R-57), and the
    NIH (CA088868).
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 NR 22
 TC 2
 PU NATURE PUBLISHING GROUP
 PI LONDON
 PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
 SN 1350-9047
 J9 CELL DEATH DIFFERENTIATION
 JI Cell Death Differ.
 PD NOV
 PY 2009
 VL 16
 IS 11
 BP 1493
 EP 1504
 DI 10.1038/cdd.2009.89
 PG 12
 SC Biochemistry & Molecular Biology; Cell Biology
 GA 505GE
 UT ISI:000270679000008
 ER
 
 PT J
 AU Oehler, VG
    Guthrie, KA
    Cummings, CL
    Sabo, K
    Wood, BL
    Gooley, T
    Yang, TM
    Epping, MT
    Shou, YP
    Pogosova-Agadjanyan, E
    Ladne, P
    Stirewalt, DL
    Abkowitz, JL
    Radich, JP
 AF Oehler, Vivian G.
    Guthrie, Katherine A.
    Cummings, Carrie L.
    Sabo, Kathleen
    Wood, Brent L.
    Gooley, Ted
    Yang, Taimei
    Epping, Mirjam T.
    Shou, Yaping
    Pogosova-Agadjanyan, Era
    Ladne, Paula
    Stirewalt, Derek L.
    Abkowitz, Janis L.
    Radich, Jerald P.
 TI The preferentially expressed antigen in melanoma (PRAME) inhibits
    myeloid differentiation in normal hematopoietic and leukemic progenitor
    cells
 SO BLOOD
 LA English
 DT Article
 ID HISTONE DEACETYLASE INHIBITORS; ACUTE LYMPHOBLASTIC-LEUKEMIA; RETINOIC
    ACID RECEPTORS; IN-VITRO; GENE-EXPRESSION; STEM-CELLS; PROGNOSIS;
    CANCER; MARKER; VIVO
 AB The preferentially expressed antigen in melanoma (PRAME) is expressed
    in several hematologic malignancies, but either is not expressed or is
    expressed at only low levels in normal hematopoietic cells, making it a
    target for cancer therapy. PRAME is a tumor-associated antigen and has
    been described as a corepressor of retinoic acid signaling in solid
    tumor cells, but its function in hematopoietic cells is unknown. PRAME
    mRNA expression increased with chronic myeloid leukemia (CML) disease
    progression and its detection in late chronic-phase CML patients before
    tyrosine kinase inhibitor therapy was associated with poorer
    therapeutic responses and ABL tyrosine kinase domain point mutations.
    In leukemia cell lines, PRAME protein expression inhibited granulocytic
    differentiation only in cell lines that differentiate along this
    lineage after all-trans retinoic acid (ATRA) exposure. Forced PRAME
    expression in normal hematopoietic progenitors, however, inhibited
    myeloid differentiation both in the presence and absence of ATRA, and
    this phenotype was reversed when PRAME was silenced in primary CML
    progenitors. These observations suggest that PRAME inhibits myeloid
    differentiation in certain myeloid leukemias, and that its function in
    these cells is lineage and phenotype dependent. Lastly, these
    observations suggest that PRAME is a target for both prognostic and
    therapeutic applications. (Blood. 2009; 114: 3299-3308)
 C1 [Oehler, Vivian G.; Guthrie, Katherine A.; Cummings, Carrie L.; Gooley, Ted; Yang, Taimei; Pogosova-Agadjanyan, Era; Ladne, Paula; Stirewalt, Derek L.; Radich, Jerald P.] Fred Hutchinson Canc Res Ctr, Div Clin Res, Seattle, WA 98104 USA.
    [Sabo, Kathleen; Abkowitz, Janis L.] Univ Washington, Div Hematol, Seattle, WA 98195 USA.
    [Wood, Brent L.] Univ Washington, Dept Lab Med, Seattle, WA 98195 USA.
    [Epping, Mirjam T.] Netherlands Canc Inst, Div Mol Carcinogenesis, Amsterdam, Netherlands.
    [Shou, Yaping] Novartis Pharmaceut, Novartis Inst BioMed Res, Cambridge, MA USA.
 RP Oehler, VG, 1100 Fairview Ave N,D4-100,Box 19024, Seattle, WA 98109 USA.
 EM voehler@u.washington.edu
 FU National Cancer Institute (NCI) [CA18029, CA106796]; Leukemia &
    Lymphoma Society Translational Research Program ; V Foundation for
    Cancer Research V Scholar 
 FX We are grateful to the following people: Drs Pierre Coulie and Rene
    Bernards for providing the original PRAME antibody and retroviral shRNA
    vectors used in these experiments; Dr C. A. Blau for providing the
    lentiviral expression vectors; Dr Stephen Collins for the kind loan of
    the K562 RARA and control cell lines; and Dr Hans P. Kiem and his
    laboratory for lentiviral shRNA vectors and assistance with the
    preparation of viral supernatants (Core Grant no. DK56465). We also
    thank Karen McDougall and August J. Salvado of Novartis Pharmaceuticals
    Corporation for providing outcomes data for the RIGHT study patients
    and Hongyue Dai of Rosetta Inpharmatics, Merck and Co for assistance
    with microarray analysis of the CML progression data.
    This work was supported by National Cancer Institute (NCI) grants
    CA18029 (J. P. R.) and CA106796, a Leukemia & Lymphoma Society
    Translational Research Program grant, and a V Foundation for Cancer
    Research V Scholar grant (V. G. O.).
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 NR 44
 TC 8
 PU AMER SOC HEMATOLOGY
 PI WASHINGTON
 PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
 SN 0006-4971
 J9 BLOOD
 JI Blood
 PD OCT 8
 PY 2009
 VL 114
 IS 15
 BP 3299
 EP 3308
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 PG 10
 SC Hematology
 GA 504DW
 UT ISI:000270595700023
 ER
 
 PT J
 AU Zhao, BQ
    Chauhan, AK
    Canault, M
    Patten, IS
    Yang, JJ
    Dockal, M
    Scheiflinger, F
    Wagner, DD
 AF Zhao, Bing-Qiao
    Chauhan, Anil K.
    Canault, Matthias
    Patten, Ian S.
    Yang, Janie J.
    Dockal, Michael
    Scheiflinger, Friedrich
    Wagner, Denisa D.
 TI vonWillebrand factor-cleaving protease ADAMTS13 reduces ischemic brain
    injury in experimental stroke
 SO BLOOD
 LA English
 DT Article
 ID VON-WILLEBRAND-FACTOR; THROMBOTIC THROMBOCYTOPENIC PURPURA; MOUSE
    MODEL; P-SELECTIN; INFLAMMATION; DISEASE; MICE; HEMOSTASIS; HEMORRHAGE;
    FIBRINOGEN
 AB Stroke is a leading cause of death and disability. The only therapy
    available is recombinant tissue plasminogen activator, but side effects
    limit its use. Platelets play a crucial role during stroke, and the
    inflammatory reaction promotes neurodegeneration. von Willebrand factor
    (VWF), an adhesion molecule for platelets, is elevated in patients with
    acute stroke. The activity of VWF is modulated by ADAMTS13 (a
    disintegrin-like and metalloprotease with thrombospondin type I
    repeats-13) that cleaves VWF to smaller less-active forms. We recently
    documented that ADAMTS13 negatively regulates both thrombosis and
    inflammation. We report that deficiency or reduction of VWF reduces
    infarct volume up to 2-fold after focal cerebral ischemia in mice, thus
    showing the importance of VWF in stroke injury. In contrast, ADAMTS13
    deficiency results in larger infarctions, but only in mice that have
    VWF. Importantly, infusion of a high dose of recombinant human ADAMTS13
    into a wild-type mouse immediately before reperfusion reduces infarct
    volume and improves functional outcome without producing cerebral
    hemorrhage. Furthermore, recombinant ADAMTS13 did not enhance bleeding
    in a hemorrhagic stroke model. Our findings show the importance of VWF
    in regulating infarction and suggest that recombinant ADAMTS13 could be
    considered as a new therapeutic agent for prevention and/or treatment
    of stroke. (Blood. 2009; 114: 3329-3334)
 C1 [Zhao, Bing-Qiao; Chauhan, Anil K.; Canault, Matthias; Patten, Ian S.; Yang, Janie J.; Wagner, Denisa D.] Immune Dis Inst, Boston, MA 02115 USA.
    [Zhao, Bing-Qiao; Chauhan, Anil K.; Canault, Matthias; Patten, Ian S.; Yang, Janie J.; Wagner, Denisa D.] Childrens Hosp, Program Cellular & Mol Med, Boston, MA 02115 USA.
    [Zhao, Bing-Qiao; Chauhan, Anil K.; Canault, Matthias; Wagner, Denisa D.] Harvard Univ, Sch Med, Dept Pathol, Boston, MA 02115 USA.
    [Dockal, Michael; Scheiflinger, Friedrich] Baxter Biosci, Vienna, Austria.
 RP Wagner, DD, Immune Dis Inst, 3 Blackfan Cir, Boston, MA 02115 USA.
 EM wagner@idi.harvard.edu
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 NR 34
 TC 9
 PU AMER SOC HEMATOLOGY
 PI WASHINGTON
 PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
 SN 0006-4971
 J9 BLOOD
 JI Blood
 PD OCT 8
 PY 2009
 VL 114
 IS 15
 BP 3329
 EP 3334
 DI 10.1182/blood-2009-03-213264
 PG 6
 SC Hematology
 GA 504DW
 UT ISI:000270595700027
 ER
 
 PT J
 AU Liu, LY
    Xie, R
    Yang, CF
    McKeehan, WL
 AF Liu, Leyuan
    Xie, Rui
    Yang, Chaofeng
    McKeehan, Wallace L.
 TI Dual function microtubule- and mitochondria-associated proteins mediate
    mitotic cell death
 SO CELLULAR ONCOLOGY
 LA English
 DT Article
 DE Aneuploidy; C19ORF5; genetic instability; LRPPRC; microtubule dynamics;
    mitochondrial dynamics; RASSF1A; paclitaxel; tumor suppression;
    mitochondria aggregation
 ID TUMOR-SUPPRESSOR RASSF1; SPINDLE POLES; CANCER; DYNAMICS; AGGREGATION;
    ANEUPLOIDY; MACHINERY; COMPLEX; C19ORF5; FAMILY
 AB Background: Survival and evolution of aneuploid cells after an
    asymmetric segregation of chromosomes at mitosis may be the common
    initiating event and underlying cause of the genetic diversity and
    adaptability of cancers. We hypothesize that mechanisms exist to detect
    impending aneuploidy and prevent it before completion of an aberrant
    mitosis.
    Methods: The distribution of isoforms of C19ORF5, an interactive
    partner with mitochondria-associated LRPPRC and tumor suppressor
    RASSF1A, state of spindle microtubules and mitochondrial aggregation
    was analyzed in synchronized mitotic cells and cells stalled in mitosis
    after treatment with paclitaxel.
    Results: C19ORF5 distributed broadly across the mitotic spindle and
    reversibly accumulated during reversible mitotic arrest. Prolonged
    stabilization of microtubules caused an accumulation of a C19ORF5
    product with dual MAP and MtAP properties that caused irreversible
    aggregation of mitochondria and death of mitotic cells.
    Conclusion: Dual function microtubule-associated (MAP) and
    mitochondria-associated (MtAP) proteins generated by prolonged mitotic
    arrest trigger mitochondrial-induced mitotic cell death. This is a
    potential mechanism to prevent minimal survivable aneuploidy resulting
    from an aberrant cell division and cancers in general at their earliest
    common origin.
 C1 [Liu, Leyuan; Xie, Rui; Yang, Chaofeng; McKeehan, Wallace L.] Texas A&M Hlth Sci Ctr, Inst Biosci & Technol, Ctr Canc & Stem Cell Biol, Houston, TX 77030 USA.
 RP McKeehan, WL, Texas A&M Hlth Sci Ctr, Inst Biosci & Technol, Ctr Canc &
    Stem Cell Biol, Houston, TX 77030 USA.
 EM wmckeehan@ibt.tamhsc.edu
 FU Public Health Service [CA59971, DK35310]; DOD New Investigator Award
    [W81XWH-08-1-0475]; John S. Dunn Research Foundation 
 FX We thank Dr. Le Sun and Joe Corvera (A&G Pharmaceuticals, Inc.,
    Columbia, MD) for anti-C19ORF5 mouse monoclonal antibody 4G1. This work
    was supported by Public Health Service Grants CA59971 and DK35310
    (WLM), DOD New Investigator Award W81XWH-08-1-0475 (LL), and aid from
    the John S. Dunn Research Foundation (WLM).
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 NR 28
 TC 2
 PU IOS PRESS
 PI AMSTERDAM
 PA NIEUWE HEMWEG 6B, 1013 BG AMSTERDAM, NETHERLANDS
 SN 1570-5870
 J9 CELL ONCOL
 JI Cell. Oncol.
 PY 2009
 VL 31
 IS 5
 BP 393
 EP 405
 DI 10.3233/CLO-2009-0484
 PG 13
 SC Oncology; Cell Biology; Pathology
 GA 502MD
 UT ISI:000270463400007
 ER
 
 PT J
 AU Yoo, KH
    Jang, IK
    Lee, MW
    Kim, HE
    Yang, MS
    Eom, Y
    Lee, JE
    Kim, YJ
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    Sung, KW
    Kim, CW
    Koo, HH
 AF Yoo, Keon Hee
    Jang, In Keun
    Lee, Myoung Woo
    Kim, Hyo Eun
    Yang, Mal Sook
    Eom, Youngwoo
    Lee, Jong Eun
    Kim, Young Jin
    Yang, Seong Kyu
    Jung, Hye Lim
    Sung, Ki Woong
    Kim, Cheol Woo
    Koo, Hong Hoe
 TI Comparison of immunomodulatory properties of mesenchymal stem cells
    derived from adult human tissues
 SO CELLULAR IMMUNOLOGY
 LA English
 DT Article
 DE Mesenchymal stem cells; Immunomodulation; IFN-gamma; TNF-alpha;
    Indoleamine 2,3-dioxygenase
 ID MARROW STROMAL CELLS; BONE-MARROW; LYMPHOCYTE-PROLIFERATION;
    INTERFERON-GAMMA; PROGENITOR CELLS; ADIPOSE-TISSUE; TRANSPLANTATION;
    INHIBIT; RESPONSES; REPAIR
 AB Mesenchymal stem cells (MSCs), which evoke only minimal immune
    reactivity, may have anti-inflammatory and immunomodulatory effects. In
    this study, we conducted a comparative analysis of the immunomodulatory
    properties of MSCs derived from adult human tissues including bone
    marrow (BM), adipose tissues (AT), umbilical cord blood (CB), and cord
    Wharton's jelly (WJ). Using a multiple cytokine detection assay, we
    showed that there were no significant differences in levels of secreted
    factors from non-stimulated MSCs. We compared the immunosuppressive
    effect of BM-MSCs, AT-MSCs, CB-MSCs, and WJ-MSCs on
    phytohemagglutinin-induced T-cell proliferation. AT-MSCs, CB-MSCs, and
    WJ-MSCs effectively suppressed mitogen-induced T-cell proliferation as
    effectively as did BM-MSCs. Levels of interferon (IFN)-gamma and tumor
    necrosis factor (TNF)-alpha secreted from activated T-cells increased
    over time, but these levels were significantly reduced when cocultured
    with each type of MSCs. In addition, the expression of hepatocyte
    growth factor, IL-10, transforming growth factor-beta(1),
    cyclooxygenase (COX)-1, and COX-2 were unchanged in MSCs treated with
    IFN-gamma and/or TNF-alpha, while indoleamine 2,3-dioxygenase (IDO)
    expression increased. IFN-gamma and/or TNF-alpha produced by activated
    T-cells were correlated with induction of IDO expression by MSCs,
    which, in turn, suppressed T-cell proliferation. These findings suggest
    that MSCs derived from AT, CB, or WJ could be substituted for BM-MSCs
    for treatment of allogeneic conflicts. (C) 2009 Elsevier Inc. All
    rights reserved.
 C1 [Yoo, Keon Hee; Lee, Myoung Woo; Yang, Seong Kyu; Jung, Hye Lim; Sung, Ki Woong; Koo, Hong Hoe] Sungkyunkwan Univ, Samsung Med Ctr, Sch Med, Dept Pediat, Seoul 135710, South Korea.
    [Jang, In Keun; Kim, Hyo Eun; Yang, Mal Sook; Eom, Youngwoo; Lee, Jong Eun; Kim, Young Jin] LifeCord Inc, Biomed Res Inst, Suwon, South Korea.
    [Yoo, Keon Hee; Kim, Cheol Woo] Seoul Natl Univ, Dept Pathol, Sch Med, Seoul, South Korea.
 RP Koo, HH, Sungkyunkwan Univ, Samsung Med Ctr, Sch Med, Dept Pediat, 50
    Irwon Dong, Seoul 135710, South Korea.
 EM hhkoo@skku.edu
 FU National R&D Program for Cancer Control ; Ministry for Health, Welfare
    and Family affairs ; Republic of Korea [0720230]
 FX This study was supported by a grant from the National R&D Program for
    Cancer Control, Ministry for Health, Welfare and Family affairs,
    Republic of Korea (Project No: 0720230).
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 NR 42
 TC 20
 PU ACADEMIC PRESS INC ELSEVIER SCIENCE
 PI SAN DIEGO
 PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
 SN 0008-8749
 J9 CELL IMMUNOL
 JI Cell. Immunol.
 PY 2009
 VL 259
 IS 2
 BP 150
 EP 156
 DI 10.1016/j.cellimm.2009.06.010
 PG 7
 SC Cell Biology; Immunology
 GA 501IG
 UT ISI:000270374300006
 ER
 
 PT J
 AU Wang, HZ
    Xiao, W
    Zhou, QB
    Chen, Y
    Yang, S
    Sheng, JS
    Yin, YQ
    Fan, J
    Zhou, JW
 AF Wang, Hanzhi
    Xiao, Wei
    Zhou, Qinbo
    Chen, Yun
    Yang, Shuo
    Sheng, Jiansong
    Yin, Yanqing
    Fan, Jia
    Zhou, Jiawei
 TI Bystin-like protein is upregulated in hepatocellular carcinoma and
    required for nucleologenesis in cancer cell proliferation
 SO CELL RESEARCH
 LA English
 DT Article
 DE Bystin-like; nucleologenesis; nucleolar proteins; cell growth;
    hepatocellular carcinoma
 ID PRE-RIBOSOMAL-RNA; ENDOMETRIAL EPITHELIAL-CELLS; C-MYC AMPLIFICATION;
    PRENUCLEOLAR BODIES; LIVING CELLS; U3 SNRNA; EXPRESSION; NUCLEOLUS;
    TROPHININ; MITOSIS
 AB The bystin-like (BYSL) gene was previously characterized to encode an
    accessory protein for cell adhesion that participates in early embryo
    implantation. It is also involved in 40S ribosomal subunit biogenesis
    and is found to be expressed in rapidly growing embryo and cancer cell
    lines. In order to explore the role of BYSL in cancer cell
    proliferation and growth, we used hepatocellular carcinoma (HCC) as a
    model. Here, we report that BYSL is crucial for HCC cell growth both in
    vitro and in vivo. Expression levels of BYSL mRNA and protein in human
    HCC specimens were markedly increased compared with those seen in
    adjacent non-cancerous tissue. In vitro, inhibition of BYSL by short
    hairpin RNA decreased HCC cell proliferation, induced apoptosis and
    partially arrested the cell cycle in the G2/M phase. In vivo, HCC cells
    treated with BYSL siRNA failed to form tumors in nude mice after
    subcutaneous implantation. To determine the cellular basis for BYSL
    RNAi-induced cell growth arrest, BYSL subcellular localization in
    mitotic and interphase HepG2 cells was examined. BYSL was present at
    multiple stages during nucleologenesis, including in nucleolus-derived
    foci (NDF), perichromosomal regions and the prenucleolar body (PNB)
    during mitosis. BYSL depletion remarkably suppressed NDF and PNB
    formation, and disrupted nucleoli assembly after mitosis, resulting in
    increased apoptosis and reduced tolerance of HCC cells to serum
    starvation. Taken together, our studies indicate that upregulated BYSL
    expression plays a role in hepatocarcinogenesis.
 C1 [Wang, Hanzhi; Zhou, Qinbo; Yang, Shuo; Sheng, Jiansong; Zhou, Jiawei] Chinese Acad Sci, Shanghai Inst Biol Sci, Inst Biochem & Cell Biol, Mol Cell Biol Lab, Shanghai 200031, Peoples R China.
    [Wang, Hanzhi; Zhou, Qinbo; Yin, Yanqing; Zhou, Jiawei] Chinese Acad Sci, Shanghai Inst Biol Sci, Inst Neurosci, State Key Lab Neurosci, Shanghai 200031, Peoples R China.
    [Xiao, Wei] First Peoples Hosp, Dept Pathol, Taizhou 225300, Jiangsu, Peoples R China.
    [Chen, Yun] 411 Hosp, Dept Pathol, Shanghai 200081, Peoples R China.
    [Fan, Jia] Fudan Univ, Shanghai Med Coll, Zhongshan Hosp,Liver Canc Inst, Key Lab Carcinogenesis & Canc Invas, Shanghai 200032, Peoples R China.
 RP Zhou, JW, Chinese Acad Sci, Shanghai Inst Biol Sci, Inst Biochem & Cell
    Biol, Mol Cell Biol Lab, Shanghai 200031, Peoples R China.
 EM jwzhou@ion.ac.cn
 FU Chinese Academy of Sciences ; National Natural Science Foundation of
    China [30525041, 30623003]; State Key Program for Basic Research of
    China [2006CB500704]
 FX We thank Dr ZJ Chen of Institute of Biochemistry and Cell Biology,
    Shanghai Institutes for Biological Sciences, Chinese Academy of
    Sciences for kindly providing HCC samples and Dr YZ Wang of Institute
    of Neuroscience, Shanghai Institutes for Biological Science, Chinese
    Academy of Sciences for the nucleolin antibody. We also thank Dr G Chen
    of Shanghai Chest Hospital for help in examining human pathological
    specimens. This work was supported by grants from the Chinese Academy
    of Sciences, National Natural Science Foundation of China ( Nos.
    30525041 and 30623003) and State Key Program for Basic Research of
    China ( No. 2006CB500704).
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 NR 54
 TC 1
 PU NATURE PUBLISHING GROUP
 PI NEW YORK
 PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
 SN 1001-0602
 J9 CELL RES
 JI Cell Res.
 PD OCT
 PY 2009
 VL 19
 IS 10
 BP 1150
 EP 1164
 DI 10.1038/cr.2009.99
 PG 15
 SC Cell Biology
 GA 503IP
 UT ISI:000270527600004
 ER
 
 PT J
 AU Ren, B
    Liang, Y
    Deng, Y
    Chen, QG
    Zhang, J
    Yang, XH
    Zuo, JR
 AF Ren, Bo
    Liang, Yan
    Deng, Yan
    Chen, Qingguo
    Zhang, Jian
    Yang, Xiaohui
    Zuo, Jianru
 TI Genome-wide comparative analysis of type-A Arabidopsis response
    regulator genes by overexpression studies reveals their diverse roles
    and regulatory mechanisms in cytokinin signaling
 SO CELL RESEARCH
 LA English
 DT Article
 DE Arabidopsis; cytokinin; MG132; protein stability; type-A ARR
 ID TO-ASP PHOSPHORELAY; HISTIDINE KINASE; NEGATIVE REGULATOR;
    CIRCADIAN-CLOCK; PHYTOCHROME-B; HIS-KINASE; TRANSDUCTION; THALIANA;
    RECEPTOR; GROWTH
 AB Cytokinin is a critical growth regulator for various aspects of plant
    growth and development. In Arabidopsis, cytokinin signaling is mediated
    by a two-component system-based phosphorelay that transmits a signal
    from the receptors, through histidine phosphotransfer proteins, to the
    downstream response regulators (ARRs). Of these ARRs, type-A ARR genes,
    whose transcription can be rapidly induced by cytokinin, act as
    negative regulators of cytokinin signaling. However, because of
    functional redundancy, the function of type-A ARR genes in plant growth
    and development is not well understood by analyzing loss-of-function
    mutants. In this study, we performed a comparative functional study on
    all ten type-A ARR genes by analyzing transgenic plants overexpressing
    these ARR genes fused to a MYC epitope tag. Overexpression of ARR genes
    results in a variety of cytokinin-associated phenotypes. Notably,
    overexpression of different ARR transgenes causes diverse phenotypes,
    even between phylogenetically closely-related gene pairs, such as
    within the ARR3-ARR4 and ARR5-ARR6 pairs. We found that the
    accumulation of a subset of ARR proteins (ARR3, ARR5, ARR7, ARR16 and
    ARR17; possibly ARR8 and ARR15) is increased by MG132, a specific
    proteasomal inhibitor, indicating that stability of these proteins is
    regulated by proteasomal degradation. Moreover, similar to that of
    previously characterized ARR5, ARR6 and ARR7, stability of ARR16 and
    ARR17, possibly including ARR8 and ARR15, is regulated by cytokinin.
    These results suggest that type-A ARR proteins are regulated by a
    combinatorial mechanism involving both the cytokinin and proteasome
    pathways, thereby executing distinctive functions in plant growth and
    development.
 C1 [Ren, Bo; Liang, Yan; Deng, Yan; Chen, Qingguo; Zhang, Jian; Yang, Xiaohui; Zuo, Jianru] Chinese Acad Sci, Inst Genet & Dev Biol, State Key Lab Plant Genom, Beijing 100101, Peoples R China.
    [Ren, Bo; Liang, Yan; Deng, Yan; Chen, Qingguo; Zhang, Jian; Yang, Xiaohui; Zuo, Jianru] Chinese Acad Sci, Inst Genet & Dev Biol, Natl Plant Gene Res Ctr Beijing, Beijing 100101, Peoples R China.
    [Ren, Bo; Deng, Yan; Chen, Qingguo] Chinese Acad Sci, Grad Sch, Beijing 100049, Peoples R China.
 RP Zuo, JR, Chinese Acad Sci, Inst Genet & Dev Biol, State Key Lab Plant
    Genom, Beijing 100101, Peoples R China.
 EM jrzuo@genetics.ac.cn
 FU National Natural Science Foundation of China [90817107]; Ministry of
    Science and Technology of China [2007CB948203]; Chinese Academy of
    Sciences [KSCX2-YW-N-015]
 FX We thank Dr Joe Kieber ( University of North Carolina, USA) and the
    Arabidopsis Biological Resource Center ( Ohio State University) for
    providing seeds. We thank Dr Shuhua Yang ( China Agricultural
    University) for critically reading the manuscript. This work was
    supported by grants from the National Natural Science Foundation of
    China ( 90817107), the Ministry of Science and Technology of China
    (2007CB948203) and Chinese Academy of Sciences (KSCX2-YW-N-015).
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 NR 60
 TC 1
 PU NATURE PUBLISHING GROUP
 PI NEW YORK
 PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
 SN 1001-0602
 J9 CELL RES
 JI Cell Res.
 PD OCT
 PY 2009
 VL 19
 IS 10
 BP 1178
 EP 1190
 DI 10.1038/cr.2009.88
 PG 13
 SC Cell Biology
 GA 503IP
 UT ISI:000270527600006
 ER
 
 PT J
 AU Huang, XZ
    Zhang, XY
    Yang, SH
 AF Huang, Xiaozhen
    Zhang, Xiaoyan
    Yang, Shuhua
 TI A novel chloroplast-localized protein EMB1303 is required for
    chloroplast development in Arabidopsis
 SO CELL RESEARCH
 LA English
 DT Article
 DE EMB1303; albino; chloroplast development; embryogenesis; Arabidopsis
 ID NUCLEAR GENE-EXPRESSION; EMBRYO DEVELOPMENT; PLASTID DIFFERENTIATION;
    4-PHOSPHATE PATHWAY; PLANT DEVELOPMENT; PHOTOSYSTEM-II; THALIANA;
    BIOSYNTHESIS; CELL; PHOTOSYNTHESIS
 AB To understand the molecular mechanisms underlying chloroplast
    development, we isolated and characterized the albino mutant emb1303-1
    in Arabidopsis. The mutant displayed a severe dwarf phenotype with
    small albino rosette leaves and short roots on a synthetic medium
    containing sucrose. It is pigment-deficient and seedling lethal when
    grown in soil. Embryo development was delayed in the mutant, although
    seed germination was not significantly impaired. The plastids of
    emb1303-1 were arrested in early developmental stages without the
    classical stack of thylakoid membrane. Genetic and molecular analyses
    uncovered that the EMB1303 gene encodes a novel chloroplast-localized
    protein. Microarray and RT-PCR analyses revealed that a number of
    nuclear- and plastid-encoded genes involved in photosynthesis and
    chloroplast biogenesis were substantially downregulated in the mutant.
    Moreover, the accumulation of several major chloroplast proteins was
    severely compromised in emb1303-1. These results suggest that EMB1303
    is essential for chloroplast development.
 C1 [Huang, Xiaozhen; Zhang, Xiaoyan; Yang, Shuhua] China Agr Univ, Coll Biol Sci, State Key Lab Plant Physiol & Biochem, Beijing 100193, Peoples R China.
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 RP Yang, SH, China Agr Univ, Coll Biol Sci, State Key Lab Plant Physiol &
    Biochem, Beijing 100193, Peoples R China.
 EM yangshuhua@cau.edu.cn
 FU National Natural Science Foundation of China [30670181, 30770202];
    Ministry of Science and Technology of China [2009CB119103]; Program for
    New Century Excellent Talents in University [NCET-05-0124]; Key Project
    of Chinese Ministry of Education [106037]
 FX We thank Dr Lixin Zhang ( Institute of Botany, Chinese Academy of
    Sciences) for providing antibodies of D1, D2, LHCII, and AtpB; and
    Arabidopsis Biological Research Center for T-DNA mutant seeds. We are
    grateful to Drs Jian Hua ( Cornell University) and Hao Yu ( National
    University of Singapore) for critically reviewing the manuscript. This
    work was supported by grants from National Natural Science Foundation
    of China ( Nos. 30670181 and 30770202), the Ministry of Science and
    Technology of China ( No. 2009CB119103), Program for New Century
    Excellent Talents in University ( No. NCET-05-0124), and the Key
    Project of Chinese Ministry of Education ( No. 106037).
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 PU NATURE PUBLISHING GROUP
 PI NEW YORK
 PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
 SN 1001-0602
 J9 CELL RES
 JI Cell Res.
 PD OCT
 PY 2009
 VL 19
 IS 10
 BP 1205
 EP 1216
 DI 10.1038/cr.2009.84
 PG 12
 SC Cell Biology
 GA 503IP
 UT ISI:000270527600008
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 LA English
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 ID TRIMETHYLATION
 C1 [Jia, Guangshuai; Wang, Weixiang; Li, Hong; Mao, Zhuo; Cai, Gaihong; Sun, Jian; Wu, Hui; Xu, Mo; Yang, Peng; Yuan, Wen; Chen, She; Zhu, Bing] Natl Inst Biol Sci, Beijing 102206, Peoples R China.
    [Jia, Guangshuai] Chinese Acad Sci, Kunming Inst Zool, Immunobiol Lab & Overseas Team, Key Lab Anim Model & Human Dis Mech, Kunming 650223, Peoples R China.
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 RP Zhu, B, Natl Inst Biol Sci, Beijing 102206, Peoples R China.
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 NR 10
 TC 3
 PU NATURE PUBLISHING GROUP
 PI NEW YORK
 PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
 SN 1001-0602
 J9 CELL RES
 JI Cell Res.
 PD OCT
 PY 2009
 VL 19
 IS 10
 BP 1217
 EP 1220
 DI 10.1038/cr.2009.110
 PG 4
 SC Cell Biology
 GA 503IP
 UT ISI:000270527600009
 ER
 
 PT J
 AU Yu, KQ
    Luo, C
    Qin, GR
    Xu, ZJ
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 SO CELL RESEARCH
 LA English
 DT Letter
 ID AVIAN INFLUENZA; NEURAMINIDASE NA; DRUG DESIGN; H5N1; INHIBITORS
 C1 [Yu, Kunqian; Luo, Cheng; Qin, Guangrong; Xu, Zhijian; Li, Ning; Liu, Hong; Shen, Xu; Yang, Caiguang; Zhu, Weiliang; Jiang, Hualiang] Chinese Acad Sci, Shanghai Inst Mat Med, State Key Lab Drug Res, Drug Discovery & Design Ctr, Shanghai 201203, Peoples R China.
    [Ma, Jianpeng; Wang, Qinghua] Baylor Coll Med, Dept Biochem & Mol Biol, Houston, TX 77030 USA.
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 RP Jiang, HL, Chinese Acad Sci, Shanghai Inst Mat Med, State Key Lab Drug
    Res, Drug Discovery & Design Ctr, Shanghai 201203, Peoples R China.
 EM wlzhu@mail.shcnc.ac.cn
    hljiang@mail.shcnc.ac.cn
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 NR 15
 TC 2
 PU NATURE PUBLISHING GROUP
 PI NEW YORK
 PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
 SN 1001-0602
 J9 CELL RES
 JI Cell Res.
 PD OCT
 PY 2009
 VL 19
 IS 10
 BP 1221
 EP 1224
 DI 10.1038/cr.2009.111
 PG 4
 SC Cell Biology
 GA 503IP
 UT ISI:000270527600010
 ER
 
 PT J
 AU Huang, XZ
    Zhang, XY
    Yang, SH
 AF Huang, Xiaozhen
    Zhang, Xiaoyan
    Yang, Shuhua
 TI A novel chloroplast-localized protein EMB1303 is required for
    chloroplast development in Arabidopsis (vol 19, pg 1205, 2009)
 SO CELL RESEARCH
 LA English
 DT Correction
 ID GENES
 CR HUANG XZ, 2009, CELL RES, V19, P1205, DOI 10.1038/cr.2009.84
    MEINKE D, 2008, TRENDS PLANT SCI, V13, P483, DOI
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 NR 3
 TC 0
 PU NATURE PUBLISHING GROUP
 PI NEW YORK
 PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
 SN 1001-0602
 J9 CELL RES
 JI Cell Res.
 PD OCT
 PY 2009
 VL 19
 IS 10
 BP 1225
 EP 1225
 DI 10.1038/cr.2009.116
 PG 1
 SC Cell Biology
 GA 503IP
 UT ISI:000270527600011
 ER
 
 PT J
 AU Xie, XY
    Chen, Y
    Xue, P
    Fan, Y
    Deng, YQ
    Peng, G
    Yang, FQ
    Xu, T
 AF Xie, Xiangyang
    Chen, Yu
    Xue, Peng
    Fan, Yong
    Deng, Yongqiang
    Peng, Gong
    Yang, Fuquan
    Xu, Tao
 TI RUVBL2, a novel AS160-binding protein, regulates insulin-stimulated
    GLUT4 translocation
 SO CELL RESEARCH
 LA English
 DT Article
 DE GLUT4; AS160; RUVBL2; tandem affinity purification (TAP); adipocytes;
    insulin
 ID GTPASE-ACTIVATING-PROTEIN; SKELETAL-MUSCLE; RABGAP AS160; DNA HELICASE;
    TRAFFICKING; DOMAIN; GLUCOSE-TRANSPORTER-4; INHIBITION; MEMBRANE; TBC1D1
 AB In fat and muscle cells, insulin-stimulated glucose uptake is mainly
    mediated by glucose transporter 4 (GLUT4), which translocates from
    intracellular compartments to the cell surface in response to insulin
    stimulation. AS160 is one of the substrates of Akt and plays important
    roles in insulin-regulated GLUT4 translocation. In this study,
    RuvB-like protein 2 (RUVBL2) is identified as a new AS160-binding
    protein using mammalian tandem affinity purification (TAP) combined
    with mass spectrometry. In 3T3-L1 adipocytes, RUVBL2 is highly
    expressed and is mainly distributed in the cytosol. Depletion of RUVBL2
    in adipocytes inhibits insulin-stimulated GLUT4 translocation and
    glucose uptake through reducing insulin-stimulated AS160
    phosphorylation. However, introduction of human RUVBL2 can reverse this
    inhibitory effect. These data suggest that RUVBL2 plays an important
    role in insulin-stimulated GLUT4 translocation through its interaction
    with AS160.
 C1 [Xie, Xiangyang; Chen, Yu; Xue, Peng; Fan, Yong; Deng, Yongqiang; Peng, Gong; Yang, Fuquan; Xu, Tao] Chinese Acad Sci, Inst Biophys, Natl Key Lab Biomacromol, Beijing 100101, Peoples R China.
    [Xie, Xiangyang; Chen, Yu; Fan, Yong; Deng, Yongqiang; Peng, Gong] Chinese Acad Sci, Grad Sch, Beijing 100101, Peoples R China.
 RP Xu, T, Chinese Acad Sci, Inst Biophys, Natl Key Lab Biomacromol,
    Beijing 100101, Peoples R China.
 EM fqyang@ibp.ac.cn
    xutao@ibp.ac.cn
 FU National Natural Science Foundation of China [30630020]; National Basic
    Research Program of China [2004CB720000]; CAS Project [KSCX1-YW-02-1]
 FX We would like to thank our colleagues, Prof Hong Tang for providing
    pCTAP-A expression vector and Dr Li Zheng for valuable discussion. This
    work is supported by the National Natural Science Foundation of China
    (NO. 30630020), the National Basic Research Program of China
    (2004CB720000), and the CAS Project (KSCX1-YW-02-1).
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 NR 22
 TC 3
 PU NATURE PUBLISHING GROUP
 PI NEW YORK
 PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
 SN 1001-0602
 J9 CELL RES
 JI Cell Res.
 PD SEP
 PY 2009
 VL 19
 IS 9
 BP 1090
 EP 1097
 DI 10.1038/cr.2009.68
 PG 8
 SC Cell Biology
 GA 503IN
 UT ISI:000270527400007
 ER
 
 PT J
 AU Yuk, JM
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    Lee, HM
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 AF Yuk, Jae-Min
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    Jo, Eun-Kyeong
 TI Vitamin D3 Induces Autophagy in Human Monocytes/Macrophages via
    Cathelicidin
 SO CELL HOST & MICROBE
 LA English
 DT Article
 ID INNATE IMMUNE-RESPONSES; TOLL-LIKE RECEPTORS;
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    PROTEIN-KINASE; HOST-DEFENSE; C/EBP-BETA; MACROPHAGES; CELLS; INHIBITION
 AB Autophagy and vitamin D3-mediated innate immunity have been shown to
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    are physiologically linked via a regulatory function of human
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    cathelicidin, which activated transcription of the autophagy-related
    genes Beclin-1 and Atg5. 1,25D3 also induced the colocalization of
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    cathelicidin-dependent manner. Furthermore, the antimycobacterial
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 C1 [Yuk, Jae-Min; Shin, Dong-Min; Lee, Hye-Mi; Yang, Chul-Su; Jin, Hyo Sun; Kim, Kwang-Kyu; Jo, Eun-Kyeong] Chungnam Natl Univ, Coll Med, Dept Microbiol, Taejon 301747, South Korea.
    [Yuk, Jae-Min; Shin, Dong-Min; Lee, Hye-Mi; Yang, Chul-Su; Jin, Hyo Sun; Kim, Kwang-Kyu; Kim, Jin-Man; Jo, Eun-Kyeong] Chungnam Natl Univ, Coll Med, Infect Signaling Network Res Ctr, Taejon 301747, South Korea.
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 RP Jo, EK, Chungnam Natl Univ, Coll Med, Dept Microbiol, Taejon 301747,
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 EM hayoungj@cnu.ac.kr
 FU Korea Science & Engineering Foundation through Infection Signaling
    Network Research Center [R13-2007-020-01000-0]
 FX We thank K.S. Song, G.M. Hur, K.K. Kim, and J.W. Shon for discussion
    and reagents; T. Yoshimori for plasmids; and J.S. Kim for critical
    reading of the manuscript. This work was supported by the Korea Science
    & Engineering Foundation through the Infection Signaling Network
    Research Center (R13-2007-020-01000-0) at Chungnam National University.
    The authors have no financial conflict of interest.
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 TC 35
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 PI CAMBRIDGE
 PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
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 J9 CELL HOST MICROBE
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 NR 1
 TC 0
 PU AMER SOC HEMATOLOGY
 PI WASHINGTON
 PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
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 J9 BLOOD
 JI Blood
 PD OCT 1
 PY 2009
 VL 114
 IS 14
 BP 3131
 EP 3131
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 PG 1
 SC Hematology
 GA 501MX
 UT ISI:000270387100040
 ER
 
 PT J
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    Roberts, KA
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 AF Blachon, Stephanie
    Cai, Xuyu
    Roberts, Kela A.
    Yang, Kevin
    Polyanovsky, Andrey
    Church, Allen
    Avidor-Reiss, Tomer
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 SO GENETICS
 LA English
 DT Article
 ID 9-FOLD SYMMETRY; BASAL BODIES; PROTEIN; CENTROSOME; MELANOGASTER;
    TUBULIN; GENES; SPERMATOGENESIS; SPERMIOGENESIS; GAMETOGENESIS
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    centriolar protein POC1 which is part of the daughter centriole
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    centriole, which may explain why no typical centriolar structure is
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    a unique model to study early steps of centriole formation.
 C1 [Blachon, Stephanie; Cai, Xuyu; Roberts, Kela A.; Yang, Kevin; Church, Allen; Avidor-Reiss, Tomer] Harvard Univ, Sch Med, Dept Cell Biol, Boston, MA 02115 USA.
    [Polyanovsky, Andrey] Russian Acad Sci, Sechenov Inst, St Petersburg 194223, Russia.
 RP Avidor-Reiss, T, Harvard Univ, Sch Med, Dept Cell Biol, 250 Longwood
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 EM tomer_avidor-reiss@hms.harvard.edu
 FU Fondation pour la Recherche Medicale ; Russian Foundation for Basic
    Research [07-04-01127]
 FX We thank the Havard Medical School EM facility for their help with
    electron microscopy, J. W. Raff for the GFP-PACT flies, and T C.
    Kaufman for Cnn antibodies. This work was supported partially by a
    grant from the Hellman Family Fund Program. Stephanie Blachon was
    Supported partially by a Fondation pour la Recherche Medicale grant.
    Andrey Polyanovsky way supported by the Russian Foundation for Basic
    Research grant no. 07-04-01127.
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 PA 428 EAST PRESTON ST, BALTIMORE, MD 21202 USA
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 PD MAY
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 PT J
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 AF Hines, Karrie A.
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 LA English
 DT Article
 ID POSITION-EFFECT VARIEGATION; NONHISTONE CHROMOSOMAL PROTEIN; ORIGIN
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 EM lori-wallrath@uiowa.edu
 FU National Institutes of Health (NIH) [GM61511]; American Heart
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    Science Foundation (NSF) [MCB-0821893]
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    are grateful for research support from the National Institutes of
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    Kirschtein National Research Service Award postdoctoral fellowship
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 NR 67
 TC 2
 PU GENETICS
 PI BALTIMORE
 PA 428 EAST PRESTON ST, BALTIMORE, MD 21202 USA
 SN 0016-6731
 J9 GENETICS
 JI Genetics
 PD AUG
 PY 2009
 VL 182
 IS 4
 BP 967
 EP 977
 DI 10.1534/genetics.109.105338
 PG 11
 SC Genetics & Heredity
 GA 499IZ
 UT ISI:000270214000005
 ER
 
 PT J
 AU Uebele, VN
    Nuss, CE
    Fox, SV
    Garson, SL
    Cristescu, R
    Doran, SM
    Kraus, RL
    Santarelli, VP
    Li, YX
    Barrow, JC
    Yang, ZQ
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    Ballard, JE
    Tang, CY
    Dai, G
    McManus, OB
    Koblan, KS
    Renger, JJ
 AF Uebele, Victor N.
    Nuss, Cindy E.
    Fox, Steven V.
    Garson, Susan L.
    Cristescu, Razvan
    Doran, Scott M.
    Kraus, Richard L.
    Santarelli, Vincent P.
    Li, Yuxing
    Barrow, James C.
    Yang, Zhi-Qiang
    Schlegel, Kelly-Ann S.
    Rittle, Kenneth E.
    Reger, Thomas S.
    Bednar, Rodney A.
    Lemaire, Wei
    Mullen, Faith A.
    Ballard, Jeanine E.
    Tang, Cuyue
    Dai, Ge
    McManus, Owen B.
    Koblan, Kenneth S.
    Renger, John J.
 TI Positive Allosteric Interaction of Structurally Diverse T-Type Calcium
    Channel Antagonists
 SO CELL BIOCHEMISTRY AND BIOPHYSICS
 LA English
 DT Article
 DE T-type calcium channel; CaV3; CACNA1I; Synergy; Radioligand; Absence
    epilepsy; Seizure
 ID CA2+ CHANNELS; ABSENCE EPILEPSY; BLOCKERS; MECHANISMS; PHARMACOLOGY;
    DISCOVERY; CANCER; PROLIFERATION; INHIBITORS; THALAMUS
 AB Low-voltage-activated (T-type) calcium channels play a role in diverse
    physiological responses including neuronal burst firing, hormone
    secretion, and cell growth. To better understand the biological role
    and therapeutic potential of the target, a number of structurally
    diverse antagonists have been identified. Multiple drug interaction
    sites have been identified for L-type calcium channels, suggesting a
    similar possibility exists for the structurally related T-type
    channels. Here, we radiolabel a novel amide T-type calcium channel
    antagonist (TTA-A1) and show that several known antagonists, including
    mibefradil, flunarizine, and pimozide, displace binding in a
    concentration-dependent manner. Further, we identify a novel
    quinazolinone T-type antagonist (TTA-Q4) that enhanced amide
    radioligand binding, increased affinity in a saturable manner and
    slowed dissociation. Functional evaluation showed these compounds to be
    state-dependent antagonists which show a positive allosteric
    interaction. Consistent with slowing dissociation, the duration of
    efficacy was prolonged when compounds were co-administered to WAG/Rij
    rats, a genetic model of absence epilepsy. The development of a T-type
    calcium channel radioligand has been used to demonstrate structurally
    distinct TTAs interact at allosteric sites and to confirm the potential
    for synergistic inhibition of T-type calcium channels with structurally
    diverse antagonists.
 C1 [Uebele, Victor N.; Nuss, Cindy E.; Fox, Steven V.; Garson, Susan L.; Cristescu, Razvan; Doran, Scott M.; Kraus, Richard L.; Santarelli, Vincent P.; Li, Yuxing; Renger, John J.] Merck Res Labs, Dept Depress & Circadian Disorders, West Point, PA 19486 USA.
    [Barrow, James C.; Yang, Zhi-Qiang; Schlegel, Kelly-Ann S.; Rittle, Kenneth E.; Reger, Thomas S.; Bednar, Rodney A.; Lemaire, Wei; Mullen, Faith A.] Merck Res Labs, Dept Med Chem, West Point, PA 19486 USA.
    [Dai, Ge; McManus, Owen B.; Koblan, Kenneth S.] Merck Res Labs, Dept Ion Channels, Rahway, NJ 07065 USA.
 RP Uebele, VN, Merck Res Labs, Dept Depress & Circadian Disorders, 770
    Sumneytown Pike,WP26-270, West Point, PA 19486 USA.
 EM victor_uebele@merck.com
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 NR 44
 TC 9
 PU HUMANA PRESS INC
 PI TOTOWA
 PA 999 RIVERVIEW DRIVE SUITE 208, TOTOWA, NJ 07512 USA
 SN 1085-9195
 J9 CELL BIOCHEM BIOPHYS
 JI Cell Biochem. Biophys.
 PD NOV
 PY 2009
 VL 55
 IS 2
 BP 81
 EP 93
 DI 10.1007/s12013-009-9057-4
 PG 13
 SC Biochemistry & Molecular Biology; Biophysics; Cell Biology
 GA 495WO
 UT ISI:000269926100002
 ER
 
 PT J
 AU Fandy, TE
    Herman, JG
    Kerns, P
    Jiemjit, A
    Sugar, EA
    Choi, SH
    Yang, AS
    Aucott, T
    Dauses, T
    Odchimar-Reissig, R
    Licht, J
    McConnell, MJ
    Nasrallah, C
    Kim, MKH
    Zhang, WJ
    Sun, YZ
    Murgo, A
    Espinoza-Delgado, I
    Oteiza, K
    Owoeye, I
    Silverman, LR
    Gore, SD
    Carraway, HE
 AF Fandy, Tamer E.
    Herman, James G.
    Kerns, Patrick
    Jiemjit, Anchalee
    Sugar, Elizabeth A.
    Choi, Si-Ho
    Yang, Allen S.
    Aucott, Timothy
    Dauses, Tianna
    Odchimar-Reissig, Rosalie
    Licht, Jonathan
    McConnell, Melanie J.
    Nasrallah, Chris
    Kim, Marianne K. H.
    Zhang, Weijia
    Sun, Yezou
    Murgo, Anthony
    Espinoza-Delgado, Igor
    Oteiza, Katharine
    Owoeye, Ibitayo
    Silverman, Lewis R.
    Gore, Steven D.
    Carraway, Hetty E.
 TI Early epigenetic changes and DNA damage do not predict clinical
    response in an overlapping schedule of 5-azacytidine and entinostat in
    patients with myeloid malignancies
 SO BLOOD
 LA English
 DT Article
 ID HISTONE DEACETYLASE INHIBITION; 5-AZA-2'-DEOXYCYTIDINE DECITABINE
    TREATMENT; MYELODYSPLASTIC SYNDROME; VALPROIC ACID; METHYLTRANSFERASE
    INHIBITORS; HEMATOPOIETIC MALIGNANCIES; HEMATOLOGIC MALIGNANCIES;
    METHYLATION STATUS; HUMAN CANCER; LEUKEMIA
 AB Sequential administration of DNA methyltransferase (DNMT) inhibitors
    and histone deacetylase (HDAC) inhibitors has demonstrated clinical
    efficacy in patients with hematologic malignancies. However, the
    mechanism behind their clinical efficacy remains controversial. In this
    study, the methylation dynamics of 4 TSGs (p15(INK4B), CDH-1, DAPK-1,
    and SOCS-1) were studied in sequential bone marrow samples from 30
    patients with myelodysplastic syndrome (MDS) or acute myeloid leukemia
    (AML) who completed a minimum of 4 cycles of therapy with 5-azacytidine
    and entinostat. Reversal of promoter methylation after therapy was
    observed in both clinical responders and nonresponders across all
    genes. There was no association between clinical response and either
    baseline methylation or methylation reversal in the bone marrow or
    purified CD34(+) population, nor was there an association with change
    in gene expression. Transient global hypomethylation was observed in
    samples after treatment but was not associated with clinical response.
    Induction of histone H3/H4 acetylation and the DNA damage-associated
    variant histone gamma-H2AX was observed in peripheral blood samples
    across all dose cohorts. In conclusion, methylation reversal of
    candidate TSGs during cycle 1 of therapy was not predictive of clinical
    response to combination "epigenetic" therapy. This trial is registered
    with http://www.clinicaltrials.gov under NCT00101179. (Blood.
    2009;114:2764-2773)
 C1 [Fandy, Tamer E.; Herman, James G.; Kerns, Patrick; Jiemjit, Anchalee; Aucott, Timothy; Dauses, Tianna; Oteiza, Katharine; Owoeye, Ibitayo; Gore, Steven D.; Carraway, Hetty E.] Johns Hopkins Univ, Sidney Kimmel Comprehens Canc Ctr, Baltimore, MD USA.
    [Sugar, Elizabeth A.] Johns Hopkins Univ, Dept Epidemiol, Bloomberg Sch Publ Hlth, Baltimore, MD USA.
    [Sugar, Elizabeth A.] Johns Hopkins Univ, Dept Biostat, Bloomberg Sch Publ Hlth, Baltimore, MD 21205 USA.
    [Choi, Si-Ho; Yang, Allen S.] Univ So Calif, Norris Canc Ctr, Div Hematol, Los Angeles, CA USA.
    [Odchimar-Reissig, Rosalie; Silverman, Lewis R.] Mt Sinai Med Ctr, Div Med Oncol, New York, NY 10029 USA.
    [Licht, Jonathan; Kim, Marianne K. H.] Northwestern Univ, Feinberg Sch Med, Robert H Lurie Comprehens Canc Ctr, Div Hematol Oncol, Chicago, IL 60611 USA.
    [McConnell, Melanie J.] Malaghan Inst Med Res, Wellington, New Zealand.
    [Nasrallah, Chris] Univ Calif Berkeley, Ctr Theoret Evolutionary Genet, Berkeley, CA 94720 USA.
    [Zhang, Weijia] Mt Sinai Sch Med, Div Hematol Oncol, New York, NY USA.
    [Sun, Yezou] Mt Sinai Sch Med, Personalized Med Res Program, New York, NY USA.
    [Murgo, Anthony; Espinoza-Delgado, Igor] NCI, Canc Therapy Evaluat Program, Rockville, MD USA.
 RP Gore, SD, 1650 Orleans St,Canc Res Bldg 1,Rm 288, Baltimore, MD 21231
    USA.
 EM gorest@jhmi.edu
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 NR 44
 TC 40
 PU AMER SOC HEMATOLOGY
 PI WASHINGTON
 PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
 SN 0006-4971
 J9 BLOOD
 JI Blood
 PD SEP 24
 PY 2009
 VL 114
 IS 13
 BP 2764
 EP 2773
 DI 10.1182/blood-2009-02-203547
 PG 10
 SC Hematology
 GA 498KK
 UT ISI:000270138600029
 ER
 
 PT J
 AU Lin, CC
    Kuo, CT
    Cheng, CY
    Wu, CY
    Lee, CW
    Hsieh, HL
    Lee, IT
    Yang, CM
 AF Lin, Chih-Chung
    Kuo, Chang-Ting
    Cheng, Ching-Yi
    Wu, Cheng-Ying
    Lee, Chiang-Wen
    Hsieh, Hsi-Lung
    Lee, I-Ta
    Yang, Chuen-Mao
 TI IL-1 beta promotes A549 cell migration via MAPKs/AP-1-and NF-kappa
    B-dependent matrix metalloproteinase-9 expression
 SO CELLULAR SIGNALLING
 LA English
 DT Article
 DE Cytokines; Matrix metalloproteinases; Mitogen-activated protein
    kinases; Transcription factors; Pulmonary epithelial cells
 ID SMOOTH-MUSCLE-CELLS; ACTIVATED PROTEIN-KINASE; NECROSIS-FACTOR-ALPHA;
    P42/P44 MAPK; TNF-ALPHA; P38 MAPK; MATRIX METALLOPROTEINASES;
    EXTRACELLULAR-MATRIX; TRANSCRIPTION FACTOR; DIVERGENT REGULATION
 AB Matrix metalloproteinases (MMPs), in particular MMP-9, is induced by
    cytokines including IL-1 beta and contributes to airway injury and
    remodeling. However, the mechanisms underlying IL-1 beta-induced MMP-9
    expression and cell migration in human A549 cells remain unclear. Here,
    we report that the IL-1 beta-induced MMP-9 gene expression was mediated
    through the activation of p42/p44 MAPK, p38 MAPK, and JNK1/2 in A549
    cells, determined by zymographic RT-PCR. and Westem blotting. The
    involvement of MAPKs in the IL-1 beta-induced responses was further
    ensured by transfection with siRNA of MEK1, p42, p38, or JNK2.
    Moreover, the IL-1 beta-induced MMP-9 gene expression was also mediated
    through the translocation of NF-kappa B (p65) into the nucleus and the
    degradation of I kappa B alpha In addition, the IL-1 beta-induced c-Jun
    phosphorylation was reduced by pretreatment with U0126 or SP600125.
    ILAP stimulated the transcriptional activity of wild-type MMP-9
    promoter in A549 cells, which was inhibited by U0126, SB203580,
    SP600125, and helenalin. In contrast, IL-1 beta had no effect on the
    cells transfected with a NF-kappa B-mutated MMP-9 promoter construct,
    suggesting that NF-kappa B is required for this response. Finally, the
    IL-1 beta-inducecl MMP-9 expression led to cell migration which was
    attenuated by pretreatment with U0126, SB203580, SP600125, helenalin,
    or MMP-2/9 inhibitor. These results suggested that in A549 cells, the
    activation of p42/p44 MAPK p38 MAPK JNK1/2, NF-kappa B, and AP-1 are
    essential for the IL-1 beta-induced MMP-9 gene expression and cell
    migration. (C) 2009 Elsevier Inc. All rights reserved.
 C1 [Cheng, Ching-Yi; Wu, Cheng-Ying; Lee, I-Ta; Yang, Chuen-Mao] Chang Gung Univ, Dept Pharmacol, Tao Yuan, Taiwan.
    [Lin, Chih-Chung] Chang Gung Mem Hosp, Tao Yuan, Taiwan.
    [Kuo, Chang-Ting] Buddhist Tzu Chi Gen Hosp, Taipei Branch, Dept Pharm, Taipei, Taiwan.
    [Lin, Chih-Chung] Chang Gung Univ, Dept Anesthet, Tao Yuan, Taiwan.
    [Lee, Chiang-Wen] Chang Gung Inst Technol, Div Basic Med Sci, Dept Nursing, Chiayi, Taiwan.
    [Hsieh, Hsi-Lung] Chang Gung Inst Technol, Dept Nursing, Tao Yuan, Taiwan.
 RP Yang, CM, Chang Gung Univ, Dept Pharmacol, 259 Wen Hwa 1st Rd, Tao
    Yuan, Taiwan.
 EM chuenmao@mail.cgu.edu.tw
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 NR 47
 TC 11
 PU ELSEVIER SCIENCE INC
 PI NEW YORK
 PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
 SN 0898-6568
 J9 CELL SIGNAL
 JI Cell. Signal.
 PD NOV
 PY 2009
 VL 21
 IS 11
 BP 1652
 EP 1662
 DI 10.1016/j.cellsig.2009.07.002
 PG 11
 SC Cell Biology
 GA 496VJ
 UT ISI:000270007300013
 ER
 
 PT J
 AU Hoshida, Y
    Nijman, SMB
    Kobayashi, M
    Chan, JA
    Brunet, JP
    Chiang, DY
    Villanueva, A
    Newell, P
    Ikeda, K
    Hashimoto, M
    Watanabe, G
    Gabriel, S
    Friedman, SL
    Kumada, H
    Llovet, JM
    Golub, TR
 AF Hoshida, Yujin
    Nijman, Sebastian M. B.
    Kobayashi, Masahiro
    Chan, Jennifer A.
    Brunet, Jean-Philippe
    Chiang, Derek Y.
    Villanueva, Augusto
    Newell, Philippa
    Ikeda, Kenji
    Hashimoto, Masaji
    Watanabe, Goro
    Gabriel, Stacey
    Friedman, Scott L.
    Kumada, Hiromitsu
    Llovet, Josep M.
    Golub, Todd R.
 TI Integrative Transcriptome Analysis Reveals Common Molecular Subclasses
    of Human Hepatocellular Carcinoma
 SO CANCER RESEARCH
 LA English
 DT Article
 ID GENE-EXPRESSION; BETA-CATENIN; INTRAHEPATIC RECURRENCE; FUNCTIONAL
    GENOMICS; HUMAN CANCER; TGF-BETA; CLASSIFICATION; DEFINES; PROGRESSION;
    INTERFERON
 AB Hepatocellular carcinoma (HCC) is a highly heterogeneous disease, and
    prior attempts to develop genomic-based classification for HCC have
    yielded highly divergent results, indicating difficulty in identifying
    unified molecular anatomy. We performed a meta-analysis of gene
    expression profiles in data sets from eight independent patient cohorts
    across the world. In addition, aiming to establish the real world
    applicability of a classification system, we profiled 118
    formalin-fixed, paraffin-embedded tissues from an additional patient
    cohort. A total of 603 patients were analyzed, representing the major
    etiologies of HCC (hepatitis B and C) collected from Western and
    Eastern countries. We observed three robust HCC subclasses (termed S1,
    S2, and S3), each correlated with clinical parameters such as tumor
    size, extent of cellular differentiation, and serum alpha-fetoprotein
    levels. An analysis of the components of the signatures indicated that
    S1 reflected aberrant activation of the WNT signaling pathway, S2 was
    characterized by proliferation as well as MYC and AKT activation, and
    S3 was associated with hepatocyte differentiation. Functional studies
    indicated that the WNT pathway activation signature characteristic of
    St tumors was not simply the result of beta-catenin mutation but rather
    was the result of transforming growth factor-beta activation, thus
    representing a new mechanism of WNT pathway activation in HCC. These
    experiments establish the first consensus classification framework for
    HCC based on gene expression profiles and highlight the power of
    integrating multiple data sets to define a robust molecular taxonomy of
    the disease. [Cancer Res 2009;69(18):7385-92]
 C1 [Hoshida, Yujin; Nijman, Sebastian M. B.; Chan, Jennifer A.; Brunet, Jean-Philippe; Chiang, Derek Y.; Gabriel, Stacey; Golub, Todd R.] Harvard Univ, Broad Inst, Cambridge, MA 02142 USA.
    [Hoshida, Yujin; Nijman, Sebastian M. B.; Chan, Jennifer A.; Brunet, Jean-Philippe; Chiang, Derek Y.; Gabriel, Stacey; Golub, Todd R.] Harvard Univ, Cambridge, MA 02138 USA.
    [Hoshida, Yujin; Golub, Todd R.] Dana Farber Canc Inst, Boston, MA 02115 USA.
    [Golub, Todd R.] Harvard Univ, Childrens Hosp Boston, Sch Med, Boston, MA 02115 USA.
    [Golub, Todd R.] Howard Hughes Med Inst, Boston, MA 02115 USA.
    [Nijman, Sebastian M. B.] Austrian Acad Sci, Ctr Mol Med, A-1010 Vienna, Austria.
    [Kobayashi, Masahiro; Ikeda, Kenji; Hashimoto, Masaji; Watanabe, Goro; Kumada, Hiromitsu] Toranomon Gen Hosp, Tokyo, Japan.
    [Chan, Jennifer A.] Univ Calgary, Calgary, AB, Canada.
    [Villanueva, Augusto; Llovet, Josep M.] IDIBAPS, Hosp Clin, CIBERehd, Barcelona Clin Liver Canc Grp,Liver Unit, Barcelona, Spain.
    [Llovet, Josep M.] Inst Catalana Recerca Estudis Avancats, Barcelona, Spain.
    [Newell, Philippa; Friedman, Scott L.; Llovet, Josep M.] Mt Sinai Sch Med, Liver Canc Program, New York, NY USA.
 RP Golub, TR, Harvard Univ, Broad Inst, 7 Cambridge Ctr, Cambridge, MA
    02142 USA.
 EM golub@broad.mit.edu
 FU NIH/National Cancer Institute [5U54 CA112962-03]; NIH/National
    Institutes of Diabetes, Digestive and Kidney Diseases [1R01DK076986];
    NIH (Spain) [SAF-2007-61898]; Samuel Waxman Cancer Research Foundation
    ; Charles A. King Trust fellowship ; Netherlands Organisation for
    Scientific Research (Rubicon) ; Dutch Cancer Society fellowships 
 FX Grant support: NIH/National Cancer Institute grant 5U54 CA112962-03
    (T.R. Golub), NIH/National Institutes of Diabetes, Digestive and Kidney
    Diseases grant 1R01DK076986 (J.M. Llovet), NIH (Spain) grant I+D
    Program SAF-2007-61898 (J.M. Llovet), and Samuel Waxman Cancer Research
    Foundation. Y. Hoshida is supported by Charles A. King Trust
    fellowship. S.M.B. Nijman was supported by the Netherlands Organisation
    for Scientific Research (Rubicon) and Dutch Cancer Society fellowships.
    The costs of publication of this article were defrayed in part by the
    payment of page charges. This article must therefore be hereby marked
    advertisement in accordance with 18 U.S.C. Section 1734 solely to
    indicate this fact.
    We thank Menno Creyghton for reagents and helpful suggestion; So Young
    Kim, Ron Firestein, William Hahn. and David Root for the shRNA
    constructs; Megan Hanna for technical help; Weijia Zhang for critical
    reading of the manuscript; and Jadwiga. Grabarek and Mariko Kobayashi
    for general support.
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 NR 38
 TC 39
 PU AMER ASSOC CANCER RESEARCH
 PI PHILADELPHIA
 PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
 SN 0008-5472
 J9 CANCER RES
 JI Cancer Res.
 PD SEP 15
 PY 2009
 VL 69
 IS 18
 BP 7385
 EP 7392
 DI 10.1158/0008-5472.CAN-09-1089
 PG 8
 SC Oncology
 GA 496FC
 UT ISI:000269954000033
 ER
 
 PT J
 AU Zhang, X
    Zhang, CS
    Liu, YC
    Yang, XQ
    Xiong, SH
    Wen, Y
    Jiang, EP
    Li, R
    Zhang, ZY
    Liu, F
    Ye, Y
 AF Zhang, Xi
    Zhang, Chuan-Sen
    Liu, Yan-Chun
    Yang, Xiang-Qun
    Xiong, Shao-Hu
    Wen, Yu
    Jiang, Er-Peng
    Li, Rui
    Zhang, Zhi-Ying
    Liu, Fang
    Ye, Yong
 TI Isolation, Culture and Characterization of Cardiac Progenitor Cells
    Derived from Human Embryonic Heart Tubes
 SO CELLS TISSUES ORGANS
 LA English
 DT Article
 DE Cardiac pacemaking cells; Cardiac progenitor cells; Cardiomyocytes;
    Smooth muscle cells
 ID GATA-4 TRANSCRIPTION FACTOR; STEM-CELLS; MYOCARDIAL REGENERATION;
    INFARCTED MYOCARDIUM; CONDUCTION SYSTEM; PRECURSOR CELLS;
    SMOOTH-MUSCLE; ADULT; DIFFERENTIATION; MULTIPOTENT
 AB A variety of studies have reported on the isolation and expansion of
    cardiac stem cells from adult hearts. However, there is little
    information concerning cardiac stem/progenitor cells derived from
    embryonic hearts/heart tubes. To provide more evidence for embryonic
    heart-derived stem/progenitor cells, Nkx2.5+ human cardiac progenitor
    cells (hCPCs) were isolated and cloned from human heart tubes. The
    cells stained positive for Nkx2.5 and Oct-4, and negative for
    alpha-smooth muscle actin (alpha-SMA), cytokeratin, factor-VIII,
    alpha-sarcomeric actin and c-Kit. GATA-4 expression of Nkx2.5+ hCPCs
    was higher than that of embryonic limb bud mesenchymal cells of the
    control group (p < 0.05). These cells were passaged continuously for >3
    months (23 passages) and proliferated actively in vitro. After being
    treated with 5-azacytidine, Nkx2.5+ hCPCs underwent cardiomyogenic
    differentiation. Ultrastructural observation confirmed that the
    longitudinal section of these cardiomyogenic differentiation cells
    clearly revealed typical sarcomeres and intercalated discs. alpha-MHC,
    alpha-sarcomeric actin and GATA-4 levels were increased in Nkx2.5+
    hCPCs treated with 5-azacytidine compared to untreated cells. Nkx2.5+
    hCPCs exhibited positive staining and had a higher expression for
    alpha-SMA when cocultured with canine vascular endothelial cells. After
    Nkx2.5+ hCPCs were treated with endothelin-1, all cells displayed
    spontaneous electrical activity and spontaneous beating. Connexin-40
    and -45 were stained positive in the treated cells. In conclusion,
    Nkx2.5+ hCPCs derived from heart tubes have been isolated and cloned in
    vitro. These cells are capable of long-term self-renewal and possess a
    potential to differentiate into cardiac muscle-like cells, cardiac
    pacemaking cells and smooth muscle-like cells. They could have a
    significant impact on cardiac regeneration medicine and developmental
    biology. Copyright (C) 2009 S. Karger AG, Basel
 C1 [Zhang, Chuan-Sen] Mil Med Coll 2, Inst Biomed Engn, Dept Anat, Shanghai 200433, Peoples R China.
 RP Zhang, CS, Mil Med Coll 2, Inst Biomed Engn, Dept Anat, 800 Xiangyin
    Rd, Shanghai 200433, Peoples R China.
 EM chuansen@yahoo.com
 FU National Natural Science Foundation of China [30772158]; Shanghai
    Natural Science Foundation of China [07ZR14140, 05JC14045, 06DJ1402]
 FX This work was supported by the National Natural Science Foundation of
    China (No. 30772158), the Shanghai Natural Science Foundation of China
    (No. 07ZR14140, No. 05JC14045) and in part by the Shanghai Natural
    Science Foundation of China (No. 06DJ1402). The authors would like to
    thank H. U. Kaimeng for his help during the performance of PCR, and are
    grateful to all professors who helped us improve the quality of the
    manuscript.
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 NR 29
 TC 0
 PU KARGER
 PI BASEL
 PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND
 SN 1422-6405
 J9 CELLS TISSUES ORGANS
 JI Cells Tissues Organs
 PY 2009
 VL 190
 IS 4
 BP 194
 EP 208
 DI 10.1159/000204750
 PG 15
 SC Anatomy & Morphology; Cell Biology; Developmental Biology
 GA 494DD
 UT ISI:000269788800002
 ER
 
 PT J
 AU Gan, L
    Liu, P
    Lu, H
    Chen, S
    Yang, J
    McCarthy, JB
    Knudsen, KE
    Huang, H
 AF Gan, L.
    Liu, P.
    Lu, H.
    Chen, S.
    Yang, J.
    McCarthy, J. B.
    Knudsen, K. E.
    Huang, H.
 TI Cyclin D1 promotes anchorage-independent cell survival by inhibiting
    FOXO-mediated anoikis
 SO CELL DEATH AND DIFFERENTIATION
 LA English
 DT Article
 DE FOXO1; FOXO3a; cyclin D1; cyclin-dependent kinase; anoikis; prostate
    cancer
 ID TRANSCRIPTION FACTORS; PROSTATE-CANCER; GENE-EXPRESSION;
    DOWN-REGULATION; NUCLEAR EXPORT; PHOSPHORYLATION; APOPTOSIS; BIM;
    INTEGRINS; PROLIFERATION
 AB O-class forkhead box (FOXO) transcription factors are critical
    regulators of diverse cellular processes, including apoptosis,
    cell-cycle arrest, DNA damage repair and oxidative stress resistance.
    Here, we show that FOXO1 and FOXO3a have an essential function in
    promoting cell detachment-induced anoikis, resistance to which is
    implicated in cancer development and metastasis. In contrast, the
    oncoprotein cyclin D1 inhibits anoikis. We further show that cyclin D1
    interacts with FOXO proteins and impedes their transcriptional
    regulatory and anoikis-promoting functions. This effect of cyclin D1
    requires its transcription repression domain but is independent of
    cyclin-dependent kinases CDK4 and CDK6. Moreover, we show that
    cancer-derived mutants of cyclin D1 are much more stable than wild-type
    cyclin D1 under anchorage-independent conditions and possess a greater
    antagonistic effect on FOXO-regulated anoikis and anchorage-independent
    growth of cancer cells. These data suggest that cyclin D1 may have a
    critical function in tumorigenesis and cancer metastasis by inhibiting
    the anoikis-promoting function of FOXO proteins.
 C1 [Gan, L.; Liu, P.; Lu, H.; Chen, S.; Huang, H.] Univ Minnesota, Mason Canc Ctr, Minneapolis, MN 55455 USA.
    [Gan, L.; Liu, P.; Lu, H.; Chen, S.; Yang, J.; McCarthy, J. B.; Huang, H.] Univ Minnesota, Sch Med, Dept Lab Med & Pathol, Minneapolis, MN 55455 USA.
    [Knudsen, K. E.] Thomas Jefferson Med Coll, Kimmel Canc Ctr, Dept Canc Biol, Philadelphia, PA USA.
 RP Huang, H, Univ Minnesota, Mason Canc Ctr, MMC 806,420 Delaware St SE,
    Minneapolis, MN 55455 USA.
 EM huang253@umn.edu
 FU Department of Defense [W81XWH-07-1-0137, PC080591]; Brainstorm Award
    from the University of Minnesota Masonic Cancer Center ; National
    Institutes of Health [CA82295, CA099996]; National Natural Science
    Foundation of China [30500109]
 FX We thank DJ Tindall, KL Guan, M Pagano, CY Young, and SW Hayward for
    plasmids and cell lines, Y Shimizu, V Bardwell, KL Schwertfeger, SM
    Dehm and members of Huang laboratory, especially LR Bohrer for critical
    reading of the manuscript. This work was supported in part by funds
    from the Department of Defense (W81XWH-07-1-0137 and PC080591) and the
    Brainstorm Award from the University of Minnesota Masonic Cancer Center
    (to HH), the National Institutes of Health (CA82295 to JBM and CA099996
    to KEK), and the National Natural Science Foundation of China (30500109
    to LG). All authors claim no conflict of interest with this study.
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 NR 39
 TC 5
 PU NATURE PUBLISHING GROUP
 PI LONDON
 PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
 SN 1350-9047
 J9 CELL DEATH DIFFERENTIATION
 JI Cell Death Differ.
 PD OCT
 PY 2009
 VL 16
 IS 10
 BP 1408
 EP 1417
 DI 10.1038/cdd.2009.86
 PG 10
 SC Biochemistry & Molecular Biology; Cell Biology
 GA 494BU
 UT ISI:000269785100011
 ER
 
 PT J
 AU Choong, ML
    Yang, H
    Lee, MA
    Lane, DP
 AF Choong, Meng Ling
    Yang, Henry
    Lee, May Ann
    Lane, David P.
 TI Specific activation of the p53 pathway by low dose actinomycin D A new
    route to p53 based cyclotherapy
 SO CELL CYCLE
 LA English
 DT Article
 DE microarray; apoptosis; cell cycle; tumor; drug combinations
 ID MICROTUBULE-ACTIVE DRUGS; P53-DEPENDENT APOPTOSIS;
    CHECKPOINT-DEFICIENT; MDM2 ANTAGONISTS; TARGET GENES; CANCER-CELLS;
    HUMAN GENOME; PHOSPHORYLATION; THERAPY; TRANSLOCATION
 AB The activation of p53 has been proposed as a novel anti-cancer
    treatment in two distinct contexts. In the first activation of p53 in
    tumor cells can promote apoptosis and senescence and enhance the
    anti-tumor activity of cytotoxic chemotherapeutic drugs. In the second
    application activation of p53 in normal tissues can cause a reversible
    cell cycle arrest that can be used to protect normal cells from the
    action of anti-mitotics. In this cyclotherapy role p53 mutant tumor
    cells are not arrested and remain sensitive to anti- mitotics. The
    advent of specific p53 activating molecules such as nutlin-3 has
    encouraged both approaches. We have sought for a clinically approved
    drug that can mimic nutlin-3. We show here that low doses of
    actinomycin D mimic nutlin-3 in the highly specific activation of p53
    dependant transcription, in the induction of a reversible protective
    growth arrest in normal cells and in the enhancement of the activity of
    chemotherapeutic drug induced killing of p53 positive human tumor
    cells. While high doses of actinomycin D reveal its more non-specific
    activities, low doses of the drug will allow exploration of the value
    of p53 activation in preclinical and clinical models before nutlin-3
    like drugs are approved.
 C1 [Lane, David P.] Agcy Sci Technol & Res, Lab P53, Singapore 138668, Singapore.
    [Choong, Meng Ling; Lee, May Ann] Ctr Expt Therapeut, Singapore, Singapore.
    [Yang, Henry] Singapore Immunol Network, Singapore, Singapore.
 RP Lane, DP, Agcy Sci Technol & Res, Lab P53, 20 Biopolis Way,08-01 Ctr,
    Singapore 138668, Singapore.
 EM dplane@p53Lab.a-star.edu.sg
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 NR 39
 TC 17
 PU LANDES BIOSCIENCE
 PI AUSTIN
 PA 1002 WEST AVENUE, 2ND FLOOR, AUSTIN, TX 78701 USA
 SN 1538-4101
 J9 CELL CYCLE
 JI Cell Cycle
 PD SEP 1
 PY 2009
 VL 8
 IS 17
 BP 2810
 EP 2818
 PG 9
 SC Cell Biology
 GA 494FK
 UT ISI:000269795800029
 ER
 
 PT J
 AU Tobinai, K
    Ishizawa, K
    Ogura, M
    Itoh, K
    Morishima, Y
    Ando, K
    Taniwaki, M
    Watanabe, T
    Yamamoto, J
    Uchida, T
    Nakata, M
    Terauchi, T
    Nawano, S
    Matsusako, M
    Hayashi, M
    Hotta, T
 AF Tobinai, Kensei
    Ishizawa, Ken-ichi
    Ogura, Michinori
    Itoh, Kuniaki
    Morishima, Yasuo
    Ando, Kiyoshi
    Taniwaki, Masafumi
    Watanabe, Takashi
    Yamamoto, Joji
    Uchida, Toshiki
    Nakata, Masanobu
    Terauchi, Takashi
    Nawano, Shigeru
    Matsusako, Masaki
    Hayashi, Masaki
    Hotta, Tomomitsu
 TI Phase II study of oral fludarabine in combination with rituximab for
    relapsed indolent B-cell non-Hodgkin lymphoma
 SO CANCER SCIENCE
 LA English
 DT Article
 ID LOW-GRADE LYMPHOMA; COOPERATIVE-ONCOLOGY-GROUP; BENDAMUSTINE PLUS
    RITUXIMAB; FOLLICULAR LYMPHOMA; MANTLE CELL; CHOP CHEMOTHERAPY;
    RESPONSE CRITERIA; FOLLOW-UP; CYCLOPHOSPHAMIDE; PHOSPHATE
 AB Oral fludarabine is more convenient than intravenous fludarabine in an
    outpatient setting. To assess the efficacy and toxicity of oral
    fludarabine in combination with rituximab in patients with relapsed
    indolent B-cell non-Hodgkin lymphoma (B-NHL), we conducted a
    multicenter phase II study. Patients with relapsed indolent B-NHL with
    two or fewer prior regimens and up to 16 doses of rituximab were
    eligible. Patients received 375 mg/m<SU2</SU rituximab on day 1, and 40
    mg/m<SU2</SU oral fludarabine once daily on days 1 through 5 every 28
    days for up to six cycles. The primary endpoint was the overall
    response rate. Forty-one patients were enrolled, including 38 (93%)
    with follicular lymphoma. Thirty-four patients (83%) had received
    rituximab as prior therapy. Twenty-seven patients (66%) completed the
    planned six cycles. Dose reduction of oral fludarabine was required in
    17 patients (41%). The overall response rate was 76% (31 of 41
    patients; 95% confidence interval, 60-88%) with a complete response
    rate of 68% (28 of 41 patients; 95% confidence interval, 52-82%).
    Median progression-free survival for the 41 patients was 19.7 months
    (95% confidence interval, 12.3-26.5 months). Hematological toxicities,
    including grade 4 neutropenia (68%), were the most frequent toxicities.
    Non-hematological toxicities were mild, except for one patient who died
    of Pneumocystis jiroveci pneumonia 4 months after the protocol
    treatment. In conclusion, oral fludarabine in combination with
    rituximab is a highly effective and convenient therapy for patients
    with relapsed indolent B-NHL who have mostly been pretreated with
    rituximab. (ClinicalTrials.gov number, NCT00311129.) (Cancer Sci 2009;
    100: 1951-1956).
 C1 [Tobinai, Kensei; Watanabe, Takashi] Natl Canc Ctr, Hematol & Stem Cell Transplantat Div, Tokyo, Japan.
    [Ishizawa, Ken-ichi; Yamamoto, Joji] Tohoku Univ Hosp, Sendai, Miyagi, Japan.
    [Ogura, Michinori; Uchida, Toshiki] Nagoya Daini Red Cross Hosp, Dept Hematol & Oncol, Nagoya, Aichi, Japan.
    [Itoh, Kuniaki; Nakata, Masanobu] Natl Canc Ctr Hosp E, Div Hematol & Oncol, Chiba, Japan.
    [Nawano, Shigeru] Natl Canc Ctr Hosp E, Div Diagnost Radiol, Chiba, Japan.
    [Morishima, Yasuo] Aichi Canc Ctr Hosp, Dept Hematol & Cell Therapy, Nagoya, Aichi 464, Japan.
    [Ando, Kiyoshi] Tokai Univ, Sch Med, Dept Hematol & Oncol, Kanagawa 2591100, Japan.
    [Taniwaki, Masafumi] Kyoto Prefectural Univ Med, Dept Hematol & Oncol, Kyoto, Japan.
    [Terauchi, Takashi] Natl Canc Ctr, Res Ctr Canc Prevent & Screening, Screening Technol & Dev Div, Tokyo 104, Japan.
    [Matsusako, Masaki] St Lukes Int Hosp, Dept Radiol, Tokyo, Japan.
    [Hayashi, Masaki] Bayer HealthCare, Dept Clin Dev, Osaka, Japan.
    [Hotta, Tomomitsu] Nagoya Med Ctr, Nagoya, Aichi, Japan.
    [Nakata, Masanobu] Sapporo Hokuyu Hosp, Dept Internal Med, Sapporo, Hokkaido, Japan.
    [Nawano, Shigeru] Int Univ Hlth & Welf, Mita Hosp, Dept Radiol, Tokyo, Japan.
    [Hayashi, Masaki] Nakagami Hosp, Dept Internal Med, Okinawa, Japan.
 RP Tobinai, K, Natl Canc Ctr, Hematol & Stem Cell Transplantat Div, 1-1
    Tsukiji 5 chome, Tokyo, Japan.
 EM ktobinai@ncc.go.jp
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 NR 34
 TC 2
 PU WILEY-BLACKWELL PUBLISHING, INC
 PI MALDEN
 PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
 SN 1347-9032
 J9 CANCER SCI
 JI Cancer Sci.
 PD OCT
 PY 2009
 VL 100
 IS 10
 BP 1951
 EP 1956
 DI 10.1111/j.1349-7006.2009.01247.x
 PG 6
 SC Oncology
 GA 494HH
 UT ISI:000269802000025
 ER
 
 PT J
 AU Konishi, K
    Shen, L
    Jelinek, J
    Watanabe, Y
    Ahmed, S
    Kaneko, K
    Kogo, M
    Takano, T
    Imawari, M
    Hamilton, SR
    Issa, JPJ
 AF Konishi, Kazuo
    Shen, Lanlan
    Jelinek, Jaroslav
    Watanabe, Yoshiyuki
    Ahmed, Saira
    Kaneko, Kazuhiro
    Kogo, Mari
    Takano, Toshihumi
    Imawari, Michio
    Hamilton, Stanley R.
    Issa, Jean-Pierre J.
 TI Concordant DNA Methylation in Synchronous Colorectal Carcinomas
 SO CANCER PREVENTION RESEARCH
 LA English
 DT Article
 ID CPG ISLAND METHYLATION; ULCERATIVE-COLITIS; COLON-CANCER;
    MICROSATELLITE INSTABILITY; THERAPEUTIC IMPLICATIONS; RECTUM;
    PHENOTYPE; P53; MUTATIONS; POLYPS
 AB Epigenetic changes have been proposed as mediators of the field defect
    in colorectal carcinogenesis, which has implications for risk
    assessment and cancer prevention. As a test of this hypothesis, we
    evaluated the methylation status of eight genes (MINT1, 2, 31, MLH1,
    p16, p14, MGMT, and ESR1), as well as BRAF and KRAS mutations, in 57
    multiple colorectal neoplasias (M-CRN) and compared these to 69
    solitary colorectal cancers (S-CRC). There were no significant
    differences in methylation between M-CRNs and S-CRCs except for p14 and
    MGMT that was significantly higher in M-CRNs than S-CRCs (16.1% versus
    9.3%; 26.5% versus 17.3%, respectively; P < 0.05). We found significant
    (P < 0.05) correlations for MINT1 (r = 0.8), p16 (r = 0.8), MLH1 (r =
    0.9), and MGMT (r = 0.6) methylation between tumors pairs of the same
    site (proximal/proximal and distal/distal). KRAS showed no concordance
    in mutations. BRAF mutation showed concordance in proximal site pairs
    but was discordant in different site pairs. Histologically, eight of 10
    paired cancers with similar locations were concordant for a cribriform
    glandular configuration. We conclude that synchronous colorectal tumors
    of the same site are highly concordant for methylation of multiple
    genes, BRAF mutations, and a cribriform glandular configuration, all
    consistent with a patient-specific predisposition to particular
    subtypes of colorectal cancers. Screening for and secondary prevention
    of colon cancer should take this fact into account.
 C1 [Issa, Jean-Pierre J.] Univ Texas MD Anderson Canc Ctr, Dept Leukemia, Unit428, Houston, TX 77030 USA.
    [Hamilton, Stanley R.] Univ Texas MD Anderson Canc Ctr, Dept Pathol, Houston, TX 77030 USA.
    [Konishi, Kazuo; Kaneko, Kazuhiro; Imawari, Michio] Showa Univ, Sch Med, Dept Gastroenterol, Tokyo 142, Japan.
    [Kogo, Mari] Showa Univ, Sch Pharm, Promot Ctr Pharmaceut Educ, Tokyo 142, Japan.
    [Watanabe, Yoshiyuki] St Marianna Univ, Sch Med, Dept Internal Med, Div Gastroenterol & Hepatol, Kawasaki, Kanagawa, Japan.
    [Takano, Toshihumi] St Marianna Univ, Sch Med, Dept Diagnost Pathol, Kanagawa, Japan.
 RP Issa, JPJ, Univ Texas MD Anderson Canc Ctr, Dept Leukemia, Unit428,
    1515 Holcombe Blvd, Houston, TX 77030 USA.
 EM jpissa@mdanderson.org
 FU NIH [CA098006, CA105346]; F. M. Kirby Foundation 
 FX Grant support: NIH grants CA098006 and CA105346. J.P. Issa is an
    American Cancer Society Clinical Research Professor supported by a
    generous gift from the F. M. Kirby Foundation.
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 NR 48
 TC 4
 PU AMER ASSOC CANCER RESEARCH
 PI PHILADELPHIA
 PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
 SN 1940-6207
 J9 CANCER PREV RES
 JI Cancer Prev. Res.
 PD SEP
 PY 2009
 VL 2
 IS 9
 BP 814
 EP 822
 DI 10.1158/1940-6207.CAPR-09-0054
 PG 9
 SC Oncology
 GA 492YY
 UT ISI:000269700400008
 ER
 
 PT J
 AU Zhou, YQ
    Yang, ZL
    Xu, L
    Li, P
    Hu, YZ
 AF Zhou, Yong-Qiang
    Yang, Zhong-Lin
    Xu, Lei
    Li, Ping
    Hu, Yu-Zhu
 TI Akebia saponin D, a saponin component from Dipsacus asper Wall,
    protects PC 12 cells against amyloid-beta induced cytotoxicity
 SO CELL BIOLOGY INTERNATIONAL
 LA English
 DT Article
 DE Dipsacus asper Wall; Akebia Saponin D; Amyloid beta; Alzheimer's disease
 ID SALVIANOLIC-ACID-B; BLOOD-BRAIN-BARRIER; ALZHEIMERS-DISEASE; IN-VITRO;
    TAU-PHOSPHORYLATION; MODEL; NANOPARTICLES; ANTIOXIDANT; MECHANISMS;
    ESTROGEN
 AB According to Traditional Chinese Medicine, Alzheimer's disease (AD) is
    regarded as senile dementia, and the etiopathogenesis lies in kidney
    deficiency during aging. Dipsacus asper Wall (DAW), a well-known
    traditional Chinese medicine for enhancing kidney activity, may possess
    the therapeutic effects against AD. Our objectives were to investigate
    the protective effects of DAW against the amyloid-beta peptide (A
    beta)-induced cytotoxicity and explore its major active components.
    Injury of PC 12 cells mediated by A beta(25-35) was adopted to assess
    the cytoprotective effects of DAW aqueous extract and various
    fractions. Salvianolic acid B, a polyphenol compound isolated from
    Salvia miltiorrhiza, was employed as a positive control agent due to
    its markedly protective effect against neurotoxicity of amyloid beta.
    Five chemical fractions (i.e. alkaloids, essential oil, saponins,
    iridoid glucoside and polysaccharides) were prepared for activity test
    and analyzed by HPLC for active components identification. In addition,
    Akebia saponin D (the most important compound in DAW saponins) and
    hederagenin (the mother nucleus of akebia saponin D) were prepared for
    testing of their activity. DAW water extract, saponins fraction and
    akebia saponin D had the neuroprotective capacity to antagonize A
    beta(25-35)-induced cytotoxicity in PC 12 cells. In contrast, other
    fractions and hederagenin had no cytoprotective action. This research
    suggests that DAW may represent a potential treatment strategy for AD
    and akebia saponin D is one of its active components. (C) 2009
    International Federation for Cell Biology. Published by Elsevier Ltd.
    All rights reserved.
 C1 [Zhou, Yong-Qiang; Yang, Zhong-Lin; Xu, Lei; Li, Ping] China Pharmaceut Univ, Key Lab Modern Chinese Med, Minist Educ, Nanjing 210009, Peoples R China.
    [Hu, Yu-Zhu] Minist Educ, Key Lab Drug Qual Control & Pharmacovigilance, Nanjing 210009, Peoples R China.
 RP Yang, ZL, China Pharmaceut Univ, Key Lab Modern Chinese Med, Minist
    Educ, 24 Tongjia Lane, Nanjing 210009, Peoples R China.
 EM yzl1950cpu@163.com
 FU National Natural Science Foundation of China [30730113]
 FX This work was supported by the National Natural Science Foundation of
    China (Grant no. 30730113).
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 NR 26
 TC 0
 PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
 PI LONDON
 PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
 SN 1065-6995
 J9 CELL BIOL INT
 JI Cell Biol. Int.
 PD OCT
 PY 2009
 VL 33
 IS 10
 BP 1102
 EP 1110
 DI 10.1016/j.cellbi.2009.06.028
 PG 9
 SC Cell Biology
 GA 491JA
 UT ISI:000269573500009
 ER
 
 PT J
 AU Wilcox, RA
    Feldman, AL
    Wada, DA
    Yang, ZZ
    Comfere, NI
    Dong, HD
    Kwon, ED
    Novak, AJ
    Markovic, SN
    Pittelkow, MR
    Witzig, TE
    Ansell, SM
 AF Wilcox, Ryan A.
    Feldman, Andrew L.
    Wada, David A.
    Yang, Zhi-Zhang
    Comfere, Nneka I.
    Dong, Haidong
    Kwon, Eugene D.
    Novak, Anne J.
    Markovic, Svetomir N.
    Pittelkow, Mark R.
    Witzig, Thomas E.
    Ansell, Stephen M.
 TI B7-H1 (PD-L1, CD274) suppresses host immunity in T-cell
    lymphoproliferative disorders
 SO BLOOD
 LA English
 DT Article
 ID ABSOLUTE LYMPHOCYTE COUNT; LEUKOCYTE ANTIGEN-DR; NON-HODGKIN-LYMPHOMA;
    FOLLICULAR LYMPHOMAS; PROGNOSTIC MARKER; TYROSINE KINASE;
    TUMOR-IMMUNITY; EXPRESSION; SURVIVAL; IDENTIFICATION
 AB Stromal elements present within the tumor microenvironment may suppress
    host immunity and promote the growth of malignant lymphocytes in B
    cell-derived non-Hodgkin lymphoma (NHL). In contrast, little is known
    about the microenvironment's role in T cell-derived NHL. B7-H1 (PD-L1,
    CD274), a member of the B7 family of costimulatory/coinhibitory ligands
    expressed by both malignant cells and stromal cells within the tumor
    microenvironment, has emerged as an important immune modulator capable
    of suppressing host immunity. Therefore, B7-H1 expression and function
    were analyzed in cutaneous and peripheral T-cell NHL. B7-H1 was
    expressed by tumor cells, monocytes, and monocyte-derived cells within
    the tumor microenvironment in T-cell NHL and was found to inhibit
    T-cell proliferation and promote the induction of FoxP3(+) regulatory T
    cells. Collectively, the data presented provide the first evidence
    implicating B7-H1 in the suppression of host immunity in T-cell
    lymphoproliferative disorders and suggest that the targeting of B7-H1
    may represent a novel therapeutic approach. (Blood. 2009; 114:
    2149-2158)
 C1 [Wilcox, Ryan A.; Yang, Zhi-Zhang; Novak, Anne J.; Markovic, Svetomir N.; Witzig, Thomas E.; Ansell, Stephen M.] Mayo Clin, Div Hematol, Rochester, MN 55905 USA.
    [Feldman, Andrew L.] Mayo Clin, Dept Lab Med & Pathol, Rochester, MN 55905 USA.
    [Wada, David A.; Comfere, Nneka I.; Pittelkow, Mark R.] Mayo Clin, Dept Dermatol, Rochester, MN 55905 USA.
    [Dong, Haidong] Mayo Clin, Dept Immunol, Rochester, MN 55905 USA.
    [Kwon, Eugene D.] Mayo Clin, Dept Urol, Rochester, MN 55905 USA.
 RP Ansell, SM, Mayo Clin, Div Hematol & Internal Med, 200 1st St SW,
    Rochester, MN 55905 USA.
 EM ansell.stephen@mayo.edu
 FU National Institutes of Health [CA92104, CA97274]
 FX This work was supported in part by the National Institutes of Health
    (grants CA92104 and CA97274).
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 NR 50
 TC 8
 PU AMER SOC HEMATOLOGY
 PI WASHINGTON
 PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
 SN 0006-4971
 J9 BLOOD
 JI Blood
 PD SEP 3
 PY 2009
 VL 114
 IS 10
 BP 2149
 EP 2158
 DI 10.1182/blood-2009-04-216671
 PG 10
 SC Hematology
 GA 490RZ
 UT ISI:000269523300021
 ER
 
 PT J
 AU Cao, DY
    Yang, JY
    Yue, SQ
    Tao, KS
    Song, ZS
    Wang, DS
    Yang, YL
    Dou, KF
 AF Cao, Da-Yong
    Yang, Jing-Yue
    Yue, Shu-Qiang
    Tao, Kai-Shan
    Song, Zhen-Shun
    Wang, De-Sheng
    Yang, Yan-Ling
    Dou, Ke-Feng
 TI Comparative analysis of DC fused with allogeneic hepatocellular
    carcinoma cell line HepG2 and autologous tumor cells as potential
    cancer vaccines against hepatocellular carcinoma
 SO CELLULAR IMMUNOLOGY
 LA English
 DT Article
 DE Dendritic cells; Cytotoxic T lymphocytes; Immunotherapy; Allogeneic;
    HepG2
 ID DENDRITIC CELLS; ANTITUMOR IMMUNITY; T-CELLS; VACCINATION; RESPONSES;
    IMMUNOTHERAPY; GENERATION; LYSATE; EPIDEMIOLOGY; MELANOMA
 AB Fusions of patient-derived dendritic cells (DCs) and autologous tumor
    cells induce T-cell responses against autologous tumors in animal
    models and human clinical trials. These fusion cells require
    patient-derived tumor cells, which are not, however, always available.
    Here we fused autologous DCs from patients with hepatocellular
    carcinoma (HCC) to an allogeneic HCC cell line (HepG2). These fusion
    cells co-expressed tumor-associated antigens (TAAs) and DC-derived
    costimulatory and MHC molecules. Both CD4(+) and CD8(+) T cells were
    activated by the fusion cells. Cytotoxic T lymphocytes (C7Ls) induced
    by the fusion cells were able to kill autologous HCC by HLA-A2- and/or
    HLA-A24-restricted mechanisms. CTL activity against shared TAAs
    indicates that the presence of alloantigens does not prevent the
    development of CTLs with activity against autologous HCC cells. These
    fusion cells may have applications in anti-tumor immunotherapy through
    cross-priming against shared tumor antigens and may provide a platform
    for adoptive immunotherapy. Crown Copyright (C) 2009 Published by
    Elsevier Inc. All rights reserved.
 C1 [Cao, Da-Yong; Yue, Shu-Qiang; Tao, Kai-Shan; Song, Zhen-Shun; Wang, De-Sheng; Yang, Yan-Ling; Dou, Ke-Feng] Fourth Mil Med Univ, Dept Hepatobiliary Surg, State Key Discipline Cell Biol, Xijing Hosp, Xian 710032, Shaanxi, Peoples R China.
    [Yang, Jing-Yue] Fourth Mil Med Univ, Dept Clin Oncol, State Key Discipline Cell Biol, Xijing Hosp, Xian 710032, Shaanxi, Peoples R China.
 RP Dou, KF, Fourth Mil Med Univ, Dept Hepatobiliary Surg, State Key
    Discipline Cell Biol, Xijing Hosp, 17 Chonglexi Rd, Xian 710032,
    Shaanxi, Peoples R China.
 EM DouKF@sohu.com
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 NR 26
 TC 2
 PU ACADEMIC PRESS INC ELSEVIER SCIENCE
 PI SAN DIEGO
 PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
 SN 0008-8749
 J9 CELL IMMUNOL
 JI Cell. Immunol.
 PY 2009
 VL 259
 IS 1
 BP 13
 EP 20
 DI 10.1016/j.cellimm.2009.05.007
 PG 8
 SC Cell Biology; Immunology
 GA 488NJ
 UT ISI:000269356200003
 ER
 
 PT J
 AU Lin, WT
    Huang, CC
    Lin, TJ
    Chen, JR
    Shieh, MJ
    Peng, HC
    Yang, SC
    Huang, CY
 AF Lin, Wan-Teng
    Huang, Chi-Chang
    Lin, Tien-Jen
    Chen, Jiun-Rong
    Shieh, Ming-Jer
    Peng, Hsiang-Chi
    Yang, Suh-Ching
    Huang, Chih-Yang
 TI Effects of beta-carotene on antioxidant status in rats with chronic
    alcohol consumption
 SO CELL BIOCHEMISTRY AND FUNCTION
 LA English
 DT Article
 DE alcoholic liver disease; antioxidant capacity; beta-carotene; lipid
    peroxidation; oxidative stress
 ID ALPHA-TOCOPHEROL; LIVER-DISEASE; LIPID-PEROXIDATION; OXIDATIVE STRESS;
    ASCORBIC-ACID; IN-VIVO; ETHANOL; ENZYMES; DIET
 AB This study examined the effects of beta-carotene on antioxidant status
    in rats with chronic alcohol consumption. At the beginning of
    experiment (week 0), according to both the plasma aspartate
    aminotransferase (AST) and alanine aminotransferase (ALT) activities,
    rats (n = 24) were divided into 3 groups and fed with a standard diet
    (group C), a diet containing ethanol (group E), or a diet containing
    ethanol and beta-carotene (group E+B). After 10 weeks, plasma AST and
    ALT, fat accumulation in the liver, antioxidant enzyme activities in
    erythrocytes and the liver, malondialdehyde (MDA), and alpha-tocopherol
    and retinol in plasma and hepatic samples were analyzed. The chronic
    alcohol diet significantly increased AST and ALT levels in plasma, and
    these changes were prevented by supplementing the diet with
    beta-carotene. Glutathione (GSH) in erythrocytes and in the liver was
    significantly elevated in rats fed with a diet containing
    beta-carotene. The results indicate that beta-carotene supplementation
    can prevent ethanol-induced liver damage and increase GSH
    concentrations in erythrocytes and the liver. Copyright (C) 2009 John
    Wiley & Sons, Ltd.
 C1 [Chen, Jiun-Rong; Shieh, Ming-Jer; Peng, Hsiang-Chi; Yang, Suh-Ching] Taipei Med Univ, Sch Nutr & Hlth Sci, Taipei 11031, Taiwan.
    [Lin, Wan-Teng] Tunghai Univ, Coll Agr, Dept Hospitality Management, Taichung 40704, Taiwan.
    [Huang, Chi-Chang] Acad Sinica, Agr Biotechnol Res Ctr, Taipei 115, Taiwan.
    [Lin, Tien-Jen] Municipal Wan Fang Hosp, Dept Surg, Div Neurosurg, Taipei, Taiwan.
    [Lin, Tien-Jen] Taipei Med Univ, Grad Inst Injury Prevent, Taipei 11031, Taiwan.
    [Huang, Chih-Yang] Grad Inst Chinese Med Sci, Grad Inst Basic Med Sci, Taichung, Taiwan.
    [Huang, Chih-Yang] China Med Univ, Taichung, Taiwan.
    [Huang, Chih-Yang] Asia Univ, Dept Hlth & Nutr Biotechnol, Taichung, Taiwan.
 RP Yang, SC, Taipei Med Univ, Sch Nutr & Hlth Sci, 250 Wu Xin St, Taipei
    11031, Taiwan.
 EM sokei@tmu.edu.tw
    cyhuang@mail.cmu.edu.tw
 FU National Science Council of Taiwan [NSC89-2320-B-038-034]
 FX This study is supported by the National Science Council of Taiwan
    (NSC89-2320-B-038-034).
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 NR 27
 TC 2
 PU JOHN WILEY & SONS LTD
 PI CHICHESTER
 PA THE ATRIUM, SOUTHERN GATE, CHICHESTER PO19 8SQ, W SUSSEX, ENGLAND
 SN 0263-6484
 J9 CELL BIOCHEM FUNCT
 JI Cell Biochem. Funct.
 PD AUG
 PY 2009
 VL 27
 IS 6
 BP 344
 EP 350
 DI 10.1002/cbf.1579
 PG 7
 SC Biochemistry & Molecular Biology; Cell Biology
 GA 488XX
 UT ISI:000269384800003
 ER
 
 PT J
 AU Zhang, HQ
    Yang, RW
    Zhang, L
    Ding, CB
    Zeng, J
    Zhou, YH
 AF Zhang, Hai-Qin
    Yang, Rui-Wu
    Zhang, Li
    Ding, Chun-Bang
    Zeng, Jian
    Zhou, Yong-Hong
 TI Genetic diversity and phylogeny in Hystrix (Poaceae, Triticeae) and
    related genera inferred from Giemsa C-banded karyotypes
 SO GENETICS AND MOLECULAR BIOLOGY
 LA English
 DT Article
 DE C-banding; Elymus; genome; Hystrix; Leymus; Triticeae
 ID MEIOTIC PAIRING BEHAVIOR; PSATHYROSTACHYS-JUNCEA; SYNTHETIC HYBRIDS;
    LEYMUS POACEAE; ELYMUS; SEQUENCES; PATULA
 AB The phylogenetic relationships of 15 taxa from Hystrix and the related
    genera Leymus (NsXm), Elymus (StH), Pseudoroegneria (St), Hordeum (H),
    Psathyrostachys (Ns), and Thinopyrum (E) were examined by using the
    Giemsa C-banded karyotype. The Hy. patula C-banding pattern was similar
    to those of Elymus species, whereas C-banding patterns of the other
    Hystrix species were similar to those of Leymus species. The results
    suggest high genetic diversity within Hystrix, and support treating Hy.
    patula as E. hystrix L., and transferring Hy. coreana, Hy. duthiei ssp.
    duthiei and Hy. duthiei ssp. longearistata to the genus Leymus. On
    comparing C-banding patterns of Elymus species with their diploid
    ancestors (Pseudoroegneria and Hordeum), there are indications that
    certain chromosomal re-arrangements had previously occurred in the St
    and H genomes. Furthermore, a comparison of the C-banding patterns of
    the Hystrix and Leymus species with the potential diploid progenitors
    (Psathyrostachys and Thinopyrum) suggests that Hy. coreana and some
    Leymus species are closely related to the Ns genome of Psathyrostachys,
    whereas Hy. duthiei ssp. duthiei, Hy. duthiei ssp. longearistata and
    some of the Leymus species have a close relationship with the E genome.
    The results suggest a multiple origin of the polyploid genera Hystrix
    and Leymus.
 C1 [Zhang, Hai-Qin; Zeng, Jian; Zhou, Yong-Hong] Sichuan Agr Univ, Triticeae Res Inst, Wenjiang 611130, Sichuan, Peoples R China.
    [Zhang, Hai-Qin; Zhou, Yong-Hong] Sichuan Agr Univ, Minist Educ, Key Lab Crop Genet Resources & Improvement, Wenjiang 611130, Sichuan, Peoples R China.
    [Yang, Rui-Wu; Zhang, Li; Ding, Chun-Bang] Sichuan Agr Univ, Coll Biol & Sci, Wenjiang 611130, Sichuan, Peoples R China.
 RP Zhou, YH, Sichuan Agr Univ, Triticeae Res Inst, Wenjiang 611130,
    Sichuan, Peoples R China.
 EM zhouyh@sicau.edu.cn
 FU Program for Changjiang Scholars ; Innovative Research Team in
    University (PCSIRT) China [IRT 0453]; National Natural Science
    Foundation of China [30670150]; Science and Technology Bureau ;
    Education Bureau of Sichuan Province, China 
 FX We wish to thank Mr. Huan-Lin Shu (Triticeae Research Institute,
    Sichuan Agricultural University, China) for his valuable suggestions on
    C-banding analysis. We are grateful to Dr. S. Sakamoto (Kyoto
    University, Japan) and the American National Plant Germplasm System
    (Pullman, Washington, USA) for providing a part of the seed-material
    used in this study. This study was support by grants from the Program
    for Changjiang Scholars and the Innovative Research Team in University
    (PCSIRT) China (No. IRT 0453), the National Natural Science Foundation
    of China (No. 30670150) and the Science and Technology Bureau and the
    Education Bureau of Sichuan Province, China.
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 NR 34
 TC 0
 PU SOC BRASIL GENETICA
 PI RIBEIRAO PRET
 PA RUA CAP ADELMIO NORBET DA SILVA, 736, ALTO DA BOA VISTA, 14025-670
    RIBEIRAO PRET, BRAZIL
 SN 1415-4757
 J9 GENET MOL BIOL
 JI Genet. Mol. Biol.
 PY 2009
 VL 32
 IS 3
 BP 521
 EP 527
 PG 7
 SC Biochemistry & Molecular Biology; Genetics & Heredity
 GA 485MT
 UT ISI:000269128100015
 ER
 
 PT J
 AU Wang, Y
    Zhang, H
    Chen, YP
    Sun, YM
    Yang, F
    Yu, WH
    Liang, J
    Sun, LY
    Yang, XH
    Shi, L
    Li, RF
    Li, YY
    Zhang, Y
    Li, Q
    Yi, X
    Shang, YF
 AF Wang, Yan
    Zhang, Hua
    Chen, Yupeng
    Sun, Yimin
    Yang, Fen
    Yu, Wenhua
    Liang, Jing
    Sun, Luyang
    Yang, Xiaohan
    Shi, Lei
    Li, Ruifang
    Li, Yanyan
    Zhang, Yu
    Li, Qian
    Yi, Xia
    Shang, Yongfeng
 TI LSD1 Is a Subunit of the NuRD Complex and Targets the Metastasis
    Programs in Breast Cancer
 SO CELL
 LA English
 DT Article
 ID RECEPTOR-REGULATED TRANSCRIPTION; HISTONE LYSINE DEMETHYLASES;
    TGF-BETA; ENDOMETRIAL CARCINOGENESIS; MESENCHYMAL TRANSITIONS;
    MOLECULAR-MECHANISMS; MI-2/NURD COMPLEX; GENE-REGULATION; EMERGING
    ROLES; ESTROGEN
 AB Lysine-specific demethylase 1 (LSD1) exerts pathway-specific activity
    in animal development and has been linked to several high-risk cancers.
    Here, we report that LSD1 is an integral component of the
    Mi-2/nucleosome remodeling and deacetylase (NuRD) complex.
    Transcriptional target analysis revealed that the LSD1/NuRD complexes
    regulate several cellular signaling pathways including TGF beta 1
    signaling pathway that are critically involved in cell proliferation,
    survival, and epithelial-to-mesenchymal transition. We demonstrated
    that LSD1 inhibits the invasion of breast cancer cells in vitro and
    suppresses breast cancer metastatic potential in vivo. We found that
    LSD1 is downregulated in breast carcinomas and that its level of
    expression is negatively correlated with that of TGFb1. Our data
    provide a molecular basis for the interplay of histone demethylation
    and deacetylation in chromatin remodeling. By enlisting LSD1, the NuRD
    complex expands its chromatin remodeling capacity to include ATPase,
    histone deacetylase, and histone demethylase.
 C1 [Wang, Yan; Zhang, Hua; Chen, Yupeng; Sun, Yimin; Yang, Fen; Yu, Wenhua; Liang, Jing; Sun, Luyang; Yang, Xiaohan; Shi, Lei; Li, Ruifang; Li, Yanyan; Zhang, Yu; Li, Qian; Yi, Xia; Shang, Yongfeng] Peking Univ, Hlth Sci Ctr, Dept Biochem & Mol Biol, Key Lab Carcinogenesis & Translat Res,Minist Educ, Beijing 100191, Peoples R China.
 RP Shang, YF, Peking Univ, Hlth Sci Ctr, Dept Biochem & Mol Biol, Key Lab
    Carcinogenesis & Translat Res,Minist Educ, Beijing 100191, Peoples R
    China.
 EM yshang@hsc.pku.edu.cn
 FU National Natural Science Foundation of China [30830032, 30621002,
    30470912]; Ministry of Science and Technology of China [2006AA02Z466,
    2005CB522404, 2007CB914503]
 FX We thank Joanne Balmer Green (Penn State University) for editorial
    assistance. This work was supported by grants (30830032, 30621002 and
    30470912, to Y.S.) from the National Natural Science Foundation of
    China and grants (863 Program: 2006AA02Z466 and 973 Program:
    2005CB522404 and 2007CB914503, to Y.S.) from the Ministry of Science
    and Technology of China.
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 NR 44
 TC 39
 PU CELL PRESS
 PI CAMBRIDGE
 PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
 SN 0092-8674
 J9 CELL
 JI Cell
 PD AUG 21
 PY 2009
 VL 138
 IS 4
 BP 660
 EP 672
 DI 10.1016/j.cell.2009.05.050
 PG 13
 SC Biochemistry & Molecular Biology; Cell Biology
 GA 485WS
 UT ISI:000269156100009
 ER
 
 PT J
 AU Yamada, Y
    Itoh, Y
    Aoki, S
    Nakamura, K
    Taki, T
    Naruse, K
    Tobiume, M
    Zennami, K
    Katsuda, R
    Kato, Y
    Watanabe, M
    Nishikawa, G
    Minami, M
    Nakahira, M
    Ukai, S
    Sawada, M
    Kitamura, A
    Honda, N
 AF Yamada, Yoshiaki
    Itoh, Youko
    Aoki, Shigeyuki
    Nakamura, Kogenta
    Taki, Tomohiro
    Naruse, Katsuya
    Tobiume, Motoi
    Zennami, Kenji
    Katsuda, Remi
    Kato, Yoshiharu
    Watanabe, Masahito
    Nishikawa, Genya
    Minami, Miwako
    Nakahira, Mariko
    Ukai, Sayaka
    Sawada, Masaki
    Kitamura, Akiko
    Honda, Nobuaki
 TI Preliminary results of M-VAC chemotherapy combined with mild
    hyperthermia, a new therapeutic strategy for advanced or metastatic
    transitional cell carcinoma of the urothelium
 SO CANCER CHEMOTHERAPY AND PHARMACOLOGY
 LA English
 DT Article
 DE Mild hyperthermia; M-VAC chemotherapy; Heat-shock protein (HSP);
    Transitional cell carcinoma; Urothelial cancer
 ID GEMCITABINE PLUS CISPLATIN; MOLECULAR TARGETED THERAPY; IN-SITU
    HYBRIDIZATION; BLADDER-CANCER; RADICAL CYSTECTOMY; PHASE-III;
    METHOTREXATE; VINBLASTINE; DOXORUBICIN; COMBINATION
 AB We evaluated the efficacy and safety of M-VAC chemotherapy combined
    with mild hyperthermia, a new therapeutic strategy for advanced
    metastatic transitional cell carcinoma of the urothelium.
    The subjects were 12 patients diagnosed with advanced metastatic
    transitional cell carcinoma of the urothelium. For mild hyperthermia,
    the patients' oral temperature was elevated to about 38A degrees C by
    heating for 20 min and retaining the heat for 20 min with a
    far-infrared heater. The antitumor effect was evaluated according to
    the RECIST, while adverse drug reactions were assessed based on the
    NCI-CTC.
    The antitumor effect was rated as partial remission (PR) in 10 of the
    12 patients and stable disease in 2 patients, with an efficacy rate of
    83% (10/12). All 10 patients who had achieved PR received three courses
    of treatment. Of the 12 patients, 5 died during the observation period,
    with survival for 9-23 months (mean: 15.6 months). Adverse drug
    reactions included myelosuppression in all patients (Grade 3 in 4
    patients, Grade 4 in 8), and gastrointestinal toxicity, such as nausea
    or vomiting, which was mild (Grade 0 in 2 patients, Grade 1 in 8, Grade
    2 in 1, Grade 3 in 1).
    The results of the present study suggest that M-VAC chemotherapy
    combined with mild hyperthermia, which potentiates the anticancer
    effect and reduces adverse drug reactions such as gastrointestinal
    symptoms, is a useful and safe method for the treatment of advanced
    transitional cell carcinoma of the urothelium.
 C1 [Yamada, Yoshiaki; Aoki, Shigeyuki; Nakamura, Kogenta; Taki, Tomohiro; Naruse, Katsuya; Tobiume, Motoi; Zennami, Kenji; Katsuda, Remi; Kato, Yoshiharu; Watanabe, Masahito; Nishikawa, Genya; Honda, Nobuaki] Aichi Med Univ, Dept Urol, Sch Med, Aichi 4801195, Japan.
    [Itoh, Youko] Aichi Med Univ, Radioisotope Res Ctr, Sch Med, Aichi, Japan.
    [Minami, Miwako; Nakahira, Mariko; Ukai, Sayaka; Sawada, Masaki; Kitamura, Akiko] Aichi Med Univ Hosp, Div Nursing, Aichi, Japan.
 RP Yamada, Y, Aichi Med Univ, Dept Urol, Sch Med, Aichi 4801195, Japan.
 EM yy1124@aichi-med-u.ac.jp
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 NR 24
 TC 4
 PU SPRINGER
 PI NEW YORK
 PA 233 SPRING ST, NEW YORK, NY 10013 USA
 SN 0344-5704
 J9 CANCER CHEMOTHER PHARMACOL
 JI Cancer Chemother. Pharmacol.
 PD NOV
 PY 2009
 VL 64
 IS 6
 BP 1079
 EP 1083
 DI 10.1007/s00280-009-0964-2
 PG 5
 SC Oncology; Pharmacology & Pharmacy
 GA 485HU
 UT ISI:000269112600003
 ER
 
 PT J
 AU Yang, B
    Zwaans, BMM
    Eckersdorff, M
    Lombard, DB
 AF Yang, Bo
    Zwaans, Bernadette M. M.
    Eckersdorff, Mark
    Lombard, David B.
 TI The sirtuin SIRT6 deacetylates H3 K56Ac in vivo to promote genomic
    stability
 SO CELL CYCLE
 LA English
 DT Letter
 DE sirtuin; SIRT6; H3 K56Ac; DNA damage; Sir2; chromatin
 ID HISTONE H3; ACETYLATION
 C1 [Yang, Bo; Zwaans, Bernadette M. M.; Eckersdorff, Mark; Lombard, David B.] Univ Michigan, Dept Pathol, Ann Arbor, MI 48109 USA.
    [Lombard, David B.] Univ Michigan, Inst Gerontol, Ann Arbor, MI 48109 USA.
 RP Lombard, DB, Univ Michigan, Dept Pathol, 3015 BSRB,109 Zina Pitcher Pl,
    Ann Arbor, MI 48109 USA.
 EM davidlom@umich.edu
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 NR 10
 TC 19
 PU LANDES BIOSCIENCE
 PI AUSTIN
 PA 1002 WEST AVENUE, 2ND FLOOR, AUSTIN, TX 78701 USA
 SN 1538-4101
 J9 CELL CYCLE
 JI Cell Cycle
 PD AUG 15
 PY 2009
 VL 8
 IS 16
 BP 2662
 EP 2663
 PG 2
 SC Cell Biology
 GA 483QY
 UT ISI:000268983900035
 ER
 
 PT J
 AU Watanabe, J
    Nishimura, Y
    Tsunoda, S
    Kawaguchi, M
    Okayasu, I
    Kuramoto, H
 AF Watanabe, Jun
    Nishimura, Yukari
    Tsunoda, Shinpei
    Kawaguchi, Miwa
    Okayasu, Isao
    Kuramoto, Hiroyuki
 TI Liquid-Based Preparation for Endometrial Cytology-Usefulness for
    Predicting the Prognosis of Endometrial Carcinoma Preoperatively
 SO CANCER CYTOPATHOLOGY
 LA English
 DT Article
 DE endometrial carcinoma; endometrial cytology; liquid-based cytology;
    immunocytochemistry; immunohistochemistry; clinicopathologic parameter;
    prognosis
 ID PROGESTERONE RECEPTOR-A; ESTROGEN-RECEPTOR; STEROID-RECEPTORS;
    ER-ALPHA; CYCLIN-A; PAP TEST; ADENOCARCINOMA; EXPRESSION; P53;
    PERFORMANCE
 AB The authors evaluated the applicability and usefulness of
    immunocytochemical staining for cyclin A, p53, estrogen receptor alpha
    (ER-alpha), and progesterone receptor B (PR-B) as a preoperative
    prognostic indicators for endometrial carcinoma using endometrial
    cytology with the liquid-based cytology (LBC) method. METHODS:
    Cytologic specimens from 44 patients who had endometrial carcinoma were
    prepared with the LBC method. The results of immunocytochemical and
    immunohistochemical staining for cyclin A, p53, ER-alpha, and PR-B were
    compared with clinicopathologic parameters and prognosis. RESULTS:
    Patients who had positive results for cyclin A and p53 and negative
    results for ER-alpha and PR-B appeared to have unfavorable
    clinicopathologic characteristics, such as high-grade histology,
    advanced clinical stage, lymphovascular space involvement (LVSI), and
    deeper myometrial invasion (MI), and had a poor prognosis. In contrast,
    patients who had positive results for ER-alpha and PR-B, and negative
    results for cyclin A and p53 had favorable characteristics, such well
    differentiated tumor, early clinical stage, negative LVSI, and less MI,
    and had a good prognosis. Immunostaining results from cytologic
    specimens obtained in the clinic and at surgery and from histologic
    specimens obtained at surgery were correlated positively. CONCLUSIONS:
    Consistent specimens that were prepared using the LBC method
    facilitated multiple immunocytochemical analyses. Endometrial cytology
    with the LBC method was useful for predicting the prognosis of patients
    with endometrial carcinoma before therapy. Cancer (Cancer Cytopathol)
    2009;117:254-63. (c) 2009 American Cancer Society.
 C1 [Watanabe, Jun; Okayasu, Isao] Kitasato Univ, Sch Med, Dept Pathol, Kanagawa 2288555, Japan.
    [Watanabe, Jun; Nishimura, Yukari; Kuramoto, Hiroyuki] Kitasato Univ, Grad Sch Med Sci, Dept Clin Cytol, Kanagawa 2288555, Japan.
    [Tsunoda, Shinpei; Kawaguchi, Miwa; Kuramoto, Hiroyuki] Kitasato Univ, Sch Med, Dept Obstet & Gynecol, Kanagawa 2288555, Japan.
    [Kuramoto, Hiroyuki] Kanagawa Hlth Serv Assoc, Kanagawa, Japan.
 RP Watanabe, J, Kitasato Univ, Sch Med, Dept Pathol, 1-15-1 Kitasato,
    Kanagawa 2288555, Japan.
 EM watajun@med.kitasato-u.ac.jp
 FU Graduate School of Medical Sciences, Kitasato University, Japan
    [1998-A03, 2002-A07]
 FX Supported by grants-in-aid for the Integrated Research Program
    (1998-A03 and 2002-A07) of the Graduate School of Medical Sciences,
    Kitasato University, Japan.
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 NR 34
 TC 0
 PU JOHN WILEY & SONS INC
 PI HOBOKEN
 PA 111 RIVER ST, HOBOKEN, NJ 07030 USA
 SN 1934-662X
 J9 CANCER CYTOPATHOL
 JI Cancer Cytopathol.
 PD AUG 25
 PY 2009
 VL 117
 IS 4
 BP 254
 EP 263
 DI 10.1002/cncy.20035
 PG 10
 SC Oncology; Pathology
 GA 484CX
 UT ISI:000269022000003
 ER
 
 PT J
 AU Tsukuda, M
    Ishitoya, J
    Mikami, Y
    Matsuda, H
    Horiuchi, C
    Taguchi, T
    Satake, K
    Kawano, T
    Takahashi, M
    Nishimura, G
    Kawakami, M
    Sakuma, Y
    Watanabe, M
    Shiono, O
    Komatsu, M
    Yamashita, Y
 AF Tsukuda, Mamoru
    Ishitoya, Junichi
    Mikami, Yasukazu
    Matsuda, Hideki
    Horiuchi, Choichi
    Taguchi, Takahide
    Satake, Kenichi
    Kawano, Toshiro
    Takahashi, Masahiro
    Nishimura, Goshi
    Kawakami, Mariko
    Sakuma, Yasunori
    Watanabe, Makiko
    Shiono, Osamu
    Komatsu, Masanori
    Yamashita, Yukiko
 TI Analysis of feasibility and toxicity of concurrent chemoradiotherapy
    with S-1 for locally advanced squamous cell carcinoma of the head and
    neck in elderly cases and/or cases with comorbidity
 SO CANCER CHEMOTHERAPY AND PHARMACOLOGY
 LA English
 DT Article
 DE S-1; Chemoradiotherapy; Elderly cases; Cases with comorbidity
 ID POOR PERFORMANCE STATUS; RADIATION-THERAPY; ORAL FLUOROPYRIMIDINE;
    ORGAN PRESERVATION; PHASE-I; CANCER; 5-FLUOROURACIL; CISPLATIN;
    CHEMOTHERAPY; RADIOTHERAPY
 AB The aim of this study was to evaluate the feasibility and toxicity of
    concurrent chemoradiotherapy (CCRT) with S-1 in patients with locally
    advanced squamous cell carcinoma of the head and neck (SCCHN) in
    elderly cases and/or cases with comorbidity.
    Fifty eligible patients with stage III (15 cases) or stage IV (35
    cases) SCCHN were treated with CCRT. Thirteen cases had an advanced age
    of over 75 years and 37 cases had comorbidity. Definitive radiotherapy
    was delivered up to a total dose of 66-70.2 Gy. The patients received
    two courses of oral S-1 (40 or 50 mg twice a day [80 or 100 mg/day])
    for 2 weeks followed by 1 week of rest while receiving CCRT.
    All the patients received the planned radiotherapy and at least one
    course of S-1. Grade 3 mucositis occurred in 20% of the patients
    (10/50). Grade 3 neutropenia occurred in 12% (6/50) and leukocytopenia
    occurred in 6% (3/50) of the cases. Pathologically, the complete
    response rates were 93% in stage III and 54% in stage IV.
    Concurrent chemoradiotherapy with S-1 is a safe, well-tolerated and
    effective regimen for locally advanced SCCHN in elderly cases and/or
    cases with comorbidity.
 C1 [Tsukuda, Mamoru; Mikami, Yasukazu; Matsuda, Hideki; Horiuchi, Choichi; Taguchi, Takahide; Satake, Kenichi; Takahashi, Masahiro; Nishimura, Goshi; Kawakami, Mariko; Watanabe, Makiko] Yokohama City Univ, Sch Med, Dept Otorhinolaryngol Head & Neck Surg, Kanazawa Ku, Yokohama, Kanagawa 2360004, Japan.
    [Ishitoya, Junichi; Kawano, Toshiro; Sakuma, Yasunori; Shiono, Osamu; Komatsu, Masanori; Yamashita, Yukiko] Yokohama City Univ, Med Ctr, Dept Otorhinolaryngol, Minami Ku, Yokohama, Kanagawa 2320024, Japan.
 RP Tsukuda, M, Yokohama City Univ, Sch Med, Dept Otorhinolaryngol Head &
    Neck Surg, Kanazawa Ku, 3-9 Fukuura, Yokohama, Kanagawa 2360004, Japan.
 EM mtsukuda@med.yokohama-cu.ac.jp
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 NR 31
 TC 4
 PU SPRINGER
 PI NEW YORK
 PA 233 SPRING ST, NEW YORK, NY 10013 USA
 SN 0344-5704
 J9 CANCER CHEMOTHER PHARMACOL
 JI Cancer Chemother. Pharmacol.
 PD OCT
 PY 2009
 VL 64
 IS 5
 BP 945
 EP 952
 DI 10.1007/s00280-009-0946-4
 PG 8
 SC Oncology; Pharmacology & Pharmacy
 GA 484VN
 UT ISI:000269076700011
 ER
 
 PT J
 AU Peng, PD
    Cohen, CJ
    Yang, S
    Hsu, C
    Jones, S
    Zhao, Y
    Zheng, Z
    Rosenberg, SA
    Morgan, RA
 AF Peng, P. D.
    Cohen, C. J.
    Yang, S.
    Hsu, C.
    Jones, S.
    Zhao, Y.
    Zheng, Z.
    Rosenberg, S. A.
    Morgan, R. A.
 TI Efficient nonviral Sleeping Beauty transposon-based TCR gene transfer
    to peripheral blood lymphocytes confers antigen-specific antitumor
    reactivity
 SO GENE THERAPY
 LA English
 DT Article
 DE Sleeping Beauty transposon; TCR gene therapy; adoptive immunotherapy;
    nonviral vector; T-cell gene transfer
 ID ADOPTIVE CELL TRANSFER; PRIMARY T-CELLS; HUMAN TUMOR; MUTATIONAL
    ANALYSIS; RETROVIRAL VECTOR; TRANSFER THERAPY; EXPRESSION; CANCER;
    INTEGRATION; SYSTEM
 AB Genetically engineered lymphocytes hold promise for the treatment of
    genetic disease, viral infections and cancer. However, current methods
    for genetic transduction of peripheral blood lymphocytes rely on viral
    vectors, which are hindered by production and safety-related problems.
    In this study, we demonstrated an efficient novel nonviral platform for
    gene transfer to lymphocytes. The Sleeping Beauty transposon-mediated
    approach allowed for long-term stable expression of transgenes at
    similar to 50% efficiency. Utilizing transposon constructs expressing
    tumor antigen-specific T-cell receptor genes targeting p53 and MART-1,
    we demonstrated sustained expression and functional reactivity of
    transposon-engineered lymphocytes on encountering target antigen
    presented on tumor cells. We found that transposon- and
    retroviral-modified lymphocytes had comparable transgene expression and
    phenotypic function. These results demonstrate the promise of nonviral
    ex vivo genetic modification of autologous lymphocytes for the
    treatment of cancer and immunologic disease. Gene Therapy (2009) 16,
    1042-1049; doi: 10.1038/gt.2009.54; published online 4 June 2009
 C1 [Peng, P. D.; Cohen, C. J.; Yang, S.; Hsu, C.; Jones, S.; Zhao, Y.; Zheng, Z.; Rosenberg, S. A.; Morgan, R. A.] NCI, Surg Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
 RP Morgan, RA, NCI, Surg Branch, Ctr Canc Res, NIH, 10 Ctr Dr,Bldg 10,CRC
    3W-3864, Bethesda, MD 20892 USA.
 EM rmorgan@mail.nih.gov
 FU National Institute of Health, National Cancer Institute, Center for
    Cancer Research 
 FX We thank Dr Steven R Yant and Dr Mark A Kay of the Departments of
    Pediatrics and Genetics, Stanford University School of Medicine,
    Stanford, CA, for their generous gift of the Sleeping Beauty transposon
    plasmids and hyperactive transposase, as well as for their helpful
    suggestions on this project. We thank FACS lab and TIL lab in Surgery
    Branch for providing technical support and maintenance of tumor cells
    from patients. This work is supported by the Intramural Research
    Program of the National Institute of Health, National Cancer Institute,
    Center for Cancer Research.
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 NR 44
 TC 13
 PU NATURE PUBLISHING GROUP
 PI LONDON
 PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
 SN 0969-7128
 J9 GENE THERAPY
 JI Gene Ther.
 PD AUG
 PY 2009
 VL 16
 IS 8
 BP 1042
 EP 1049
 DI 10.1038/gt.2009.54
 PG 8
 SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology;
    Genetics & Heredity; Medicine, Research & Experimental
 GA 482VH
 UT ISI:000268916800012
 ER
 
 PT J
 AU Yuan, GH
    Wang, YH
    Gluhak-Heinrich, J
    Yang, GB
    Chen, L
    Li, T
    Wu, LA
    Chen, Z
    MacDougall, M
    Chen, S
 AF Yuan, Guohua
    Wang, Yinghua
    Gluhak-Heinrich, Jelica
    Yang, Guobin
    Chen, Lei
    Li, Tong
    Wu, Li-An
    Chen, Zhi
    MacDougall, Mary
    Chen, Shuo
 TI Tissue-specific expression of dentin sialophosphoprotein (DSPP) and its
    polymorphisms in mouse tissues
 SO CELL BIOLOGY INTERNATIONAL
 LA English
 DT Article
 DE Dentin sialophosphoprotein (DSPP); Dentin sialoprotein (DSP); Dentin
    phosphoprotein (DPP); Polymorphism; Dentinogenesis
 ID CASEIN KINASE-I; SUBSTRATE DETERMINANTS; SPATIAL EXPRESSION; MATRIX
    PROTEIN-1; SIALOPROTEIN DSP; GENE; PHOSPHOPROTEIN; BIOMINERALIZATION;
    PHOSPHOPHORYN; MUTATIONS
 AB Dentin sialophosphoprotein (DSPP) consists of dentin sialoprotein (DSP)
    and dentin phosphoprotein (DPP). DSPP is highly expressed in
    mineralized tissues. However, recent studies have shown that DSPP is
    also expressed in several active metabolic ductal epithelial tissues
    and exists in a variety of sequences. We have investigated DSPP
    expression in various mouse tissues using RT-PCR, in situ hybridization
    and immunohistochemical analyses. To identify DSPP gene polymorphisms,
    we screened a mouse tooth cDNA library as well as isolated and
    characterized DSPP variations. Our results show that DSPP is
    predominantly expressed in teeth and moderately in bone tissues. We
    also have characterized a full-length DSPP cDNA clone with an
    open-reading frame of 940 codons and this polyadenylation signal.
    Compared to previously reported mouse DSPP cDNAs, 13 sequence
    variations were identified, including 8 non-synonymous single
    nucleotide polymorphisms and an in-frame indel (8 amino acids) at DPP
    domain of the mouse DSPP. These 8 amino acids are rich in aspartic acid
    and serine residues. Northern blot assay showed a prominent band at 4.4
    kb. RT-PCR demonstrated that this mouse DSPP gene was dominantly
    expressed in teeth. The predicted secondary structure of DPP domain of
    this DSPP showed differences from the previously published mouse DPPs,
    implying that they play different roles during tooth development and
    formation. (C) 2009 International Federation for Cell Biology.
    Published by Elsevier Ltd. All rights reserved.
 C1 [MacDougall, Mary] Univ Alabama, Sch Dent, Dept Oral Maxillofacial Surg, Birmingham, AL 35294 USA.
    [Yuan, Guohua; Wang, Yinghua; Yang, Guobin; Chen, Lei; Li, Tong; Wu, Li-An; Chen, Shuo] Univ Texas Hlth Sci Ctr San Antonio, Dept Pediat Dent, San Antonio, TX 78229 USA.
    [Gluhak-Heinrich, Jelica] Univ Texas Hlth Sci Ctr San Antonio, Dept Orthoped, Sch Dent, San Antonio, TX 78229 USA.
    [Yuan, Guohua] Wuhan Univ, Key Lab Oral Biomed Engn, Minist Educ, Sch & Hosp Stomatol, Wuhan 430072, Peoples R China.
    [Chen, Zhi] Wuhan Univ, Dept Cariol & Endodont, Sch & Hosp Stomatol, Wuhan 430072, Peoples R China.
 RP MacDougall, M, Univ Alabama, Sch Dent, Dept Oral Maxillofacial Surg,
    1919 7th Ave S,SDB 702, Birmingham, AL 35294 USA.
 EM macdougall@uab.edu
    chens0@uthscsa.edu
 FU NIDCR, National Institutes of Health [DE113221, DE019802]; China
    Scholarship Council Award [CSC20073020]
 FX We thank Dr Russel Reiter for critical reading of the manuscript. This
    work was supported by NIDCR, National Institutes of Health, Grant
    DE113221 (M. M.), DE019802 (S. C.) and China Scholarship Council Award
    CSC20073020 (G. Y.).
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 NR 45
 TC 4
 PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
 PI LONDON
 PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
 SN 1065-6995
 J9 CELL BIOL INT
 JI Cell Biol. Int.
 PD AUG
 PY 2009
 VL 33
 IS 8
 BP 816
 EP 829
 DI 10.1016/j.cellbi.2009.05.001
 PG 14
 SC Cell Biology
 GA 481HT
 UT ISI:000268799100002
 ER
 
 PT J
 AU Yang, K
    Jiang, ZL
    Wang, D
    Lian, XH
    Yang, T
 AF Yang, Ke
    Jiang, Zilin
    Wang, Dong
    Lian, Xiaohua
    Yang, Tian
 TI Corneal epithelial-like transdifferentiation of hair follicle stem
    cells is mediated by pax6 and beta-catenin/Lef-1
 SO CELL BIOLOGY INTERNATIONAL
 LA English
 DT Article
 DE Hair follicle stem cells; Cornea; Pax6; beta-Catenin; Lef-1;
    Transdifferentiation; k12
 ID OCULAR SURFACE; BETA-CATENIN; BULGE; SKIN; DIFFERENTIATION;
    RECONSTRUCTION; ENRICHMENT; EPIDERMIS; ANIRIDIA
 AB Several types of adult stem cells are capable of transdifferentiaton
    into other types of tissues. The hair follicle bulge area is an
    abundant and easily accessible source of pluripotent adult stem cells.
    We demonstrate that the bulge KSCs have the potential for
    transdifferentiation into corneal epithelial-like cells. Bulge KSCs
    isolated by collagen type IV adhesiveness possessed the highest colony
    formation efficiency (CFE), and expressed specific markers (CD34 and
    alpha 6-integrin). The isolated cells transdifferentiate into corneal
    epithelial-like cells in conditioned medium containing corneal limbus
    soluble factors, including their specific marker, keratin12. The
    transdifferentiation depends on upregulation of pax6 and downregulation
    of beta-catenin and Lef-1. Furthermore, overexpression of pax6 in bulge
    KSCs induced their expression of k12. The expressions of beta-catenin
    and Lef-1 were not suppressed in the pax6-transfected bulge KSCs, but
    which were downregulated pax6-transfected cells cultured in the
    conditioned medium. Bulge KSCs may have potential therapeutic
    application as cell source for the construction of bioengineered
    corneas. (C) 2009 International Federation for Cell Biology. Published
    by Elsevier Ltd. All rights reserved.
 C1 [Yang, Ke; Lian, Xiaohua; Yang, Tian] Third Mil Med Univ, Dept Cell Biol, Chongqing 400038, Peoples R China.
    [Jiang, Zilin] Chongqing Univ, Bioengn Coll, Chongqing 400038, Peoples R China.
    [Wang, Dong] Third Mil Med Univ, Dept Ultrasound, XinQiao Hosp, Chongqing 400038, Peoples R China.
 RP Lian, XH, Third Mil Med Univ, Dept Cell Biol, Chongqing 400038, Peoples
    R China.
 EM tiany@163.net
 FU Chongqing Science and Technology Commission [CSTC 2004AC5074]
 FX We thank Dr. Masaharu Sakai, Hokkaido University Graduate School of
    Medicine, Japan for providing the plasmid pAct/Pax6. This work was
    supported by Chongqing Science and Technology Commission (No. CSTC
    2004AC5074).
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    10.1073/pnas.0500344102
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    10.1167/iovs.02-0576
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    10.1016/j.neulet.2006.07.049
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    TAYLOR G, 2000, CELL, V102, P451
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 NR 22
 TC 1
 PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
 PI LONDON
 PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
 SN 1065-6995
 J9 CELL BIOL INT
 JI Cell Biol. Int.
 PD AUG
 PY 2009
 VL 33
 IS 8
 BP 861
 EP 866
 DI 10.1016/j.cellbi.2009.04.009
 PG 6
 SC Cell Biology
 GA 481HT
 UT ISI:000268799100007
 ER
 
 PT J
 AU Yamaguchi, N
    Ito, T
    Azuma, S
    Ito, E
    Honma, R
    Yanagisawa, Y
    Nishikawa, A
    Kawamura, M
    Imai, J
    Watanabe, S
    Semba, K
    Inoue, J
 AF Yamaguchi, Noritaka
    Ito, Taku
    Azuma, Sakura
    Ito, Emi
    Honma, Reiko
    Yanagisawa, Yuka
    Nishikawa, Akira
    Kawamura, Mika
    Imai, Jun-ichi
    Watanabe, Shinya
    Semba, Kentaro
    Inoue, Jun-ichiro
 TI Constitutive activation of nuclear factor-kappa B is preferentially
    involved in the proliferation of basal-like subtype breast cancer cell
    lines
 SO CANCER SCIENCE
 LA English
 DT Article
 ID MAMMARY-GLAND DEVELOPMENT; REED-STERNBERG CELLS; GENE-EXPRESSION;
    MULTIPLE-MYELOMA; KINASE; PROGRESSION; TUMORS; DIFFERENTIATION;
    TUMORIGENESIS; RECEPTOR
 AB Constitutive nuclear factor (NF)-kappa B activation is thought to be
    involved in survival, invasion, and metastasis in various types of
    cancers. However, neither the subtypes of breast cancer cells with
    constitutive NF-kappa B activation nor the molecular mechanisms leading
    to its constitutive activation have been clearly defined. Here, we
    quantitatively analyzed basal NF-kappa B activity in 35 human breast
    cancer cell lines and found that most of the cell lines with high
    constitutive NF-kappa B activation were categorized in the estrogen
    receptor negative, progesterone receptor negative, ERBB2 negative
    basal-like subtype, which is the most malignant form of breast cancer.
    Inhibition of constitutive NF-kappa B activation by expression of I
    kappa B alpha super-repressor reduced proliferation of the basal-like
    subtype cell lines. Expression levels of mRNA encoding NF-kappa
    B-inducing kinase (NIK) were elevated in several breast cancer cell
    lines, and RNA interference-mediated knockdown of NIK reduced NF-kappa
    B activation in a subset of the basal-like subtype cell lines with
    upregulated NIK expression. Taken together, these results suggest that
    constitutive NF-kappa B activation, partially dependent on NIK, is
    preferentially involved in proliferation of basal-like subtype breast
    cancer cells and may be a useful therapeutic target for this subtype of
    cancer. (Cancer Sci 2009; 100: 1668-1674).
 C1 [Yamaguchi, Noritaka; Ito, Taku; Inoue, Jun-ichiro] Univ Tokyo, Inst Med Sci, Dept Cellular & Mol Biol, Tokyo, Japan.
    [Azuma, Sakura; Semba, Kentaro] Waseda Univ, Dept Life Sci & Med Biosci, Tokyo, Japan.
    [Yamaguchi, Noritaka; Semba, Kentaro] Consolidated Res Inst Adv Sci Med Care, Tokyo, Japan.
    [Ito, Emi; Honma, Reiko; Yanagisawa, Yuka; Nishikawa, Akira; Kawamura, Mika; Imai, Jun-ichi; Watanabe, Shinya] Fukushima Med Univ, Tokyo Branch, Dept Clin Genom, Translat Res Ctr, Tokyo, Japan.
    [Nishikawa, Akira] Nippon Gene Co, Toyama, Japan.
    [Kawamura, Mika] Medicrome, Kanagawa, Japan.
 RP Inoue, J, Univ Tokyo, Inst Med Sci, Dept Cellular & Mol Biol, 4-6-1
    Shirokanedai, Tokyo, Japan.
 EM jun-i@ims.u-tokyo.ac.jp
 FU Ministry of Education, Culture, Sports, Science, and Technology, Japan 
 FX We thank Dr Y. Kanegae and Dr I. Saito (University of Tokyo, Japan) for
    preparation of the adenoviral vectors. We also thank Ms K. Shimizu, M.
    Hashimoto, J. Kuritani, and K. Semba for secretarial assistance. This
    study was supported by a Grant-in-Aid for Scientific Research on
    Priority Areas and 'Establishment of Consolidated Research Institute
    for Advanced Science and Medical Care' Project, Ministry of Education,
    Culture, Sports, Science, and Technology, Japan; 'Encouraging
    Development Strategic Research Centers Program', New Energy and
    Industrial Technology Development Organization.
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 NR 35
 TC 9
 PU WILEY-BLACKWELL PUBLISHING, INC
 PI MALDEN
 PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
 SN 1347-9032
 J9 CANCER SCI
 JI Cancer Sci.
 PD SEP
 PY 2009
 VL 100
 IS 9
 BP 1668
 EP 1674
 DI 10.1111/j.1349-7006.2009.01228.x
 PG 7
 SC Oncology
 GA 482XL
 UT ISI:000268923800016
 ER
 
 PT J
 AU Fu, HY
    Xue, DY
    Zhang, XD
    Yang, PY
 AF Fu, Hao-Yue
    Xue, Ding-Yu
    Zhang, Xiang-de
    Yang, Pei-Ying
 TI Assessing potential miRNA targets based on a Markov model
 SO GENETICS AND MOLECULAR RESEARCH
 LA English
 DT Article
 DE Markov chain model; Machine-learning method; MicroRNA target
    prediction; Maximum likelihood estimation; Potential target assessment
 ID MICRORNA TARGETS; COMPUTATIONAL IDENTIFICATION; BINDING-SITES;
    PREDICTION; DROSOPHILA; MICROINSPECTOR; SEQUENCE; GENES
 AB At present, studies on microRNA mainly focus on the identification of
    microRNA genes and their mRNA targets. Although researchers have
    identified many microRNA genes, relatively few microRNA targets have
    been identified by experimental methods. Computational programs
    designed for predicting potential microRNA targets provide numerous
    targets for experimental validation. We used a Markov model to examine
    base-pairing binding patterns of known microRNA targets. Using this
    model, potential microRNA targets in human species predicted by four
    well-known computational programs were assessed. Each potential target
    was assigned a score reflecting consistency with known target binding
    patterns. Targets with scores higher than the cutoff value would be
    identified by our model. The predicted targets identified by our model
    have base-pairing binding patterns consistent with known targets. This
    model was efficient for evaluating the extent to which a potential
    target was accurately predicted.
 C1 [Fu, Hao-Yue; Zhang, Xiang-de] Northeastern Univ, Coll Sci, Shenyang, Peoples R China.
    [Fu, Hao-Yue; Xue, Ding-Yu; Yang, Pei-Ying] Northeastern Univ, Coll Informat Sci & Engn, Shenyang, Peoples R China.
 RP Fu, HY, Northeastern Univ, Coll Sci, Shenyang, Peoples R China.
 EM fuhaoyue@tom.com
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 NR 24
 TC 0
 PU FUNPEC-EDITORA
 PI RIBEIRAO PRETO
 PA RUA HUDSON 655, JARDIM CANADA, RIBEIRAO PRETO, SP, BRAZIL
 SN 1676-5680
 J9 GENET MOL RES
 JI Genet. Mol. Res.
 PY 2009
 VL 8
 IS 3
 BP 848
 EP 860
 DI 10.4238/vol8-3gmr604
 PG 13
 SC Biochemistry & Molecular Biology; Genetics & Heredity
 GA 479BP
 UT ISI:000268634100011
 ER
 
 PT J
 AU Hu, SQ
    Song, E
    Tian, R
    Ma, SC
    Yang, T
    Mu, Y
    Li, Y
    Shao, C
    Gao, SJ
    Gao, YH
 AF Hu, Siqi
    Song, Eli
    Tian, Rui
    Ma, Sucan
    Yang, Tao
    Mu, Yi
    Li, Yuan
    Shao, Chen
    Gao, Shijuan
    Gao, Youhe
 TI Systematic Analysis of a Simple Adaptor Protein PDZK1: Ligand
    Identification, Interaction and Functional Prediction of Complex
 SO CELLULAR PHYSIOLOGY AND BIOCHEMISTRY
 LA English
 DT Article
 DE Adaptor protein; Literature mining; PDZ; PDZK1; Protein interaction
 ID DOMAIN-CONTAINING PROTEIN; TRANSMEMBRANE CONDUCTANCE REGULATOR;
    CYSTIC-FIBROSIS; MOLECULAR-MECHANISM; INTERACTION NETWORK; KINASE-C;
    BINDING; CELLS; CFTR; EXPRESSION
 AB PDZK1 is a simple adaptor protein with four protein interaction PDZ
    domains, but without any other known functional domains. Here, we used
    yeast two-hybrid screening of a random peptide library and
    high-throughput validation screening of a specialized PDZ ligand
    candidate library to systematically and comprehensively identify PDZK1
    ligands. The potential functional associations of the ligands were
    predicted by functional annotations from a MILANO literature search and
    subcellular localizations. The ligands were considered more likely to
    be functionally associated if they had similar patterns of functions or
    closely related functions. For some functionally associated ligand
    pairs, interaction with one ligand was found to be influenced by
    another ligand in a yeast three-hybrid system. Many G-protein signaling
    pathway-related proteins were found to interact with PDZK1, and they
    were likely to be functionally associated with transporters based on
    their closely related functions. This strategy can be extended to the
    study of other adaptor proteins that contain peptide-binding domains.
    Copyright (C) 2009 S. Karger AG, Basel
 C1 [Hu, Siqi; Song, Eli; Tian, Rui; Ma, Sucan; Yang, Tao; Mu, Yi; Li, Yuan; Shao, Chen; Gao, Shijuan; Gao, Youhe] Chinese Acad Sci, Peking Union Med Coll, Inst Basic Med Sci,Sch Basic Med, Natl Key Lab Med Mol Biol,Dept Physiol & Pathophy, Beijing 100005, Peoples R China.
 RP Gao, YH, Chinese Acad Sci, Peking Union Med Coll, Inst Basic Med
    Sci,Sch Basic Med, Natl Key Lab Med Mol Biol,Dept Physiol & Pathophy, 5
    Dong Dan San Tiao, Beijing 100005, Peoples R China.
 EM gaoyouhe@pumc.edu.cn
 FU National Science Fund for Distinguished Young Scholar [30725009]; The
    National High Technology Research and Development Program of China (863
    Program) [2006AA02Z308]; Ministry of Public Health [20082007]; Beijing
    Natural Science Foundation [5072037]; Specialized Research Fund for the
    Doctoral Program of Higher Education [20070023021]
 FX This work was supported by grants from National Science Fund for
    Distinguished Young Scholar 30725009, The National High Technology
    Research and Development Program of China (863 Program) 2006AA02Z308,
    The Research Grant for Public Interest from Ministry of Public Health
    20082007, Beijing Natural Science Foundation 5072037 and Specialized
    Research Fund for the Doctoral Program of Higher Education 20070023021.
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 NR 55
 TC 0
 PU KARGER
 PI BASEL
 PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND
 SN 1015-8987
 J9 CELL PHYSIOL BIOCHEM
 JI Cell. Physiol. Biochem.
 PY 2009
 VL 24
 IS 3-4
 BP 231
 EP 242
 DI 10.1159/000233258
 PG 12
 SC Cell Biology; Physiology
 GA 479RZ
 UT ISI:000268679900012
 ER
 
 PT J
 AU Liao, WB
    Zhong, J
    Yu, JX
    Xie, J
    Liu, YJ
    Du, L
    Yang, SG
    Liu, PX
    Xu, J
    Wang, JM
    Han, ZB
    Han, ZC
 AF Liao, Wenbin
    Zhong, Jian
    Yu, Jingxia
    Xie, Jiang
    Liu, Yongjun
    Du, Lei
    Yang, Shaoguang
    Liu, Pengxia
    Xu, Jie
    Wang, Jiming
    Han, Zhibo
    Han, Zhong Chao
 TI Therapeutic Benefit of Human Umbilical Cord Derived Mesenchymal Stromal
    Cells in Intracerebral Hemorrhage Rat: Implications of
    Anti-inflammation and Angiogenesis
 SO CELLULAR PHYSIOLOGY AND BIOCHEMISTRY
 LA English
 DT Article
 DE Human umbilical cord; Mesenchymal stromal cells; Intracerebral
    hemorrhage; Anti-inflammation; Angiogenesis
 ID STEM-CELLS; BONE-MARROW; IN-VITRO; IMMUNOLOGICAL-PROPERTIES;
    MYOCARDIAL-INFARCTION; PARKINSONS-DISEASE; CEREBRAL-ISCHEMIA; MOUSE
    MODEL; TRANSPLANTATION; PROLIFERATION
 AB Cell-based therapy represents a promising strategy in the treatment of
    neurological disorders. Human umbilical cord tissue has recently been
    recognized as an ideal source of mesenchymal stromal cells due to
    accessibility, vast abundance and safety. Here, an intracerebral
    hemorrhage (ICH) rat model was established by injection of bacterial
    collagenase VII and CM-Dil labeled human umbilical cord tissue derived
    mesenchymal stromal cells (UC-MSC) were intracerebrally transplanted
    into rat brain 24h after ICH. The results demonstrated that UC-MSC
    treatment significantly improved neurological function deficits and
    decreased injury volume of ICH rats. Leukocytes infiltration,
    microglial activation, ROS level and matrix metalloproteinases (MMPs)
    production were substantially reduced in peri-ICH area in cell-treated
    group as compared with PBS control at day 3 post-transplantation. In
    addition, UC-MSC treatment significantly increased vascular density in
    peri-ICH area and transplanted UC-MSC were found to be able to
    incorporate into cerebral vasculature in ipsilateral hemisphere at 14
    days after transplantation. In summary, intracerebral administration of
    UC-MSC could accelerate neurological function recovery of ICH rat, the
    underlying mechanism may ascribe to their ability to inhibit
    inflammation and promote angiogenesis. Thus UC-MSC may provide a
    potential cell candidate for cell-based therapy in neurological
    disorders. Copyright (C) 2009 S. Karger AG, Basel
 C1 [Liao, Wenbin; Yu, Jingxia; Xie, Jiang; Liu, Yongjun; Yang, Shaoguang; Liu, Pengxia; Xu, Jie; Han, Zhibo; Han, Zhong Chao] CAMS & PUMC, Inst Hematol, State Key Lab Expt Hematol, Tianjin 300020, Peoples R China.
    [Zhong, Jian; Liu, Yongjun; Wang, Jiming; Han, Zhong Chao] AmCellGene Co Ltd, Natl Engn Res Ctr Cell Prod, Tianjin, Peoples R China.
    [Zhong, Jian] Tianjin Univ, Sch Chem Engn & Technol, Tianjin 300072, Peoples R China.
    [Du, Lei] Hebei Med Univ, Shijiazhuang, Peoples R China.
 RP Han, ZC, CAMS & PUMC, Inst Hematol, State Key Lab Expt Hematol, 288
    Nanjing Rd, Tianjin 300020, Peoples R China.
 EM tihzchan@public.tpt.tj.cn
 FU Ministry Science & Technology of China [2006AA02A110]; National Natural
    Science Foundation of China [30570905, 30600238]; Tianjin Municipal
    Science and Technology Commission [07JCYBJC11200, 08ZCKFSF03200]
 FX This study was supported by 863 projects from Ministry Science &
    Technology of China (2006AA02A110), National Natural Science Foundation
    of China (30570905 and 30600238) and Tianjin Municipal Science and
    Technology Commission (07JCYBJC11200 and 08ZCKFSF03200).
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 NR 58
 TC 9
 PU KARGER
 PI BASEL
 PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND
 SN 1015-8987
 J9 CELL PHYSIOL BIOCHEM
 JI Cell. Physiol. Biochem.
 PY 2009
 VL 24
 IS 3-4
 BP 307
 EP 316
 DI 10.1159/000233255
 PG 10
 SC Cell Biology; Physiology
 GA 479RZ
 UT ISI:000268679900019
 ER
 
 PT J
 AU Yang, T
    Tsang, KS
    Poon, WS
    Ng, HK
 AF Yang, Tao
    Tsang, Kam Sze
    Poon, Wai Sang
    Ng, Ho Keung
 TI Neurotrophism of Bone Marrow Stromal Cells to Embryonic Stem Cells:
    Noncontact Induction and Transplantation to a Mouse Ischemic Stroke
    Model
 SO CELL TRANSPLANTATION
 LA English
 DT Article
 DE Embryonic stem cell; Stromal cell; Coculture; Differentiation;
    Transplantation; Ischemic stroke
 ID NEURAL PROGENITOR CELLS; DOPAMINERGIC-NEURONS; ES CELLS; BRAIN-INJURY;
    DIFFERENTIATION; GENERATION; REORGANIZATION; PROLIFERATION;
    SPECIFICATION; MIGRATION
 AB Embryonic stein (ES) cell-derived cell products may serve as it Source
    of cells for regenerative medicine. Currently available technologies
    for the induction of ES cells into neural lineage cells require
    extended culturing in vitro and complex procedural manipulations, with
    variable yields of heterogeneous Cells, which have hindered the
    prospective use of cell derivatives for treatment of ischemic stroke.
    We established a simple and efficient method to derive mouse ES cells
    into neural lineage cells using an 8-day coculture with the bone marrow
    stromal cells MS5, followed by a 6-day propagation culture and a 4-day
    selection Culture. The protocol generated a relatively high yield of
    neural lineage cells without any mesodermal and endodermal lineage
    commitment. In in vivo study, these derived cells could improve the
    cognitive function of ischemic stroke mice. Three weeks after
    transplantation, migration of implanted cells to lesioned areas was
    noted. It was also evident of a normalization of pyramidal neuron
    density and morphology in hippocampal CA1 region. One (1/17) episode of
    teratoma development was noted. Data suggested that MS5 cells may exert
    a neurotrophic effect to enhance neural differentiation of ES cells and
    MS5-induced ES cell-derived cells appeared to be applicable to cell
    therapy for ischemic stroke.
 C1 [Yang, Tao; Tsang, Kam Sze; Poon, Wai Sang; Ng, Ho Keung] Chinese Univ Hong Kong, Dept Anat & Cellular Pathol, Prince Wales Hosp, Shatin, Hong Kong, Peoples R China.
    [Yang, Tao; Tsang, Kam Sze; Ng, Ho Keung] Chinese Univ Hong Kong, Li Ka Shing Inst Hlth Sci, Shatin, Hong Kong, Peoples R China.
    [Poon, Wai Sang] Chinese Univ Hong Kong, Dept Surg, Prince Wales Hosp, Shatin, Hong Kong, Peoples R China.
 RP Tsang, KS, Chinese Univ Hong Kong, Dept Anat & Cellular Pathol, Prince
    Wales Hosp, Shatin, Hong Kong, Peoples R China.
 EM tsangks@cuhk.edu.hk
 FU Li Ka Shing Institute of Health Sciences ; The Chinese University of
    Hong Kong ; Strategic Research Program [SRP 2102]
 FX This study was supported in part by stem cell research funding from the
    Li Ka Shing Institute of Health Sciences, The Chinese University of
    Hong Kong, and by the Strategic Research Program SRP 2102, The Chinese
    University of Hong Kong.
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 NR 34
 TC 4
 PU COGNIZANT COMMUNICATION CORP
 PI ELMSFORD
 PA 3 HARTSDALE ROAD, ELMSFORD, NY 10523-3701 USA
 SN 0963-6897
 J9 CELL TRANSPLANT
 JI Cell Transplant.
 PY 2009
 VL 18
 IS 4
 BP 391
 EP 404
 PG 14
 SC Cell & Tissue Engineering; Medicine, Research & Experimental;
    Transplantation
 GA 478XW
 UT ISI:000268623100002
 ER
 
 PT J
 AU Song, L
    Shi, QM
    Yang, XH
    Xu, ZH
    Xue, HW
 AF Song, Li
    Shi, Qiu-Ming
    Yang, Xiao-Hua
    Xu, Zhi-Hong
    Xue, Hong-Wei
 TI Membrane steroid-binding protein 1 (MSBP1) negatively regulates
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 SO CELL RESEARCH
 LA English
 DT Article
 DE MSBP1; BR signaling; BAK1; endocytosiss
 ID RECEPTOR KINASE BRI1; ARABIDOPSIS-THALIANA; CELL ELONGATION;
    EXTRACELLULAR DOMAIN; PLASMA-MEMBRANE; GENE-EXPRESSION; GROWTH; AUXIN;
    TRANSDUCTION; PATHWAY
 AB Brassinosteroids (BRs) are perceived by transmembrane receptors and
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    responses to environmental stimuli. The transmembrane receptor BRI1 can
    directly bind to brassinolide (BL), and BAK1 interacts with BRI1 to
    enhance the BRI1-mediated BR signaling. Our previous studies indicated
    that a membrane steroid-binding protein 1 (MSBP1) could bind to BL in
    vitro and is negatively involved in BR signaling. To further elucidate
    the underlying mechanism, we here show that MSBP1 specifically
    interacts with the extracellular domain of BAK1 in vivo in a
    BL-independent manner. Suppressed cell expansion and BR responses by
    increased expression of MSBP1 can be recovered by overexpressing BAK1
    or its intracellular kinase domain, suggesting that MSBP1 may suppress
    BR signaling through interacting with BAK1. Subcellular localization
    studies revealed that both MSBP1 and BAK1 are localized to plasma
    membrane and endocytic vesicles and MSBP1 accelerates BAK1 endocytosis,
    which results in suppressed BR signaling by shifting the equilibrium of
    BAK1 toward endosomes. Indeed, enhanced MSBP1 expression reduces the
    interaction between BRI1 and BAK1 in vivo, demonstrating that MSBP1
    acts as a negative factor at an early step of the BR signaling pathway.
 C1 [Song, Li; Shi, Qiu-Ming; Yang, Xiao-Hua; Xu, Zhi-Hong; Xue, Hong-Wei] Chinese Acad Sci, Shanghai Inst Biol Sci, Natl Key Lab Plant Mol Genet, Inst Plant Physiol & Ecol, Shanghai 200032, Peoples R China.
 RP Xue, HW, Chinese Acad Sci, Shanghai Inst Biol Sci, Natl Key Lab Plant
    Mol Genet, Inst Plant Physiol & Ecol, 300 Fenglin Rd, Shanghai 200032,
    Peoples R China.
 EM hwxue@sibs.ac.cn
 FU Chinese Academy of Sciences and National Natural Science Foundation of
    China [30425029, 30421001, 90717001]
 FX This study was supported by the Chinese Academy of Sciences and
    National Natural Science Foundation of China (Grants 30425029,
    30421001, 90717001). We greatly thank Prof Hong Ma (Penn. State
    University, USA) for critical reading and writing improvement and Prof
    Nam-Hai Chua (The Rockefeller University, USA) for helpful comments. We
    thank the Salk Institute Genomic Analysis Laboratory for providing the
    sequence-indexed Arabidopsis T-DNA insertion mutants, and Prof Sheng
    Luan (University of California, Berkeley, USA) for providing the
    construct pATC940. We thank Prof Hong-Quan Yang (SIPPE, CAS) for
    providing LexA yeast two-hybrid system and Prof Zhi-Yong Wang (The
    Stanford University, USA) for providing the BRI1 antibody. We thank Mr
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 NR 62
 TC 2
 PU INST BIOCHEMISTRY & CELL BIOLOGY
 PI SHANGHAI
 PA SIBS, CAS, 319 YUEYAND ROAD, SHANGHAI, 200031, PEOPLES R CHINA
 SN 1001-0602
 J9 CELL RES
 JI Cell Res.
 PD JUL
 PY 2009
 VL 19
 IS 7
 BP 864
 EP 876
 DI 10.1038/cr.2009.66
 PG 13
 SC Cell Biology
 GA 480GR
 UT ISI:000268722200008
 ER
 
 PT J
 AU Yang, HY
    Yu, Y
    Li, WG
    Xu, TL
    Jiang, HL
 AF Yang, Huaiyu
    Yu, Ye
    Li, Wei-Guang
    Xu, Tian-Le
    Jiang, Hualiang
 TI Conformational sampling on acid-sensing ion channel 1 (ASIC1):
    implication for a symmetric conformation
 SO CELL RESEARCH
 LA English
 DT Letter
 C1 [Yang, Huaiyu; Jiang, Hualiang] Chinese Acad Sci, Shanghai Inst Mat Med, Drug Discovery & Design Ctr, State Key Lab Drug Res, Shanghai 201203, Peoples R China.
    [Yu, Ye; Li, Wei-Guang; Xu, Tian-Le] Chinese Acad Sci, Shanghai Inst Biol Sci, Inst Neurosci, Shanghai 200031, Peoples R China.
    [Yu, Ye; Li, Wei-Guang; Xu, Tian-Le] Chinese Acad Sci, Shanghai Inst Biol Sci, State Key Lab Neurosci, Shanghai 200031, Peoples R China.
    [Jiang, Hualiang] E China Univ Sci & Technol, Sch Pharm, Shanghai 200237, Peoples R China.
 RP Jiang, HL, Chinese Acad Sci, Shanghai Inst Mat Med, Drug Discovery &
    Design Ctr, State Key Lab Drug Res, Shanghai 201203, Peoples R China.
 EM tlxu@ion.ac.cn
    hljiang@mail.shcnc.ac.cn
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 NR 11
 TC 1
 PU INST BIOCHEMISTRY & CELL BIOLOGY
 PI SHANGHAI
 PA SIBS, CAS, 319 YUEYAND ROAD, SHANGHAI, 200031, PEOPLES R CHINA
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 J9 CELL RES
 JI Cell Res.
 PD AUG
 PY 2009
 VL 19
 IS 8
 BP 1035
 EP 1037
 DI 10.1038/cr.2009.90
 PG 3
 SC Cell Biology
 GA 480GS
 UT ISI:000268722300014
 ER
 
 PT J
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 LA English
 DT Editorial Material
 DE microRNA-221/-222; prostate cancer; CRPC; microRNA; cancer
 ID PROSTATE-CANCER; MICRORNA; EXPRESSION; P27(KIP1); RESISTANCE; MIR-222;
    CELLS
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 PU LANDES BIOSCIENCE
 PI AUSTIN
 PA 1002 WEST AVENUE, 2ND FLOOR, AUSTIN, TX 78701 USA
 SN 1538-4101
 J9 CELL CYCLE
 JI Cell Cycle
 PD AUG 1
 PY 2009
 VL 8
 IS 15
 BP 2315
 EP 2316
 PG 2
 SC Cell Biology
 GA 477RH
 UT ISI:000268535700003
 ER
 
 PT J
 AU Yang, J
    Moses, MA
 AF Yang, Jiang
    Moses, Marsha A.
 TI Lipocalin 2 A multifaceted modulator of human cancer
 SO CELL CYCLE
 LA English
 DT Article
 DE lipocalin 2; NGAL; breast cancer; epithelial to mesenchymal transition;
    biomarker; estrogen receptor; Slug
 ID GELATINASE-ASSOCIATED LIPOCALIN; ISCHEMIA-REPERFUSION INJURY; HUMAN
    NEUTROPHIL GELATINASE; GENE-EXPRESSION PROFILES; CHRONIC
    MYELOID-LEUKEMIA; BREAST-CANCER; COLORECTAL-CANCER; PANCREATIC-CANCER;
    CDNA MICROARRAY; PROTEIN FAMILY
 AB Lipocalin 2 (Lcn2), a member of the lipocalin family that transports
    small lipophilic ligands, has gained recent attention as both a
    potential biomarker and a modulator of human cancers. Here we describe
    recent findings of the functions of Lcn2 in breast cancer and the
    potential mechanisms that underlie its actions. Lcn2 has been shown to
    induce the epithelial to mesenchymal transition (EMT) in breast cancer
    cells and to promote breast tumor invasion. Estrogen receptor alpha may
    participate in the pathway that leads to Lcn2-induced EMT. Preliminary
    evidence also suggests that Lcn2 may be useful as a potential
    non-invasive urinary biomarker of breast cancer. Elevated levels of
    Lcn2 have also been reported in other human cancers. The potential
    roles of Lcn2 in epithelial tumors as well as leukemia are also
    reviewed and discussed here.
 C1 [Moses, Marsha A.] Childrens Hosp, Vasc Biol Program, Boston, MA 02115 USA.
    Childrens Hosp, Dept Surg, Boston, MA 02115 USA.
    Harvard Univ, Sch Med, Dept Surg, Boston, MA 02115 USA.
 RP Moses, MA, Childrens Hosp, Vasc Biol Program, 12-214,300 Longwood Ave,
    Boston, MA 02115 USA.
 EM marsha.moses@childrens.harvard.edu
 FU NIH [R01 CA118764]; JoAnn Webb Fund for Angiogenesis Research ; Dr. T.
    Quinto and J. Larsen, the Riehl Family Foundation ; S. Elizabeth
    O'Brien Trust ; Advanced Medical Foundation 
 FX This work was supported by NIH R01 CA118764, the JoAnn Webb Fund for
    Angiogenesis Research, Dr. T. Quinto and J. Larsen, the Riehl Family
    Foundation, the S. Elizabeth O'Brien Trust and the Advanced Medical
    Foundation. We thank K. Johnson for graphics assistance.
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 NR 58
 TC 4
 PU LANDES BIOSCIENCE
 PI AUSTIN
 PA 1002 WEST AVENUE, 2ND FLOOR, AUSTIN, TX 78701 USA
 SN 1538-4101
 J9 CELL CYCLE
 JI Cell Cycle
 PD AUG 1
 PY 2009
 VL 8
 IS 15
 BP 2347
 EP 2352
 PG 6
 SC Cell Biology
 GA 477RH
 UT ISI:000268535700016
 ER
 
 PT J
 AU Leinninger, GM
    Jo, YH
    Leshan, RL
    Louis, GW
    Yang, HY
    Barrera, JG
    Wilson, H
    Opland, DM
    Faouzi, MA
    Gong, YS
    Jones, JC
    Rhodes, CJ
    Chua, S
    Diano, S
    Horvath, TL
    Seeley, RJ
    Becker, JB
    Munzberg, H
    Myers, MG
 AF Leinninger, Gina M.
    Jo, Young-Hwan
    Leshan, Rebecca L.
    Louis, Gwendolyn W.
    Yang, Hongyan
    Barrera, Jason G.
    Wilson, Hilary
    Opland, Darren M.
    Faouzi, Miro A.
    Gong, Yusong
    Jones, Justin C.
    Rhodes, Christopher J.
    Chua, Streamson, Jr.
    Diano, Sabrina
    Horvath, Tamas L.
    Seeley, Randy J.
    Becker, Jill B.
    Muenzberg, Heike
    Myers, Martin G., Jr.
 TI Leptin Acts via Leptin Receptor-Expressing Lateral Hypothalamic Neurons
    to Modulate the Mesolimbic Dopamine System and Suppress Feeding
 SO CELL METABOLISM
 LA English
 DT Article
 ID MELANIN-CONCENTRATING HORMONE; MESSENGER-RNA EXPRESSION; BODY-WEIGHT;
    FOOD-INTAKE; ARCUATE NUCLEUS; OREXIN NEURONS; ENERGY-BALANCE; REWARD;
    BRAIN; MICE
 AB The lateral hypothalamic area (LHA) acts in concert with the ventral
    tegmental area (VTA) and other components of the mesolimbic dopamine
    (DA) system to control motivation, including the incentive to feed. The
    anorexigenic hormone leptin modulates the mesolimbic DA system,
    although the mechanisms underlying this control have remained
    incompletely understood. We show that leptin directly regulates a
    population of leptin receptor (LepRb)-expressing inhibitory neurons in
    the LHA and that leptin action via these LHA LepRb neurons decreases
    feeding and body weight. Furthermore, these LHA LepRb neurons innervate
    the VTA, and leptin action on these neurons restores VTA expression of
    the rate-limiting enzyme in DA production along with mesolimbic DA
    content in leptin-deficient animals. Thus, these findings reveal that
    LHA LepRb neurons link anorexic leptin action to the mesolimbic DA
    system.
 C1 [Leinninger, Gina M.; Leshan, Rebecca L.; Louis, Gwendolyn W.; Opland, Darren M.; Faouzi, Miro A.; Gong, Yusong; Jones, Justin C.; Muenzberg, Heike; Myers, Martin G., Jr.] Univ Michigan, Dept Internal Med, Div Endocrinol Diabet & Metab, Ann Arbor, MI 48109 USA.
    [Leshan, Rebecca L.; Louis, Gwendolyn W.; Myers, Martin G., Jr.] Univ Michigan, Dept Mol & Integrat Physiol, Ann Arbor, MI 48109 USA.
    [Yang, Hongyan; Seeley, Randy J.; Becker, Jill B.] Univ Michigan, Mol & Behav Neurosci Inst, Ann Arbor, MI 48109 USA.
    [Jo, Young-Hwan; Chua, Streamson, Jr.] Albert Einstein Coll Med, Dept Med, Bronx, NY 10461 USA.
    [Barrera, Jason G.; Wilson, Hilary] Univ Cincinnati, Dept Psychiat, Cincinnati, OH 45237 USA.
    [Barrera, Jason G.; Wilson, Hilary] Univ Cincinnati, Genome Res Inst, Cincinnati, OH 45237 USA.
    [Rhodes, Christopher J.] Univ Chicago, Dept Med, Chicago, IL 60637 USA.
    [Diano, Sabrina; Horvath, Tamas L.] Yale Univ, New Haven, CT 06511 USA.
 RP Myers, MG, Univ Michigan, Dept Internal Med, Div Endocrinol Diabet &
    Metab, Ann Arbor, MI 48109 USA.
 EM mgmyers@umich.edu
 FU Michigan Diabetes Research and Training Center ; Michigan Comprehensive
    Diabetes Center ; American Diabetes Association and American Heart
    Association ; NIH ; Obesity Society 
 FX We thank Amylin Pharmaceuticals for the generous gift of leptin and
    thank Gary Schwartz, Bob Kennedy, Maura Perry, and members of the Myers
    lab for helpful discussions. This work was supported by the Michigan
    Diabetes Research and Training Center; Michigan Comprehensive Diabetes
    Center; and grants from the American Diabetes Association and American
    Heart Association (M.G.M.), the NIH (M.G.M., C.J.R., and J.B.B.), and
    the Obesity Society (G. M. L.).
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 NR 45
 TC 44
 PU CELL PRESS
 PI CAMBRIDGE
 PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
 SN 1550-4131
 J9 CELL METAB
 JI Cell Metab.
 PD AUG 6
 PY 2009
 VL 10
 IS 2
 BP 89
 EP 98
 DI 10.1016/j.cmet.2009.06.011
 PG 10
 SC Cell Biology; Endocrinology & Metabolism
 GA 480DB
 UT ISI:000268711200006
 ER
 
 PT J
 AU Wan, Y
    Pan, F
    Liu, Y
    Liang, Y
    Yang, Z
    Zhao, HD
    Xua, YY
 AF Wan, Yi
    Pan, Feng
    Liu, Ya
    Liang, Ying
    Yang, Zhe
    Zhao, Huadong
    Xua, Yongyong
 TI Validation of the Andon KD-391 semiautomated blood pressure monitor in
    adults according to the International Protocol
 SO BLOOD PRESSURE MONITORING
 LA English
 DT Article
 DE blood pressure measurement; European Society of Hypertension;
    oscillometry; validation
 ID EUROPEAN-SOCIETY; HYPERTENSION; ACCURATE; DEVICES
 AB Objective Accurate blood pressure measurement is important for both the
    patients and the health service in appropriate treatment and estimation
    of clinical risk. Few automated devices have been shown to be accurate
    when compared with mercury sphygmomanometer. This study presents the
    validation results of the Andon KD-391 semiautomated blood pressure
    monitor according to the International Protocol of the European Society
    of Hypertension (ESH) in an adult population.
    Methods Sequential measurements of systolic and diastolic blood
    pressures were obtained in 33 participants who fulfilled the
    requirements of the International Protocol using the mercury
    sphygmomanometer (two observers) and the test device (one supervisor).
    According to the ESH validation protocol, 99 couples of test device and
    reference blood pressure measurements were obtained during the two
    phases of the study (three pairs for each of the 33 participants).
    Results In phase 1, the Andon KD-391 device produced 29, 38 and 44
    measurements for systolic blood pressure and 28, 39 and 43 for
    diastolic blood pressure failing within the zones 5, 10 and 15 mmHg,
    respectively. The test device also passed phase 2 of the validation
    study with a mean (+/- SD) device-observer difference of -0.17 +/- 7.07
    mmHg for systolic and -1.01 +/- 5.95 mmHg for diastolic blood pressure.
    Conclusion According to the results of the validation study on the
    basis of the ESH International Protocol, the Andon KD-391 can be
    recommended for clinical use in an adult population. Blood Press Monit
    14:181-184 (C) 2009 Wolters Kluwer Health | Lippincott Williams &
    Wilkins.
 C1 [Wan, Yi; Pan, Feng; Liang, Ying; Yang, Zhe; Xua, Yongyong] Fourth Mil Med Univ, Inst Hlth Informat, Xian 710032, Peoples R China.
    [Liu, Ya] Fourth Mil Med Univ, Xijing Hosp, Xian 710032, Peoples R China.
    [Zhao, Huadong] Fourth Mil Med Univ, Tangdu Hosp, Xian 710032, Peoples R China.
 RP Xua, YY, Fourth Mil Med Univ, Inst Hlth Informat, 169 W Changle Rd,
    Xian 710032, Peoples R China.
 EM yongyong_xu@yahoo.com
 FU National Natural Science Foundation of China [90612012]
 FX This study was supported by a National Natural Science Foundation of
    China (90612012). The authors declare that they have no conflicts of
    interest.
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 NR 8
 TC 1
 PU LIPPINCOTT WILLIAMS & WILKINS
 PI PHILADELPHIA
 PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
 SN 1359-5237
 J9 BLOOD PRESS MONIT
 JI Blood Press. Monit.
 PD AUG
 PY 2009
 VL 14
 IS 4
 BP 181
 EP 184
 DI 10.1097/MBP.0b013e32832db4c2
 PG 4
 SC Peripheral Vascular Disease
 GA 479VU
 UT ISI:000268690600008
 ER
 
 PT J
 AU Yu, Y
    Iclozan, C
    Yamazaki, T
    Yang, XX
    Anasetti, C
    Dong, C
    Yu, XZ
 AF Yu, Yu
    Iclozan, Cristina
    Yamazaki, Tomohide
    Yang, Xuexian
    Anasetti, Claudio
    Dong, Chen
    Yu, Xue-Zhong
 TI Abundant c-Fas-associated death domain-like interleukin-1-converting
    enzyme inhibitory protein expression determines resistance of T helper
    17 cells to activation-induced cell death
 SO BLOOD
 LA English
 DT Article
 ID SIGNALING COMPLEX; APOPTOSIS; DIFFERENTIATION; INFLAMMATION; DISTINCT;
    LINEAGE; FLIP; TH17; TH2
 AB Activation-induced cell death (AICD) plays an important role in
    peripheral T-cell tolerance. AICD in CD4 T helper (Th) cells, including
    Th1 and Th2 effectors, has been extensively studied. Recently,
    interleukin-17-producing CD4(+) T cells (Th17 cells) have been
    identified as a unique Th subset, but their susceptibility to AICD and
    the underlying molecular mechanisms have not been defined. In this
    study, we found that Th17 cells were significantly less susceptible to
    AICD than Th1 cells, and Th17 cell resistance to AICD is due to the
    high levels of c-Fas-associated death domain-like
    interleukin-1-converting enzyme inhibitory protein preventing
    Fas-mediated apoptosis. The resistance of Th17 cells to AICD reveals a
    novel mechanism to explain the high pathogenicity of Th17 cells in
    autoimmune diseases, and may also provide a rationale to generate
    tumor-specific Th17 cells for adoptive immunotherapy. (Blood. 2009;
    114: 1026-1028)
 C1 [Yu, Yu; Iclozan, Cristina; Anasetti, Claudio; Yu, Xue-Zhong] Univ S Florida, Coll Med, H Lee Moffitt Canc Ctr & Res Inst, Dept Immunol, Tampa, FL 33612 USA.
    [Yu, Yu; Iclozan, Cristina; Anasetti, Claudio; Yu, Xue-Zhong] Univ S Florida, Coll Med, H Lee Moffitt Canc Ctr & Res Inst, Dept Blood & Marrow Transplantat, Tampa, FL 33612 USA.
    [Yamazaki, Tomohide; Yang, Xuexian; Dong, Chen] Univ Texas MD Anderson Canc Ctr, Dept Immunol, Houston, TX 77030 USA.
    [Anasetti, Claudio; Yu, Xue-Zhong] Univ S Florida, Dept Oncol Sci, Tampa, FL USA.
 RP Yu, XZ, Univ S Florida, Coll Med, H Lee Moffitt Canc Ctr & Res Inst,
    Dept Immunol, SRB 2,12902 Magnolia Dr, Tampa, FL 33612 USA.
 EM Xue.Yu@moffitt.org
 FU National Institutes of Health [AI63553, CA118116, AI51693]; American
    Society for Blood and Marrow Transplantation 
 FX We thank Drs Amer Beg, Esteban Celis, and Lia Perez for their critical
    discussion on this project. We are grateful for the technical
    assistance provided by Flow Cytometry and Mouse Core Facility at the
    Moffitt Cancer Center.
    This work was supported in part by National Institutes of Health grants
    AI63553, CA118116 ( to X.-Z.Y.), and AI51693 ( to C. A.). X.-Z.Y. is a
    recipient of a New Investigator Award supported by the American Society
    for Blood and Marrow Transplantation.
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 PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
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 J9 BLOOD
 JI Blood
 PD JUL 30
 PY 2009
 VL 114
 IS 5
 BP 1026
 EP 1028
 DI 10.1182/blood-2009-03-210153
 PG 3
 SC Hematology
 GA 477BH
 UT ISI:000268491100016
 ER
 
 PT J
 AU Wang, Q
    Lin, K
    Yang, SZ
 AF Wang, Qian
    Lin, Kai
    Yang, Shu-Zheng
 TI Fermions tunnelling from the rotating 5-D Myers-Perry black hole
 SO GENERAL RELATIVITY AND GRAVITATION
 LA English
 DT Article
 DE Fermions; Hawking radiation; Tunnelling; Myers-Perry black hole
 ID DE-SITTER SPACES; HAWKING RADIATION; DIRAC PARTICLES; ANOMALIES; ENTROPY
 AB Recent researches on the Hawking radiation of black holes show that the
    Hawking temperature can be obtained by fermion tunnelling method. In
    this paper, we extend this method to a 5-D space-time and view the
    Hawking radiation of the Myers-Perry black hole with two independent
    angular momenta. As a result, the Hawking temperature is obtained,
    which is the same as that obtained by other methods.
 C1 [Wang, Qian; Lin, Kai; Yang, Shu-Zheng] China W Normal Univ, Inst Theoret Phys, Nanchong 637002, Sichuan, Peoples R China.
 RP Wang, Q, China W Normal Univ, Inst Theoret Phys, Nanchong 637002,
    Sichuan, Peoples R China.
 EM wqlhl@126.com
    lk314159@126.com
    szyang@cwnu.edu.cn
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 NR 33
 TC 1
 PU SPRINGER/PLENUM PUBLISHERS
 PI NEW YORK
 PA 233 SPRING ST, NEW YORK, NY 10013 USA
 SN 0001-7701
 J9 GEN RELATIV GRAVIT
 JI Gen. Relativ. Gravit.
 PD AUG
 PY 2009
 VL 41
 IS 8
 BP 1887
 EP 1893
 DI 10.1007/s10714-009-0765-2
 PG 7
 SC Astronomy & Astrophysics; Physics, Multidisciplinary; Physics,
    Particles & Fields
 GA 475AG
 UT ISI:000268326200013
 ER
 
 PT J
 AU Sun, WJ
    Li, HX
    Yu, Y
    Fan, YH
    Grabiner, BC
    Mao, RF
    Ge, NL
    Zhang, H
    Fu, SB
    Lin, X
    Yang, JH
 AF Sun, Wenjing
    Li, Hongxiu
    Yu, Yang
    Fan, Yihui
    Grabiner, Brian C.
    Mao, Renfang
    Ge, Ningling
    Zhang, Hong
    Fu, Songbin
    Lin, Xin
    Yang, Jianhua
 TI MEKK3 is required for lysophosphatidic acid-induced NF-kappa B
    activation
 SO CELLULAR SIGNALLING
 LA English
 DT Article
 DE NF-kappa B; LPA; GPCR; MEKK3; TAK1
 ID KINASE COMPLEX; IKK; BETA; TAK1; LIPOPOLYSACCHARIDE; PHOSPHORYLATION;
    PROTEINS; RECEPTOR; PLAYS; ALPHA
 AB Lysophosphatidic acid (LPA) is a potent agonist that exerts various
    cellular functions on many cell types through binding to its cognate G
    protein-coupled receptors (GPCRs). Although LPA induces NF-kappa B
    activation by acting on its GPCR receptor, the molecular mechanism of
    LPA receptor-mediated NF-kappa B activation remains to be well defined.
    In the present study, by using MEKK3-, TAK1-, and IKK beta-deficient
    murine embryonic fibroblasts (MEFs), we found that MEKK3 but not TAK1
    deficiency impairs LPA and protein kinase C (PKC)-induced I kappa B
    kinase (IKK)-NF-kappa B activation, and IKK beta is required for
    PKC-induced NF-kappa B activation. In addition, we demonstrate that LPA
    and PKC-induced IL-6 and MIP-2 production are abolished in the absence
    of MEKK3 but not TAK1. Together, our results provide the genetic
    evidence that MEKK3 but not TAK1 is required for LPA receptor-mediated
    IKK-NF-kappa B activation. (C) 2009 Elsevier Inc. All rights reserved.
 C1 [Sun, Wenjing; Yu, Yang; Fan, Yihui; Ge, Ningling; Yang, Jianhua] Baylor Coll Med, Dept Pediat, Texas Childrens Canc Ctr, Dan L Duncan Canc Ctr, Houston, TX 77030 USA.
    [Sun, Wenjing; Fu, Songbin] Harbin Med Coll, Med Genet Lab, Harbin 150081, Peoples R China.
    [Li, Hongxiu; Grabiner, Brian C.; Lin, Xin] Univ Texas MD Anderson Canc Ctr, Dept Mol & Cellular Oncol, Houston, TX USA.
    [Mao, Renfang; Zhang, Hong] Baylor Coll Med, Dept Pathol, Houston, TX 77030 USA.
 RP Yang, JH, Baylor Coll Med, Dept Pediat, Texas Childrens Canc Ctr, Dan L
    Duncan Canc Ctr, Houston, TX 77030 USA.
 EM jianhuay@bcm.tmc.edu
 FU National Institutes of Health [1R21CA106513-01A2, 5R01GM079451];
    American Cancer Society [RSG-06-070-01-TBE]; Fleming and Davenport
    Award 
 FX We are grateful to Susan Burlingame for the excellent technical
    assistance. We thank Drs. Paul Chiao, Bing Su and Sankar Ghosh for
    providing IKK beta-, MEKK3- and TAK1-deficient MEFs. This research was
    supported in part by the National Institutes of Health Grant
    1R21CA106513-01A2 (to J.Y.), 5R01GM079451 (to X.L.), the American
    Cancer Society grant RSG-06-070-01-TBE (to J.Y.),and the Fleming and
    Davenport Award (to H.Z.).
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 NR 34
 TC 9
 PU ELSEVIER SCIENCE INC
 PI NEW YORK
 PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
 SN 0898-6568
 J9 CELL SIGNAL
 JI Cell. Signal.
 PD OCT
 PY 2009
 VL 21
 IS 10
 BP 1488
 EP 1494
 DI 10.1016/j.cellsig.2009.05.007
 PG 7
 SC Cell Biology
 GA 475RN
 UT ISI:000268378300004
 ER
 
 PT J
 AU Zhou, YB
    Frey, TK
    Yang, JJ
 AF Zhou, Yubin
    Frey, Teryl K.
    Yang, Jenny J.
 TI Viral calciomics: Interplays between Ca2+ and virus
 SO CELL CALCIUM
 LA English
 DT Review
 DE Virus; Calcium; Signaling; EF-hand; Structure; Interaction; Apoptosis;
    Infection
 ID NONSTRUCTURAL GLYCOPROTEIN NSP4; CALCIUM-BINDING SITE; ACTIVATED
    T-CELLS; TYPE-1 ENVELOPE GLYCOPROTEIN; INDUCED STRUCTURAL-CHANGES;
    TOBACCO MOSAIC-VIRUS; EPSTEIN-BARR VIRUS; HIV-1 PROTEIN TAT; EF-HAND
    FAMILY; NF-KAPPA-B
 AB Ca2+ is one of the most universal and versatile signaling molecules and
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    adept at utilizing the universal Ca2+ signal to create a tailored
    cellular environment that meets their own demands. This review
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    homeostasis and utilize Ca2+ and cellular Ca2+-binding proteins to
    their benefit in their replication cycles. Ca2+ plays important roles
    in virion structure formation, virus entry, viral gene expression,
    posttranslational processing of viral proteins and virion maturation
    and release. As part of the review, we introduce an algorithm to
    identify linear "EF-hand" Ca2+-binding motifs which resulted in the
    prediction of a total of 93 previously unrecognized Ca2+-binding motifs
    in virus proteins. Many of these proteins are nonstructural proteins, a
    class of proteins among which Ca2+ interactions had not been formerly
    appreciated. The presence of linear Ca2+-binding motifs in viral
    proteins enlarges the spectrum of Ca2+-virus interplay and expands the
    total scenario of viral calciomics. (C) 2009 Elsevier Ltd. All rights
    reserved.
 C1 [Frey, Teryl K.] Georgia State Univ, Dept Biol, Atlanta, GA 30303 USA.
    [Zhou, Yubin; Yang, Jenny J.] Georgia State Univ, Dept Chem, Atlanta, GA 30303 USA.
 RP Frey, TK, Georgia State Univ, Dept Biol, 50 Decatur St, Atlanta, GA
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 EM tfrey@gsu.edu
    chejjy@langate.gsu.edu
 FU NIAID [R01 AI21389]; NIH [R01 GM 62999]
 FX We thank Dan Adams for his help in preparation of this manuscript. This
    work is supported in part by a grant (R01 AI21389) from NIAID to TKF
    and JJY and in part by the R01 GM 62999 (NIH) grant for JJY. YZ is a
    fellow of the Molecular Basis of Disease Area of Focus at GSU.
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 NR 171
 TC 10
 PU CHURCHILL LIVINGSTONE
 PI EDINBURGH
 PA JOURNAL PRODUCTION DEPT, ROBERT STEVENSON HOUSE, 1-3 BAXTERS PLACE,
    LEITH WALK, EDINBURGH EH1 3AF, MIDLOTHIAN, SCOTLAND
 SN 0143-4160
 J9 CELL CALCIUM
 JI Cell Calcium
 PD JUL
 PY 2009
 VL 46
 IS 1
 BP 1
 EP 17
 DI 10.1016/j.ceca.2009.05.005
 PG 17
 SC Cell Biology
 GA 474MT
 UT ISI:000268288900001
 ER
 
 PT J
 AU Chang, YK
    Yang, W
    Zhao, M
    Mok, CC
    Chan, TM
    Wong, RWS
    Lee, KW
    Mok, MY
    Wong, SN
    Ng, IOL
    Lee, TL
    Ho, MHK
    Lee, PPW
    Wong, WHS
    Lau, CS
    Sham, PC
    Lau, YL
 AF Chang, Y. K.
    Yang, W.
    Zhao, M.
    Mok, C. C.
    Chan, T. M.
    Wong, R. W. S.
    Lee, K. W.
    Mok, M. Y.
    Wong, S. N.
    Ng, I. O. L.
    Lee, T. L.
    Ho, M. H. K.
    Lee, P. P. W.
    Wong, W. H. S.
    Lau, C. S.
    Sham, P. C.
    Lau, Y. L.
 TI Association of BANK1 and TNFSF4 with systemic lupus erythematosus in
    Hong Kong Chinese
 SO GENES AND IMMUNITY
 LA English
 DT Article
 DE SLE; BANK1; TNFSF4; Chinese; genetic association
 ID GENOME-WIDE ASSOCIATION; OX40 LIGAND
 AB Systemic lupus erythematosus (SLE) is a prototypic autoimmune disease
    with complex genetic inheritance. Recently, single nucleotide
    polymorphisms (SNPs) in BANK1 and TNFSF4 have been shown to be
    associated with SLE in Caucasian populations, but it is not known
    whether they are also involved in the disease in other ethnic groups.
    Recent data from our genome-wide association study (GWAS) for 314 SLE
    cases and 920 controls collected in Hong Kong identified SNPs in and
    around BANK1 and TNFSF4 to be associated with SLE risk. On the basis of
    the results of the reported studies and our GWAS, SNPs were selected
    for further genotyping in 949 SLE patients ( overlapping with the 314
    cases in our GWAS) and non-overlapping 1042 healthy controls. We
    confirmed the associations of BANK1 and TNFSF4 with SLE in Chinese
    (BANK1, rs3733197, odds ratio (OR) = 0.84, P = 0.021; BANK1,
    rs17266594, OR = 0.61, P = 4.67 x 10(-9); TNFSF4, rs844648, OR = 1.22,
    P = 2.47 x 10(-3); TNFSF4, rs2205960, OR = 1.30, P = 2.41 x 10(-4)).
    Another SNP located in intron 1 of BANK1, rs4522865, was separately
    replicated by Sequenom in 360 cases and 360 controls and was also
    confirmed to be associated with SLE (OR = 0.725, P = 2.93 x 10(-3)).
    Logistic regression analysis showed that rs3733197 (A383T in ankyrin
    domain) and rs17266594 (a branch point-site SNP) from BANK1 had
    independent contributions towards the disease association (P = 0.037
    and 6.63 x 10(-8), respectively). In TNFSF4, rs2205960 was associated
    with SLE independently from the effect of rs844648 (P = 6.26 x 10(-3)),
    but not vice versa (P = 0.55). These findings suggest that multiple
    independent genetic variants may be present within the gene locus,
    which exert their effects on SLE pathogenesis through different
    mechanisms. Genes and Immunity (2009) 10, 414-420; doi:
    10.1038/gene.2009.16; published online 9 April 2009
 C1 [Chang, Y. K.; Yang, W.; Zhao, M.; Lee, T. L.; Ho, M. H. K.; Lee, P. P. W.; Wong, W. H. S.; Lau, Y. L.] Univ Hong Kong, Queen Mary Hosp, Dept Paediat & Adolescent Med, LKS Fac Med, Hong Kong, Hong Kong, Peoples R China.
    [Mok, C. C.] Tuen Mun Hosp, Dept Med, Hong Kong, Hong Kong, Peoples R China.
    [Chan, T. M.; Wong, R. W. S.; Mok, M. Y.; Lau, C. S.] Univ Hong Kong, Dept Med, LKS Fac Med, Hong Kong, Hong Kong, Peoples R China.
    [Lee, K. W.] Pamela Youde Nethersole Eastern Hosp, Dept Med, Hong Kong, Hong Kong, Peoples R China.
    [Wong, S. N.] Tuen Mun Hosp, Dept Paediat & Adolescent Med, Hong Kong, Hong Kong, Peoples R China.
    [Ng, I. O. L.] Univ Hong Kong, LKS Fac Med, Dept Pathol, Hong Kong, Hong Kong, Peoples R China.
    [Sham, P. C.] Univ Hong Kong, LKS Fac Med, Dept Psychiat, Hong Kong, Hong Kong, Peoples R China.
 RP Lau, YL, Univ Hong Kong, Li Ka Shing Fac Med, Hong Kong, Hong Kong,
    Peoples R China.
 EM lauylung@hkucc.hku.hk
 FU Shun Tak District Min Yuen Tong of Hong Kong ; Mr and Mrs SH Wong
    Foundation Scholarship ; BLWong Scholarship ; Yu Chun Keung Memorial
    Scholarship for Master of Research in Medicine ; Edward Sai Kim Hotung
    Paediatric Education and Research Fund ; University Postgraduate
    Studentship ; UGC, UHK [200711159155]
 FX This study is partially supported by the Shun Tak District Min Yuen
    Tong of Hong Kong. YKC thanks support from Mr and Mrs SH Wong
    Foundation Scholarship, BLWong Scholarship and Award of Yu Chun Keung
    Memorial Scholarship for Master of Research in Medicine. MZ was
    supported by Edward Sai Kim Hotung Paediatric Education and Research
    Fund, and University Postgraduate Studentship. WY thanks support from
    UGC, UHK (200711159155).
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 NR 19
 TC 17
 PU NATURE PUBLISHING GROUP
 PI LONDON
 PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
 SN 1466-4879
 J9 GENES IMMUN
 JI Genes Immun.
 PD JUL
 PY 2009
 VL 10
 IS 5
 BP 414
 EP 420
 DI 10.1038/gene.2009.16
 PG 7
 SC Genetics & Heredity; Immunology
 GA 472YH
 UT ISI:000268168800006
 ER
 
 PT J
 AU Li, QZ
    Zhou, J
    Yang, R
    Yan, M
    Ye, Q
    Liu, K
    Liu, S
    Shao, X
    Li, L
    Zhou, XJ
    Wakeland, EK
    Mohan, C
 AF Li, Q-Z
    Zhou, J.
    Yang, R.
    Yan, M.
    Ye, Q.
    Liu, K.
    Liu, S.
    Shao, X.
    Li, L.
    Zhou, X-J
    Wakeland, E. K.
    Mohan, C.
 TI The lupus-susceptibility gene kallikrein downmodulates
    antibody-mediated glomerulonephritis
 SO GENES AND IMMUNITY
 LA English
 DT Article
 DE Kallikrein; anti-GBM; glomerulonephritis; adenovirus; lupus
 ID CONVERTING ENZYME-INHIBITION; STRAIN DISTRIBUTION PATTERN; BRADYKININ
    B2 RECEPTOR; CONGENIC MOUSE STRAINS; INDUCED RENAL INJURY; TISSUE
    KALLIKREIN; ERYTHEMATOSUS PATHOGENESIS; DIABETIC-NEPHROPATHY; SLE
    PATHOGENESIS; KININ SYSTEM
 AB Sle3 is a NZM2410/NZW-derived lupus-susceptibility interval on murine
    chromosome 7, which is associated with spontaneous lupus nephritis
    (SLN), and also anti-GBM-induced glomerulonephritis (GN). The tissue
    kallikrein gene cluster is located within the Sle3 interval and
    constitutes potential candidate genes for this locus. We have recently
    reported that renal kallikrein expression was upregulated by anti-GBM
    antibody challenge in a strain-specific manner and that it was
    significantly underexpressed in the anti-GBM-sensitive strains,
    including B6.Sle3. Further sequencing and functional studies reported
    earlier provided evidence that kallikreins could constitute disease
    genes in lupus. In this report, we have used an adenoviral vector to
    deliver the klk1 gene to B6.Sle3 congenics to directly test if
    kallikreins might have a protective effect against anti-GBM-induced
    nephritis. Our data show that klk1 gene delivery ameliorated
    anti-GBM-induced nephritis in B6. Sle3 congenics. Taken together with
    earlier studies, these findings indicate that kallikreins play an
    important protective role in autoantibody-initiated GN and could
    constitute potential candidate genes for anti-GBM-induced GN and SLN.
    Genes and Immunity (2009) 10, 503-508; doi: 10.1038/gene.2009.7;
    published online 5 March 2009
 C1 [Li, Q-Z; Zhou, J.; Yang, R.; Ye, Q.; Liu, K.; Liu, S.; Shao, X.; Li, L.; Wakeland, E. K.; Mohan, C.] Univ Texas SW Med Ctr Dallas, Dept Immunol, Dallas, TX 75390 USA.
    [Li, Q-Z; Yan, M.; Mohan, C.] Univ Texas SW Med Ctr Dallas, Dept Internal Med, Dallas, TX 75390 USA.
    [Zhou, X-J] Univ Texas SW Med Ctr Dallas, Dept Pathol, Dallas, TX 75390 USA.
 RP Li, QZ, Univ Texas SW Med Ctr Dallas, Dept Immunol, 5323 Harry Hines
    Blvd, Dallas, TX 75390 USA.
 EM quan.li@utsouthwestern.edu
    Chandra.mohan@utsouthwestern.edu
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 NR 58
 TC 3
 PU NATURE PUBLISHING GROUP
 PI LONDON
 PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
 SN 1466-4879
 J9 GENES IMMUN
 JI Genes Immun.
 PD JUL
 PY 2009
 VL 10
 IS 5
 BP 503
 EP 508
 DI 10.1038/gene.2009.7
 PG 6
 SC Genetics & Heredity; Immunology
 GA 472YH
 UT ISI:000268168800016
 ER
 
 PT J
 AU Gao, D
    Wang, RP
    Li, BF
    Yang, YL
    Zhai, ZH
    Chen, DY
 AF Gao, Dong
    Wang, Ruipeng
    Li, Bingfeng
    Yang, Yongkang
    Zhai, Zhonghe
    Chen, Dan-Ying
 TI WDR34 is a novel TAK1-associated suppressor of the
    IL-1R/TLR3/TLR4-induced NF-kappa B activation pathway
 SO CELLULAR AND MOLECULAR LIFE SCIENCES
 LA English
 DT Article
 DE TAK1; WDR34; IL-1R; TLR4; TLR3; NF-kappa B
 ID BETA SIGNAL-TRANSDUCTION; INNATE IMMUNE-RESPONSES; KINASE KINASE
    KINASE; TAK1 MAPKKK; TAK1-BINDING PROTEIN-1; CRITICAL ROLES; TAB1;
    IL-1; DROSOPHILA; BINDING
 AB Toll-like receptors (TLRs) act as sensors of microbial components and
    elicit innate immune responses. All TLR signaling pathways activate the
    nuclear factor-kappaB (NF-kappa B), which controls the expression of
    inflammatory cytokine genes. Transforming growth factor-beta-activated
    kinase 1 (TAK1) is a serine/threonine protein kinase that is critically
    involved in the activation of NF-kappa B by tumor necrosis factor (TNF
    alpha), interleukin-1 beta (IL-1 beta) and TLR ligands. In this study,
    we identified a novel protein, WD40 domain repeat protein 34 (WDR34) as
    a TAK1-interacting protein in yeast two-hybrid screens. WDR34
    interacted with TAK1, TAK1-binding protein 2 (TAB2), TAK1-binding
    protein 3 (TAB3) and tumor necrosis factor receptor-associated factor 6
    (TRAF6) in overexpression and under physiological conditions.
    Overexpression of WDR34 inhibited IL-1 beta-, polyI:C- and
    lipopolysaccharide (LPS)-induced but not TNF alpha-induced NF-kappa B
    activation, whereas knockdown of WDR34 by a RNA-interference construct
    potentiated NF-kappa B activation by these ligands. Our findings
    suggest that WDR34 is a TAK1-associated inhibitor of the
    IL-1R/TLR3/TLR4-induced NF-kappa B activation pathway.
 C1 [Gao, Dong; Wang, Ruipeng; Li, Bingfeng; Yang, Yongkang; Zhai, Zhonghe; Chen, Dan-Ying] Peking Univ, Coll Life Sci, Minist Educ, Key Lab Cell Proliferat & Differentiat, Beijing 100871, Peoples R China.
 RP Chen, DY, Peking Univ, Coll Life Sci, Minist Educ, Key Lab Cell
    Proliferat & Differentiat, Beijing 100871, Peoples R China.
 EM dychen@pku.edu.cn
 FU National Natural Science Foundation of China [30421004, 30871288];
    Foundation for Authors of National Excellent Doctoral Dissertations of
    PR China [200533]; China 973 Program [2006CB504301]
 FX This work was supported by the National Natural Science Foundation of
    China (30421004 and 30871288), the Foundation for Authors of National
    Excellent Doctoral Dissertations of PR China (200533) and the China 973
    Program (2006CB504301). We thank Dr. Hong-Bing Shu and Dr. Zheng-Fan
    Jiang for stimulating discussions and members of our laboratory for
    technical help.
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 NR 33
 TC 0
 PU BIRKHAUSER VERLAG AG
 PI BASEL
 PA VIADUKSTRASSE 40-44, PO BOX 133, CH-4010 BASEL, SWITZERLAND
 SN 1420-682X
 J9 CELL MOL LIFE SCI
 JI Cell. Mol. Life Sci.
 PD AUG
 PY 2009
 VL 66
 IS 15
 BP 2573
 EP 2584
 DI 10.1007/s00018-009-0059-6
 PG 12
 SC Biochemistry & Molecular Biology; Cell Biology
 GA 472AR
 UT ISI:000268102000011
 ER
 
 PT J
 AU Yang, H
    Lang, S
    Zhai, Z
    Li, L
    Kahr, WHA
    Chen, PG
    Brkic, J
    Spring, CM
    Flick, MJ
    Degen, JL
    Freedman, J
    Ni, HY
 AF Yang, Hong
    Lang, Sean
    Zhai, Zhimin
    Li, Ling
    Kahr, Walter H. A.
    Chen, Pingguo
    Brkic, Jelena
    Spring, Christopher M.
    Flick, Matthew J.
    Degen, Jay L.
    Freedman, John
    Ni, Heyu
 TI Fibrinogen is required for maintenance of platelet intracellular and
    cell-surface P-selectin expression
 SO BLOOD
 LA English
 DT Article
 ID VON-WILLEBRAND-FACTOR; ACTIVATED HUMAN PLATELETS; DEFICIENT MICE;
    IN-VIVO; FIBRONECTIN INTERNALIZATION; INTEGRIN ALPHA(IIB)BETA(3);
    MEDIATED MODULATION; ENDOTHELIAL-CELLS; ADAPTIVE IMMUNITY;
    ALPHA-GRANULES
 AB Platelet P-selectin plays important roles in inflammation and
    contributes to thrombosis and hemostasis. Although it has been reported
    that von Willebrand factor (VWF) affects P-selectin expression on
    endothelial cells, little information is available regarding regulation
    of platelet P-selectin expression. Here, we first observed that
    P-selectin expression was significantly decreased on platelets of
    fibrinogen and VWF double-deficient mice. Subsequently, we identified
    this was due to fibrinogen deficiency. Impaired P-selectin expression
    on fibrinogen-deficient platelets was further confirmed in human
    hypofibrinogenemic patients. We demonstrated that this impairment is
    unlikely due to excessive P-selectin shedding, deficient
    fibrinogen-mediated cell surface P-selectin binding, or impaired
    platelet granule release, but rather is due to decreased platelet
    P-selectin content. Fibrinogen transfusion completely recovered this
    impairment in fibrinogen-deficient (Fg(-/-)) mice, and engagement of
    the C-terminus of the fibrinogen gamma chain with beta 3 integrin was
    required for this process. Furthermore, Fg(-/-) platelets significantly
    increased P-selectin expression following transfusion into beta 3
    integrin-deficient mice and when cultured with fibrinogen. These data
    suggest fibrinogen may play important roles in inflammation,
    thrombosis, and hemostasis via enhancement of platelet P-selectin
    expression. Since human fibrinogen levels vary significantly in normal
    and diseased populations, P-selectin as an activation marker on
    platelets should be used with caution. (Blood. 2009; 114: 425-436)
 C1 [Ni, Heyu] Univ Toronto, Canadian Blood Serv, St Michaels Hosp,Li Ka Shing Knowledge Inst, Toronto Platelet Immunobiol Grp,Keenan Res Ctr, Toronto, ON M5B 1W8, Canada.
    [Yang, Hong; Lang, Sean; Freedman, John; Ni, Heyu] Univ Toronto, Dept Lab Med & Pathobiol, Toronto, ON M5B 1W8, Canada.
    [Yang, Hong; Lang, Sean; Chen, Pingguo; Ni, Heyu] Canadian Blood Serv, Toronto, ON, Canada.
    [Yang, Hong; Lang, Sean; Chen, Pingguo; Brkic, Jelena; Spring, Christopher M.; Freedman, John; Ni, Heyu] St Michaels Hosp, Dept Lab Med, Keenan Res Ctr, Li Ka Shing Knowledge Inst, Toronto, ON M5B 1W8, Canada.
    [Lang, Sean] Univ Toronto Scarborough, Dept Biol Sci, Toronto, ON, Canada.
    [Zhai, Zhimin] Anhui Med Univ, Affiliated Hosp 2, Ctr Lab, Anhui Prov Hosp, Hefei, Anhui, Peoples R China.
    [Li, Ling; Kahr, Walter H. A.] Univ Toronto, Hosp Sick Children, Cell Biol Program, Toronto, ON M5B 1W8, Canada.
    [Kahr, Walter H. A.] Univ Toronto, Hosp Sick Children, Dept Pediat, Div Haematol Oncol, Toronto, ON M5B 1W8, Canada.
    [Flick, Matthew J.; Degen, Jay L.] Univ Cincinnati, Cincinnati, OH 45221 USA.
    [Freedman, John; Ni, Heyu] Univ Toronto, Dept Med, Toronto, ON M5B 1W8, Canada.
    [Ni, Heyu] Univ Toronto, Dept Physiol, Toronto, ON M5B 1W8, Canada.
 RP Ni, HY, Univ Toronto, Canadian Blood Serv, St Michaels Hosp,Li Ka Shing
    Knowledge Inst, Toronto Platelet Immunobiol Grp,Keenan Res Ctr, 30 Bond
    St,Rm 2-006, Toronto, ON M5B 1W8, Canada.
 EM nih@smh.toronto.on.ca
 FU Heart and Stroke Foundation of Canada (Ottawa, ON) ; Canadian
    Institutes of Health Research (CIHR) ; Canadian Blood Services ; St
    Michael's Hospital ; Canada Foundation for Innovation ; International
    Cooperation Research Fund of Anhui Provincial Scientific and
    Technologic Committee (China) ; Heart and Stroke Foundation of Ontario 
 FX This work was supported in part by the Heart and Stroke Foundation of
    Canada (Ottawa, ON); Canadian Institutes of Health Research (CIHR) and
    Canadian Blood Services; Equipment Funds from St Michael's Hospital,
    Canadian Blood Services, and Canada Foundation for Innovation; and
    International Cooperation Research Fund of Anhui Provincial Scientific
    and Technologic Committee (China). W. H. A. K. was supported by an
    operating grant from CIHR and a Phase II Clinician Scientist Salary
    Award from the Heart and Stroke Foundation of Ontario. H.Y. is a
    recipient of the Heart and Stroke/Richard Lewar Excellence award and a
    Canadian Blood Services postdoctoral fellowship award. S. L. is a
    recipient of the Canadian Blood Services summer internship program and
    the Master's Studentship Award of the Heart and Stroke Foundation of
    Ontario.
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 TC 4
 PU AMER SOC HEMATOLOGY
 PI WASHINGTON
 PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
 SN 0006-4971
 J9 BLOOD
 JI Blood
 PD JUL 9
 PY 2009
 VL 114
 IS 2
 BP 425
 EP 436
 DI 10.1182/blood-2008-03-145821
 PG 12
 SC Hematology
 GA 471MK
 UT ISI:000268061700028
 ER
 
 PT J
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    Morgan, RA
    Dudley, ME
    Cassard, L
    Yang, JC
    Hughes, MS
    Kammula, US
    Royal, RE
    Sherry, RM
    Wunderlich, JR
    Lee, CCR
    Restifo, NP
    Schwarz, SL
    Cogdill, AP
    Bishop, RJ
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    Brewer, CC
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    VanWaes, C
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    Rosenberg, SA
 AF Johnson, Laura A.
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    Dudley, Mark E.
    Cassard, Lydie
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 TI Gene therapy with human and mouse T-cell receptors mediates cancer
    regression and targets normal tissues expressing cognate antigen
 SO BLOOD
 LA English
 DT Article
 ID TUMOR-INFILTRATING LYMPHOCYTES; ADOPTIVE IMMUNOTHERAPY; METASTATIC
    MELANOMA; TCR; AUTOIMMUNITY; RECOGNITION; PERSISTENCE
 AB Gene therapy of human cancer using genetically engineered lymphocytes
    is dependent on the identification of highly reactive T-cell receptors
    (TCRs) with antitumor activity. We immunized transgenic mice and also
    conducted high-throughput screening of human lymphocytes to generate
    TCRs highly reactive to melanoma/melanocyte antigens. Genes encoding
    these TCRs were engineered into retroviral vectors and used to
    transduce autologous peripheral lymphocytes administered to 36 patients
    with metastatic melanoma. Transduced patient lymphocytes were CD45RA(-)
    and CD45RO(+) after ex vivo expansion. After infusion, the persisting
    cells displayed a CD45RA(+) and CD45RO(-) phenotype. Gene-engineered
    cells persisted at high levels in the blood of all patients 1 month
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    reactivity than nonresponders. Objective cancer regressions were seen
    in 30% and 19% of patients who received the human or mouse TCR,
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    melanocytes in the skin, eye, and ear, and sometimes required local
    steroid administration to treat uveitis and hearing loss. Thus, T cells
    expressing highly reactive TCRs mediate cancer regression in humans and
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    This trial was registered at www.ClinicalTrials.gov as NCI-07-C-0174
    and NCI-07-C-0175. (Blood. 2009; 114: 535-546)
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 RP Rosenberg, SA, NCI, Surg Branch, Hatfield Clin Res Ctr, Bldg 10CRC,
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 NR 32
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 PU AMER SOC HEMATOLOGY
 PI WASHINGTON
 PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
 SN 0006-4971
 J9 BLOOD
 JI Blood
 PD JUL 16
 PY 2009
 VL 114
 IS 3
 BP 535
 EP 546
 DI 10.1182/blood-2009-03-211714
 PG 12
 SC Hematology
 GA 471ML
 UT ISI:000268061800012
 ER
 
 PT J
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 AF Frankel, W. N.
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 TI Szt2, a novel gene for seizure threshold in mice
 SO GENES BRAIN AND BEHAVIOR
 LA English
 DT Article
 DE Epilepsy; feedback; mice; mutagenesis; mutation; seizure threshold
 ID EPILEPSY; KCNQ2; MOUSE
 AB In a chemical mutagenesis screen we identified Szt2 (seizure threshold
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    highly conserved head-to-head configuration with Med8 (which encodes a
    Mediator complex subunit), separated by only 91 nt. While the
    biological function of Szt2 remains unknown, its high conservation,
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    an important role in the central nervous system.
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 RP Frankel, WN, Jackson Lab, 600 Main St, Bar Harbor, ME 04609 USA.
 EM wayne.frankel@jax.org
 FU NIH [NS31348, HD41066, CA34196]
 FX We thank Greg Cox and Verity Letts for their feedback on this
    manuscript, Doug Hinerfeld and Rob Wilpan for their assistance with
    mass spectrometry, Ron Conaway for helpful discussions, Rod Bronson for
    reviewing our histological analysis and Steve White for sharing with us
    his pilot studies on corneal kindling in mutants. This work was
    supported by NIH grant NS31348 ( to WNF), NIH grant HD41066 ( to TPO)
    and CA34196 ( JAX Scientific Services).
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 PU WILEY-BLACKWELL PUBLISHING, INC
 PI MALDEN
 PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
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 PT J
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 LA English
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    structural changes were observed when each activator binds holo-TFIID.
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    activator-dependent TFIID assembly and transcription initiation.
 C1 [Liu, Wei-Li; Coleman, Robert A.; Ma, Elizabeth; Grob, Patricia; Yang, Joyce L.; Zhang, Yixi; Dailey, Gina; Nogales, Eva; Tjian, Robert] Univ Calif Berkeley, Howard Hughes Med Inst, Dept Mol & Cell Biol, Berkeley, CA 94720 USA.
    [Grob, Patricia; Nogales, Eva] Univ Calif Berkeley, Lawrence Berkeley Lab, Berkeley, CA 94720 USA.
 RP Tjian, R, Univ Calif Berkeley, Howard Hughes Med Inst, Dept Mol & Cell
    Biol, Berkeley, CA 94720 USA.
 EM jmlim@berkeley.edu
 FU NIH National Cancer Institute [PO1 CA112181]; NIH General Medical
    Sciences [RO1 GM63072]; Howard Hughes Medical Institute Investigators 
 FX We thank S. Zheng for providing TAF4 mAb supernatant, D. King for
    peptides, the Tjian laboratory tissue culture facility technicians, M.
    Haggart for assistance, U. Schulze- Gahmen for insect cells, and the
    Tjian laboratory members. We also thank S. Lipscomb, V. Ramey, and H.
    Wang for helpful advice and technical support. We are grateful to J.
    Yao, Z. Zhang, and U. Schulze- Gahmen for critical comments of the
    manuscript. This work was supported by NIH National Cancer Institute
    PO1 CA112181 (R. T. and E. N.), and NIH General Medical Sciences RO1
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    Investigators. R. T. is the President of the Howard Hughes Medical
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 NR 39
 TC 13
 PU COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT
 PI WOODBURY
 PA 500 SUNNYSIDE BLVD, WOODBURY, NY 11797-2924 USA
 SN 0890-9369
 J9 GENE DEVELOP
 JI Genes Dev.
 PD JUL 1
 PY 2009
 VL 23
 IS 13
 BP 1510
 EP 1521
 DI 10.1101/gad.1790709
 PG 12
 SC Cell Biology; Developmental Biology; Genetics & Heredity
 GA 470DN
 UT ISI:000267954800006
 ER
 
 PT J
 AU He, KY
    Yang, SZ
    Shen, DH
    Zhang, LM
    Lu, SD
    Sun, FY
 AF He, K-Y
    Yang, S-Z
    Shen, D-H
    Zhang, L-M
    Lu, S-D
    Sun, F-Y
 TI Excision repair cross-complementing 1 expression protects against
    ischemic injury following middle cerebral artery occlusion in the rat
    brain
 SO GENE THERAPY
 LA English
 DT Article
 DE ERCC1; cerebral ischemia; DNA repair; NER; neuroprotection; brain damage
 ID TRANSIENT FOCAL ISCHEMIA; OXIDATIVE DNA-DAMAGE; NEURONAL INJURY; STRAND
    BREAKS; GENE ERCC1; APOPTOSIS; RECOMBINATION; ENDONUCLEASE; CELLS;
    REPERFUSION
 AB To study the effects of excision repair cross-complementing 1 (ERCC1)
    on the pathophysiological process of brain ischemia, we examined the
    changes in ERCC1 expression, as well as the functional significance of
    ERCC1 in the rat brain following middle cerebral artery occlusion
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    were widely distributed in various brain regions. ERCC1 expression was
    localized to the nuclei of neurons and astrocytes. (2) ERCC1
    expression, as determined by western blot, increased at 3 days,
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    following MCAO. Immunohistochemical analysis demonstrated that ischemia
    induced increased ERCC1 expression within the periinfarct core, with
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    expression by intraventricular injection of antisense plasmids
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    ERCC1 overproduction, by injection of expression plasmids,
    significantly reduced infarct volume and the accumulation of
    DNA-damaged neurons. Taken together, these results indicate that both
    endogenous ERCC1 and exogenous ERCC1 have an important neuroprotective
    function in the brain. In addition, administration of ERCC1 to the
    brain could prove to be a successful strategy for neuronal protection
    against ischemic injury. Gene Therapy (2009) 16, 840-848;
    doi:10.1038/gt.2009.48; published online 14 May 2009
 C1 [He, K-Y; Yang, S-Z; Shen, D-H; Zhang, L-M; Lu, S-D; Sun, F-Y] Fudan Univ, Shanghai Med Coll, Dept Neurobiol, Inst Biomed Sci,State Key Lab Med Neurobiol, Shanghai 200032, Peoples R China.
 RP Sun, FY, Fudan Univ, Shanghai Med Coll, Dept Neurobiol, Inst Biomed
    Sci,State Key Lab Med Neurobiol, Shanghai 200032, Peoples R China.
 EM fysun@shmu.edu.cn
 FU National Basic Research Program of China [2006CB504100, 2006CB943702];
    National Natural Science Foundation of China [30770660]; Shanghai
    Metropolitan Fund for Research and Development [04DZ14005, 07DZ14005]
 FX This work was supported in part by grants from the National Basic
    Research Program of China (nos. 2006CB504100 and 2006CB943702),
    National Natural Science Foundation of China (no. 30770660) and
    Shanghai Metropolitan Fund for Research and Development (nos. 04DZ14005
    and 07DZ14005).
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 NR 36
 TC 1
 PU NATURE PUBLISHING GROUP
 PI LONDON
 PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
 SN 0969-7128
 J9 GENE THERAPY
 JI Gene Ther.
 PD JUL
 PY 2009
 VL 16
 IS 7
 BP 840
 EP 848
 DI 10.1038/gt.2009.48
 PG 9
 SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology;
    Genetics & Heredity; Medicine, Research & Experimental
 GA 468HB
 UT ISI:000267806600003
 ER
 
 PT J
 AU Wang, XF
    Wang, XY
    Liu, J
    Feng, JJ
    Mu, WL
    Shi, XJ
    Yang, QQ
    Duan, XC
    Xie, Y
    Lu, ZJ
 AF Wang, Xiu-Fang
    Wang, Xiaoyan
    Liu, Jing
    Feng, Jingjing
    Mu, Wenli
    Shi, Xiaojuan
    Yang, QnQing
    Duan, Xiaocui
    Xie, Ying
    Lu, Zhanjun
 TI Alu Tandem Sequences Inhibit GFP Gene Expression by Triggering
    Chromatin Wrapping
 SO GENES & GENOMICS
 LA English
 DT Article
 DE Alu; GFP; chromatin wrapping; premature transcriptional termination
 ID TRANSCRIPTIONAL REPRESSION; ELEMENTS; REPEATS; REGION; LOCUS; EXONS; DNA
 AB Alu elements belonging to the short interspersed nuclear elements
    (SINE) of repetitive elements are present in more than one million
    copies which altogether represent 10% of the whole human genome. In
    this study, the roles of Alu tandem sequences in the process of GFP
    gene (GFP) expression and packing into chromatin of its DNA were
    studied. To detect the effect of Alu repeats on gene expression,
    different copies of Alus were inserted GFP downstream respectively in
    pEGFT-C1 vector. We found that Alu sequences decreased the amount of
    GFP transcription, the percentage of GFP positive cells and the
    accessibility to DNase I in length-dependent manner. Inserting Alu
    caused the production of higher-molecular-mass RNA, indicating Ala
    sequence did not induce premature transcriptional termination. Tight
    packing chromatins keep silent and resist to DNase I digestion, which
    is a general phenomenon. We suggested that head and tail tandem Ala
    sequences suppressed GFP expression in length dependent manner by
    triggering chromatin packing.
 C1 [Wang, Xiu-Fang; Wang, Xiaoyan; Liu, Jing; Feng, Jingjing; Mu, Wenli; Shi, Xiaojuan; Yang, QnQing; Duan, Xiaocui; Xie, Ying; Lu, Zhanjun] Hebei Med Univ, Dept Genet, Hebei Key Lab Anim, Shijiazhuang, Hebei Province, Peoples R China.
 RP Lu, ZJ, Hebei Med Univ, Dept Genet, Hebei Key Lab Anim, Shijiazhuang,
    Hebei Province, Peoples R China.
 EM lslab@hebmu.edu.cn
 FU Hebei Plovillce Natural Science Foundation of China [C2008001065]
 FX This work was supported by Hebei Plovillce Natural Science Foundation
    of China (C2008001065 to Z.J.Lu).
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 NR 30
 TC 1
 PU KOREAN SOC GENETICS
 PI SEOUL
 PA KOREAN SCIENCE & TECHNOLOGY CENTER, RM 1002, 635-4 YEOKSAM-DONG,
    KANGNAM, SEOUL, 135-703, SOUTH KOREA
 SN 1976-9571
 J9 GENES GENOM
 JI Genes Genom.
 PD JUN
 PY 2009
 VL 31
 IS 3
 BP 209
 EP 215
 PG 7
 SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology;
    Genetics & Heredity
 GA 469DS
 UT ISI:000267876500001
 ER
 
 PT J
 AU Luo, YD
    Yang, CF
    Jin, CL
    Xie, R
    Wang, F
    McKeehan, WL
 AF Luo, Yongde
    Yang, Chaofeng
    Jin, Chengliu
    Xie, Rui
    Wang, Fen
    McKeehan, Wallace L.
 TI Novel phosphotyrosine targets of FGFR2IIIb signaling
 SO CELLULAR SIGNALLING
 LA English
 DT Article
 DE Receptor tyrosine kinases; Fibroblast growth factor (FGF);
    Stromal-epithelial homeostasis; Tumor suppression; Tyrosine phosphatases
 ID FIBROBLAST-GROWTH-FACTOR; RECEPTOR TYROSINE KINASE; EPITHELIAL-CELL
    ANDROMEDIN; FGF RECEPTOR; INTRAEPITHELIAL NEOPLASIA; CONDITIONAL
    ACTIVATION; CRYSTAL-STRUCTURE; ADAPTER PROTEINS; HEPARAN-SULFATE;
    PROSTATE
 AB In partnership exclusively with the epithelial FGFR2IIIb isotype and a
    structurally-specific heparan sulfate motif, stromal-derived FGF7
    delivers both growth-promoting and growth-limiting differentiation
    signals to epithelial cells that promote cellular homeostasis between
    stromal and epithelial compartments. Intercompartmental homeostasis
    supported by FGF7/FGFR2IIIb is subverted in many solid epithelial
    tumors. The normally mesenchymal-derived homologue FGFR1 drives
    proliferation and a progressive tumor-associated phenotype when it
    appears ectopically in epithelial cells. In order to understand the
    mechanism underlying the unique biological effects of FGFR2IIIb, we
    developed an inducible FGFR2IIIb expression system that is specifically
    dependent on FGF7 for activation in an initially unresponsive cell line
    to avoid selection for only the growth-promoting aspects of FGFR2IIIb
    signaling. We then determined FGF7/FGFR2IIIb signaling-specific
    tyrosine phosphorylated proteins within 5 min after FGF7 stimulation by
    phosphopeptide immunoaffinity purification and nano-LC-MS/MS. The
    FGF7/FGFR2 pair caused tyrosine phosphorylation of multiple proteins
    that have been implicated in the growth stimulating activities of FGFR1
    that included multi-substrate organizers FRS2 alpha and IRS4, ERK2 and
    phosphatases SHP2 and SHIP2. It uniquely phosphorylated CDK2 and
    phosphatase PTPN18 on sites involved in the attenuation of cell
    proliferation, and several factors that maintain nuclear-cytosolic
    relationships (emerin and LAP2), protein structure and other cellular
    fine structures as well as some proteins of unknown functions. Several
    of the FGF7/FGFR2IIIb-specific targets have been associated with
    maintenance of function and tumor suppression and disruption in tumors.
    In contrast, a number of pTyr substrates associated with FGF2/FGFR1
    that are generally associated with intracellular Ca2+-phospholipid
    signaling, membrane and cytoskeletal plasticity, cell adhesion,
    migration and the tumorigenic phenotype were not observed with
    FGF7/FGFR2IIIb. Our findings provide specific downstream targets for
    dissection of causal relationships underlying the distinct role of
    FGF7/FGFR2IIIb signaling in epithelial cell homeostasis. (C) 2009
    Elsevier Inc. All rights reserved.
 C1 [Luo, Yongde; Yang, Chaofeng; Jin, Chengliu; Xie, Rui; Wang, Fen; McKeehan, Wallace L.] Texas A&M Hlth Sci Ctr, Inst Biosci & Technol, Ctr Canc & Stem Cell Biol, Houston, TX 77030 USA.
    [Luo, Yongde; McKeehan, Wallace L.] Texas A&M Hlth Sci Ctr, Inst Biosci & Technol, IBT Prote & Nanotechnol Lab, Houston, TX 77030 USA.
    [Luo, Yongde; McKeehan, Wallace L.] Texas A&M Univ, Dept Biochem & Biophys, College Stn, TX 77843 USA.
 RP McKeehan, WL, Texas A&M Hlth Sci Ctr, Inst Biosci & Technol, Ctr Canc &
    Stem Cell Biol, 2121 W Holcombe Blvd, Houston, TX 77030 USA.
 EM wmckeehan@ibt.tamhsc.edu
 FU NIH [CA059971, DK47039]; J.S. Dunn Research Foundation ; Alliance for
    NanoHealth (Houston, TX) 
 FX This work was supported partially by NIH grant CA059971 and DK47039 (to
    W.L.M.), and by the J.S. Dunn Research Foundation and the Alliance for
    NanoHealth (Houston, TX) (to WIN and Y.L.).
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 NR 63
 TC 6
 PU ELSEVIER SCIENCE INC
 PI NEW YORK
 PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
 SN 0898-6568
 J9 CELL SIGNAL
 JI Cell. Signal.
 PD SEP
 PY 2009
 VL 21
 IS 9
 BP 1370
 EP 1378
 DI 10.1016/j.cellsig.2009.04.004
 PG 9
 SC Cell Biology
 GA 468BC
 UT ISI:000267787300004
 ER
 
 PT J
 AU Lin, WN
    Luo, SF
    Lin, CC
    Hsiao, LD
    Yang, CM
 AF Lin, Wei-Ning
    Luo, Shue-Fen
    Lin, Chih-Chung
    Hsiao, Li-Der
    Yang, Chuen-Mao
 TI Differential involvement of PKC-dependent MAPKs activation in
    lipopolysaccharide-induced AP-1 expression in human tracheal smooth
    muscle cells
 SO CELLULAR SIGNALLING
 LA English
 DT Article
 DE Lipopolysaccharide; Vascular cell adhesion molecule-1; Protein kinase
    C; Mitogen-activated protein kinase; Activator protein-1
 ID NF-KAPPA-B; PROTEIN-KINASE-C; NECROSIS-FACTOR-ALPHA; VCAM-1 EXPRESSION;
    P38 MAPK; ADHESION MOLECULE-1; JUN EXPRESSION; FOS EXPRESSION;
    TRANSCRIPTIONAL REGULATION; GENE-EXPRESSION
 AB Lipopolysaccharide (LPS) has been shown to up-regulate the expression
    of vascular cell adhesion molecule (VCAM)-1 which contributes to the
    occurrence of airway inflammatory diseases. Genetic analysis reveals
    the existence of activator protein-1 (AP-1) binding site on VCAM-1
    promoter region. However, the role of AP-1 in LPS-induced VCAM-1
    expression in human tracheal smooth muscle cells (HTSMCs) is not known.
    Here, we show that LPS increased VCAM-1 expression and adhesiveness of
    HTSMCs through AP-1, since pretreatment with an AP-1 inhibitor
    tanshinone attenuated LPS-induced VCAM-1 expression and leukocytes
    adhesion. The implication of AP-1 in LPS-induced VCAM-1 expression was
    confirmed by animal studies showing that pretreatment of mice with
    tanshinone attenuated LPS-induced VCAM-1 mRNA expression in airway
    tissues and accumulation of leukocytes in bronchoalveolar lavage. By
    using the pharmacological inhibitors and transfection with siRNA of
    PKC, p42, p38, or JNK2, LPS-induced expression of c-Fos was mediated
    through protein kinase C (PKC), p42/p44 MAPK and p38 MAPK. While, c-Jun
    expression was mediated through PKC and mitogen-activated protein
    kinases (MAPKs, p42/p44 MAPK, p38 MAPK and JNK) in HTSMCs. Pretreatment
    with the inhibitors of PKCs or MAPKs attenuated LPS-stimulated nuclear
    translocation and VCAM-1 promoter binding abilities of AP-1, which
    attenuated promoter activity and gene expression of VCAM-1 and the
    adhesiveness between HTSMCs and leukocytes. These results indicated
    that differential regulation of AP-1 through PKCs-dependent MAPKs
    activation plays central roles in LPS-induced VCAM-1 expression. The
    altered modulation of this axis with inhibitors or siRNAs may
    contribute to the improvement of airway inflammatory diseases. (C) 2009
    Elsevier Inc. All rights reserved.
 C1 [Lin, Wei-Ning; Yang, Chuen-Mao] Chang Gung Univ, Dept Physiol & Pharmacol, Tao Yuan, Taiwan.
    [Lin, Wei-Ning; Luo, Shue-Fen; Lin, Chih-Chung; Hsiao, Li-Der; Yang, Chuen-Mao] Chang Gung Mem Hosp, Tao Yuan, Taiwan.
    [Luo, Shue-Fen; Hsiao, Li-Der] Chang Gung Univ, Dept Internal Med, Tao Yuan, Taiwan.
    [Lin, Chih-Chung] Chang Gung Univ, Dept Anesthet, Tao Yuan, Taiwan.
 RP Yang, CM, Chang Gung Univ, Dept Pharmacol, 259 Wen Hwa 1st Rd, Tao
    Yuan, Taiwan.
 EM chuenmao@mail.cgu.edu.tw
 FU Chang Gung Medical Research Foundation [CMRPD170331, CMRPD140252];
    National Science Council, Taiwan [NSC95-2320-B-182047-MY3]
 FX This work was supported by grants CMRPD170331 and CMRPD140252 from
    Chang Gung Medical Research Foundation and NSC95-2320-B-182047-MY3 from
    National Science Council, Taiwan.
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 NR 44
 TC 2
 PU ELSEVIER SCIENCE INC
 PI NEW YORK
 PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
 SN 0898-6568
 J9 CELL SIGNAL
 JI Cell. Signal.
 PD SEP
 PY 2009
 VL 21
 IS 9
 BP 1385
 EP 1395
 DI 10.1016/j.cellsig.2009.04.006
 PG 11
 SC Cell Biology
 GA 468BC
 UT ISI:000267787300006
 ER
 
 PT J
 AU Chang, CJ
    Yin, PH
    Yang, DM
    Wang, CH
    Hung, WY
    Chi, CW
    Wei, YH
    Lee, HC
 AF Chang, C. -J.
    Yin, P. -H.
    Yang, D. -M.
    Wang, C. -H.
    Hung, W. -Y.
    Chi, C. -W.
    Wei, Y. -H.
    Lee, H. -C.
 TI Mitochondrial dysfunction-induced amphiregulin upregulation mediates
    chemo-resistance and cell migration in HepG2 cells
 SO CELLULAR AND MOLECULAR LIFE SCIENCES
 LA English
 DT Article
 DE ROS; Ca2+; ADAM17; EGFR; oligomycin; mtDNA depletion
 ID HUMAN HEPATOCELLULAR-CARCINOMA; GROWTH-FACTOR; DNA MUTATIONS;
    BREAST-CANCER; COPY NUMBER; D-LOOP; TUMOR PROGRESSION; RECEPTOR
    PATHWAY; PHASE-II; STRESS
 AB The aim of this study was to investigate the contribution of
    mitochondrial dysfunction to chemoresistance and migration of hepatoma
    cells. We found that inhibition of mitochondrial respiration and
    mitochondrial DNA (mtDNA) depletion resulted in induction of
    amphiregulin (AR) expression in HepG2 cells. Upon oligomycin treatment
    of HepG2 cells, the cytosolic Ca2+ was significantly raised after 30
    min, and the intracellular level of reactive oxygen species (ROS) was
    elevated 2.2-fold after 4 h. Moreover, the condition medium of
    oligomycin-treated HepG2 cells was found to stimulate the migration of
    SK-Hep-1 cells. On the other hand, oligomycin-induced
    cisplatin-resistance and cell migration of HepG2 cells were attenuated
    by AR-specific RNA interference (#L-017435, Dharmacon) and a
    neutralizing antibody (MAB262, R&D Systems), respectively. Together,
    these findings suggest that mitochondrial dysfunction induced Ca2+
    mobilization, and ROS overproduction, which modulated the
    chemo-resistance and migration of hepatoma cells through the induction
    and activation of AR.
 C1 [Chang, C. -J.; Wang, C. -H.; Hung, W. -Y.; Chi, C. -W.; Lee, H. -C.] Natl Yang Ming Univ, Inst Pharmacol, Sch Med, Taipei 112, Taiwan.
    [Chang, C. -J.; Wei, Y. -H.] Natl Yang Ming Univ, Dept Biochem & Mol Biol, Taipei 112, Taiwan.
    [Yin, P. -H.; Yang, D. -M.; Chi, C. -W.] Taipei Vet Gen Hosp, Dept Med Res & Educ, Taipei 112, Taiwan.
    [Yang, D. -M.] Natl Yang Ming Univ, Inst Biophoton, Taipei 112, Taiwan.
    [Chang, C. -J.] Chinese Culture Univ, Sch Agr, Dept Food, Hlth & Nutr Sci, Taipei, Taiwan.
 RP Wei, YH, Natl Yang Ming Univ, Dept Biochem & Mol Biol, Taipei 112,
    Taiwan.
 EM zjr6@faculty.pccu.edu.tw
    joeman@ym.edu.tw
    hclee2@ym.edu.tw
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 NR 50
 TC 2
 PU BIRKHAUSER VERLAG AG
 PI BASEL
 PA VIADUKSTRASSE 40-44, PO BOX 133, CH-4010 BASEL, SWITZERLAND
 SN 1420-682X
 J9 CELL MOL LIFE SCI
 JI Cell. Mol. Life Sci.
 PD MAY
 PY 2009
 VL 66
 IS 10
 BP 1755
 EP 1765
 DI 10.1007/s00018-009-8767-5
 PG 11
 SC Biochemistry & Molecular Biology; Cell Biology
 GA 470TO
 UT ISI:000268003600010
 ER
 
 PT J
 AU Zeng, SC
    Yang, Q
 AF Zeng, Sicong
    Yang, Qin
 TI The MUS81 endonuclease is essential for telomerase negative cell
    proliferation
 SO CELL CYCLE
 LA English
 DT Article
 DE ALT; APBs; MUS81; telomere recombination
 ID PROMYELOCYTIC LEUKEMIA BODIES; HOLLIDAY JUNCTIONS; DNA-DAMAGE;
    MAMMALIAN TELOMERES; RNA INTERFERENCE; IN-VITRO; RECOMBINATION; LOOP;
    IDENTIFICATION; MAINTENANCE
 AB A substantial number of human tumors (similar to 10%) are telomerase
    negative, and cells in such tumors have been proposed to maintain
    telomere length by the alternative lengthening of telomeres (ALT)
    pathway. Although details of the molecular mechanism of ALT are largely
    unknown, previous studies have shown that telomere homologous
    recombination (HR) is implicated in the ALT pathway. MUS81 is a DNA
    structure-specific recombination endonuclease and functions on aberrant
    DNA replication and recombination. Recently, we demonstrate that MUS81
    plays a key role in the maintenance of telomeres in ALT cells (Zeng, et
    al. Nature Cell Biology, 2009). The MUS81 endonuclease specifically
    localizes to ALT-associated promyelocytic leukemia nuclear bodies
    (APBs) and interacts with telomeres in ALT cells. Depletion of MUS81
    leads to reduced telomere recombination resulting in the growth arrest
    of ALT cells. The endonuclease activity of MUS81, regulated by its
    binding partner TRF2, is found to be essential for telomere
    post-replicative recombination. This study provides the first direct
    evidence that MUS81 specifically functions on ALT recombination-based
    cell survival. The specific function of MUS81 on the ALT pathway
    provides a potential powerful diagnostic marker and a therapeutic
    target for ALT tumors.
 C1 [Yang, Qin] Washington Univ, Sch Med, Dept Radiat Oncol, Div Radiat & Canc Biol, St Louis, MO 63108 USA.
 RP Yang, Q, Washington Univ, Sch Med, Dept Radiat Oncol, Div Radiat & Canc
    Biol, 4511 Forest Pk, St Louis, MO 63108 USA.
 EM qyang@wustl.edu
 FU Concern Foundation 
 FX We thank Roger R. Reddel for providing the ALT cells, and Clare H.
    McGowan for providing the wild- type and mutant MUS81 constructs, MUS81
    antibody and Mus81+/+ and Mus81-/MEFs. This work is supported in part
    by grants from Concern Foundation (Q.Y.).
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 NR 34
 TC 0
 PU LANDES BIOSCIENCE
 PI AUSTIN
 PA 1002 WEST AVENUE, 2ND FLOOR, AUSTIN, TX 78701 USA
 SN 1538-4101
 J9 CELL CYCLE
 JI Cell Cycle
 PD JUL 15
 PY 2009
 VL 8
 IS 14
 BP 2157
 EP 2160
 PG 4
 SC Cell Biology
 GA 470IQ
 UT ISI:000267968800016
 ER
 
 PT J
 AU Gupta, A
    Yang, Q
    Pandita, RK
    Hunt, CR
    Xiang, T
    Misri, S
    Zeng, SC
    Pagan, J
    Jeffery, J
    Puc, J
    Kumar, R
    Feng, ZH
    Powell, SN
    Bhat, A
    Yaguchi, T
    Wadhwa, R
    Kaul, SC
    Parsons, R
    Khanna, KK
    Pandita, TK
 AF Gupta, Arun
    Yang, Qin
    Pandita, Raj K.
    Hunt, Clayton R.
    Xiang, Tao
    Misri, Sandeep
    Zeng, Sicong
    Pagan, Julia
    Jeffery, Jessie
    Puc, Janusz
    Kumar, Rakesh
    Feng, Zhihui
    Powell, Simon N.
    Bhat, Audesh
    Yaguchi, Tomoko
    Wadhwa, Renu
    Kaul, Sunil C.
    Parsons, Ramon
    Khanna, Kum Kum
    Pandita, Tej K.
 TI Cell cycle checkpoint defects contribute to genomic instability in PTEN
    deficient cells independent of DNA DSB repair
 SO CELL CYCLE
 LA English
 DT Article
 DE genomic instability; checkpoint defects; DNA damage response; ATM;
    PTEN; Rad51
 ID DOUBLE-STRAND BREAKS; IONIZING-RADIATION; TUMOR-SUPPRESSOR;
    ATAXIA-TELANGIECTASIA; HISTONE H2AX; MAMMALIAN-CELLS; GAMMA-H2AX FOCI;
    PROSTATE-CANCER; X-IRRADIATION; NUCLEAR PTEN
 AB Chromosomes in PTEN deficient cells display both numerical as well as
    structural alterations including regional amplification. We found that
    PTEN deficient cells displayed a normal DNA damage response (DDR) as
    evidenced by the ionizing radiation (IR)-induced phosphorylation of
    Ataxia Telangiectasia Mutated (ATM) as well as its effectors. PTEN
    deficient cells also had no defect in Rad51 expression or DNA damage
    repair kinetics post irradiation. In contrast, caffeine treatment
    specifically increased IR-induced chromosome aberrations and mitotic
    index only in cells with PTEN, and not in cells deficient for PTEN,
    suggesting that their checkpoints were defective. Furthermore,
    PTEN-deficient cells were unable to maintain active spindle checkpoint
    after taxol treatment. Genomic instability in PTEN deficient cells
    could not be attributed to lack of PTEN at centromeres, since no
    interaction was detected between centromeric DNA and PTEN in wild type
    cells. These results indicate that PTEN deficiency alters multiple cell
    cycle checkpoints possibly leaving less time for DNA damage repair
    and/or chromosome segregation as evidenced by the increased structural
    as well as numerical alterations seen in PTEN deficient cells.
 C1 [Pandita, Tej K.] Washington Univ, Sch Med, Dept Radiat Oncol, St Louis, MO 63108 USA.
    [Pagan, Julia; Jeffery, Jessie; Khanna, Kum Kum] Queensland Inst Med Res, Brisbane, Qld 4006, Australia.
    [Puc, Janusz; Parsons, Ramon] Columbia Univ, Inst Genet, New York, NY USA.
    [Yaguchi, Tomoko; Wadhwa, Renu; Kaul, Sunil C.] Natl Inst Adv Ind Sci & Technol, Tsukuba, Ibaraki, Japan.
 RP Pandita, TK, Washington Univ, Sch Med, Dept Radiat Oncol, 4511 Forest
    Pk Ave, St Louis, MO 63108 USA.
 EM pandita@wustl.edu
 FU National Institute of Health [CA129537, CA123232]
 FX This work was supported by National Institute of Health grants CA129537
    and CA123232 (T. K. P.). We thank Shyam K. Sharan, Yuxin Yin, Titia
    DeLange, Susana Gonzalo, Todd Waldman, T. Halazonetis and C. Eng for
    providing the reagents, sharing data and advice. We thank the members
    of Pandita laboratory for their help and thoughtful discussion.
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 NR 59
 TC 9
 PU LANDES BIOSCIENCE
 PI AUSTIN
 PA 1002 WEST AVENUE, 2ND FLOOR, AUSTIN, TX 78701 USA
 SN 1538-4101
 J9 CELL CYCLE
 JI Cell Cycle
 PD JUL 15
 PY 2009
 VL 8
 IS 14
 BP 2198
 EP 2210
 PG 13
 SC Cell Biology
 GA 470IQ
 UT ISI:000267968800023
 ER
 
 PT J
 AU Yang, ZC
    Wang, KS
    Wu, Y
    Zou, XQ
    Xiang, YY
    Chen, XP
    Li, YJ
 AF Yang, Zhi-Chun
    Wang, Kuan-Song
    Wu, Yan
    Zou, Xiao-Qing
    Xiang, Yue-Yun
    Chen, Xiao-Ping
    Li, Yuan-Jian
 TI Asymmetric Dimethylarginine Impairs Glucose Utilization via ROS/TLR4
    Pathway in Adipocytes: an Effect Prevented by Vitamin E
 SO CELLULAR PHYSIOLOGY AND BIOCHEMISTRY
 LA English
 DT Article
 DE Asymmetric dimethylarginine; Glucose; Adipocytes; Oxidative stress;
    Toll-like receptor 4
 ID HUMAN ADIPOSE-TISSUE; DIET-INDUCED OBESITY; TOLL-LIKE RECEPTOR;
    NF-KAPPA-B; INSULIN-RESISTANCE; GLUT4 TRANSLOCATION; DIABETES-MELLITUS;
    3T3-L1 ADIPOCYTES; OXIDATIVE STRESS; 3T3L1 ADIPOCYTES
 AB Background: Asymmetric dimethylarginine (ADMA), the inhibitor of nitric
    oxide synthase (NOS), has been reported to be associated with glucose
    metabolism, but its mechanisms remain unknown. Methods: In 3T3-L1
    adipocytes, we measured the effects of ADMA on glucose transport
    process under basal or insulin-induced condition, and examined the
    production of nitric oxide (NO), reactive oxygen species ( ROS) and
    tumor necrosis factor alpha (TNF-alpha), and the expression of
    toll-like receptor 4 (TLR4). Results: ADMA significantly impaired basal
    or insulin-stimulated 2-deoxy- [H-3] glucose uptake, and decreased the
    expression of insulin receptor substrate-1 (IRS-1) and glucose
    transporter-4 (GLUT4). Phosphorylated protein of IRS-1 and
    translocation of GLUT4 with insulin-stimulation were also inhibited by
    ADMA. NO decreased, while production of ROS and TNF-alpha, and
    expression of TLR4 increased after ADMA treatment. Vitamin E reduced
    the effects of ADMA on glucose transport system, and on NO, ROS and
    TLR4. Moreover, vitamin E decreased ADMA contents by up-regulating
    dimethylarginine dimethylaminohydrolase (DDAH) activity in adipocytes.
    Though L-arginine also increased NO level, but failed to reduce the
    effects of ADMA. Conclusion: ADMA significantly impairs both basal and
    insulin-stimulated glucose transport in adipocytes, which may relate to
    activation of the ROS/TLR4 pathway. Copyright (C) 2009 S. Karger AG,
    Basel
 C1 [Yang, Zhi-Chun; Wu, Yan; Zou, Xiao-Qing; Chen, Xiao-Ping; Li, Yuan-Jian] Cent S Univ, Dept Pharmacol, Sch Pharmaceut Sci, Changsha 410078, Hunan, Peoples R China.
    [Wang, Kuan-Song] Cent S Univ, Dept Pathol, Sch Basic Med, Changsha 410078, Hunan, Peoples R China.
    [Xiang, Yue-Yun] Cent S Univ, Dept Docimasiol, Xiang Ya Sch Med, Changsha 410078, Hunan, Peoples R China.
 RP Li, YJ, Cent S Univ, Dept Pharmacol, Sch Pharmaceut Sci, Xiang Ya Rd
    110, Changsha 410078, Hunan, Peoples R China.
 EM yuan_jianli@yahoo.com
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 NR 35
 TC 2
 PU KARGER
 PI BASEL
 PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND
 SN 1015-8987
 J9 CELL PHYSIOL BIOCHEM
 JI Cell. Physiol. Biochem.
 PY 2009
 VL 24
 IS 1-2
 BP 115
 EP 124
 DI 10.1159/000227819
 PG 10
 SC Cell Biology; Physiology
 GA 466GY
 UT ISI:000267650600013
 ER
 
 PT J
 AU Wang, CT
    Zhang, P
    Wang, YS
    Ruan, XZ
    Li, ZY
    Peng, F
    Yang, HS
    Wei, YQ
 AF Wang, Chun-Ting
    Zhang, Peng
    Wang, Yong-Sheng
    Ruan, Xu-Zhi
    Li, Zhi-Yong
    Peng, Feng
    Yang, Han-Shuo
    Wei, Yu-Quan
 TI RNA interference against Biot2, a novel mouse testis - specific gene,
    inhibits the growth of tumor cells
 SO CELLULAR & MOLECULAR BIOLOGY LETTERS
 LA English
 DT Article
 DE RNA interference; Biot2; Testis-specific; Proliferation
 ID DIFFERENTIATION ANTIGEN; BREAST-CANCER; CANCER/TESTIS ANTIGENS;
    MULTIPLE-MYELOMA; MAMMARY-GLAND; EXPRESSION; IMMUNOTHERAPY; NY-BR-1;
    RESPONSES; PROTEIN
 AB Biot2 is a novel murine testis-specific gene that was first identified
    using the SEREX technique, and named by our laboratory. Using
    conventional RT-PCR and real time RT-PCR, we tested the expression
    profile of Biot2 in normal tissues and various murine tumor cell lines.
    Using RNA interference, we studied the biological function of Biot2 in
    tumorigenesis. We applied various types of growth assay, such as the in
    vitro MTT, colony-forming and BrdU incorporation assays, along with in
    vivo tumorigenicity assays, to reveal its inhibition of tumor cell
    proliferation. The results revealed that the Biot2 transcript was
    detected only and strongly in the testis tissues and abundantly in five
    types of murine cancer cell line. Treating B16 murine melanoma, LL/2
    murine Lewis lung carcinoma and CT26 murine colorectal adenocarcinoma
    with special shRNA targeting Biot2 can significantly reduce the
    proliferation rate of these three tumor cell lines in vitro, as
    measured by the MTT, colony-forming and BrdU incorporation assays. The
    tumorigenicity of the CT26 cells transfected with special shRNA
    targeting Biot2 was also decreased distinctly in vivo compared with the
    control. It was therefore concluded that Biot2 plays a key role in
    tumorigenesis and could be a potential target for biotherapy.
 C1 [Wang, Chun-Ting; Wang, Yong-Sheng; Ruan, Xu-Zhi; Li, Zhi-Yong; Peng, Feng; Yang, Han-Shuo; Wei, Yu-Quan] Sichuan Univ, State Key Lab Biotherapy, W China Hosp, W China Med Sch, Chengdu 610041, Sichuan, Peoples R China.
    [Zhang, Peng] Sichuan Canc Hosp, Dept Radiat Oncol, Chengdu 610041, Sichuan, Peoples R China.
    [Peng, Feng] Sichuan Univ, Dept Thorac Oncol, Ctr Canc, W China Hosp,W China Med Sch, Chengdu 610041, Sichuan, Peoples R China.
 RP Peng, F, Sichuan Univ, State Key Lab Biotherapy, W China Hosp, W China
    Med Sch, Keyuan Rd 4, Chengdu 610041, Sichuan, Peoples R China.
 EM evenforeven@yahoo.com.cn
    yhansh@scu.edu.cn
 FU National Natural Science Foundation of China [30700969, 30801048];
    National 863 Projects 
 FX This work was supported by National Natural Science Foundation of China
    (30700969 and 30801048) and National 863 Projects.
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 NR 24
 TC 2
 PU VERSITA
 PI WARSAW 41
 PA 9 DRUGA POPRZECNA ST, 04-604 WARSAW 41, POLAND
 SN 1425-8153
 J9 CELL MOL BIOL LETT
 JI Cell. Mol. Biol. Lett.
 PD SEP
 PY 2009
 VL 14
 IS 3
 BP 363
 EP 376
 DI 10.2478/s11658-009-0004-6
 PG 14
 SC Biochemistry & Molecular Biology; Cell Biology
 GA 464DF
 UT ISI:000267484600001
 ER
 
 PT J
 AU Yang, KM
    Pyo, JO
    Kim, GY
    Yu, R
    Han, IS
    Ju, SA
    Kim, WH
    Kim, BS
 AF Yang, Kyung Min
    Pyo, Jong Ok
    Kim, Gyu-Yeol
    Yu, Rina
    Han, In Seob
    Ju, Seong A.
    Kim, Won Ho
    Kim, Byung-Sam
 TI Capsaicin induces apoptosis by generating reactive oxygen species and
    disrupting mitochondrial transmembrane potential in human colon cancer
    cell lines
 SO CELLULAR & MOLECULAR BIOLOGY LETTERS
 LA English
 DT Article
 DE Capsaicin; Colon cancer cell line; Apoptosis; Mitochondrial
    transmembrane potential; Reactive oxygen species; Caspase 3
 ID VANILLOID CAPSAICIN; INDUCTION; MECHANISMS; DEATH; INHIBITION;
    COMPONENT; GROWTH; P53
 AB Although genetic factors are a well-known cause of colorectal cancer,
    environmental factors contribute more to its development. Despite
    advances in the fields of surgery, radiotherapy and chemotherapy, the
    cure rates for colon cancer have not substantially improved over the
    past few decades. Capsaicin (trans-8-methyl-N-vanillyl-6-nonenamide),
    the principal pungent ingredient of hot chili pepper, has exhibited an
    anti-tumor effect in many cell types. However, the mechanisms
    responsible for the anti-tumor effect of capsaicin are not yet
    completely understood. In this study, we investigated whether capsaicin
    induces apoptosis in colon cancer cell lines. Capsaicin decreased cell
    viability in a dose-dependent manner in Colo320DM and LoVo cells. In
    addition, capsaicin produced cell morphology changes and DNA
    fragmentation, decreased the DNA contents, and induced
    phosphatidylserine translocation, which is a hallmark of apoptotic cell
    death. We showed that capsaicin-induced apoptosis is associated with an
    increase in ROS generation and a disruption of the mitochondrial
    transmenbrane potential. A possible mechanism of capsaicin-induced
    apoptosis is the activation of caspase 3, a major apoptosis-executing
    enzyme. Treatment with capsaicin induced a dramatic increase in caspase
    3 activity, as assessed by the cleavage of Ac-DEVD-AMC, a fluorogenic
    substrate. In conclusion, our results clearly showed that capsaicin
    induced apoptosis in colon cancer cells. Although the actual mechanisms
    of capsaicin-induced apoptosis remain uncertain, it may be a beneficial
    agent for colon cancer treatment and chemoprevention.
 C1 [Han, In Seob; Kim, Byung-Sam] Univ Ulsan, Dept Biol Sci, Ulsan 680749, South Korea.
    [Yang, Kyung Min; Kim, Won Ho] Yonsei Univ, Coll Med, Dept Internal Med, Inst Gastroenterol, Seoul, South Korea.
    [Pyo, Jong Ok] Seoul Natl Univ, Sch Biol Sci, Bio MAX Inst, Seoul, South Korea.
    [Kim, Gyu-Yeol] Univ Ulsan, Dept Surg, Ulsan Univ Hosp, Coll Med, Ulsan 680749, South Korea.
    [Yu, Rina] Univ Ulsan, Dept Food Sci & Nutr, Ulsan 680749, South Korea.
    [Ju, Seong A.] Univ Ulsan, Biomed Res Ctr, Ulsan Univ Hosp, Coll Med, Ulsan 680749, South Korea.
 RP Kim, BS, Univ Ulsan, Dept Biol Sci, Ulsan 680749, South Korea.
 EM bskim@ulsan.ac.kr
 FU Korean Ministry of Education and Human Resources Development
    [KRF-2007-412-J00302]; Korea Health 21 RD project 
 FX This study was supported by the Korean Ministry of Education and Human
    Resources Development (KRF-2007-412-J00302) and the Korea Health 21 R&D
    project.
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 NR 25
 TC 4
 PU VERSITA
 PI WARSAW 41
 PA 9 DRUGA POPRZECNA ST, 04-604 WARSAW 41, POLAND
 SN 1425-8153
 J9 CELL MOL BIOL LETT
 JI Cell. Mol. Biol. Lett.
 PD SEP
 PY 2009
 VL 14
 IS 3
 BP 497
 EP 510
 DI 10.2478/s11658-009-0016-2
 PG 14
 SC Biochemistry & Molecular Biology; Cell Biology
 GA 464DF
 UT ISI:000267484600010
 ER
 
 PT J
 AU Cheng, MT
    Yang, HW
    Chen, TH
    Lee, OKS
 AF Cheng, M-T.
    Yang, H-W.
    Chen, T-H.
    Lee, O. K-S.
 TI Isolation and characterization of multipotent stem cells from human
    cruciate ligaments
 SO CELL PROLIFERATION
 LA English
 DT Article
 ID MARROW STROMAL CELLS; TERM-FOLLOW-UP; ANTERIOR CRUCIATE; BONE-MARROW;
    IN-VITRO; ADIPOSE-TISSUE; REPAIR; GROWTH; KNEES; TEARS
 AB Objectives:
    Mesenchymal stem cells have great potential for tissue regeneration,
    and these cells can be harvested from a variety of tissues; however, up
    to now it has not been clear whether stem cells could be isolated from
    cruciate ligaments of the knee joint. The aim of our study was to
    isolate and characterize stem cells from both anterior and posterior
    cruciate ligaments (ACL and PCL) of humans.
    Materials and methods:
    Cruciate igaments were obtained from patients receiving total knee
    arthroplasty for advanced osteoarthritis and plastic-adherent cells
    were serially passaged. In vitro chondrogenic, osteogenic and
    adipogenic abilities of the cells were evaluated by reverse
    transcriptase-polymerase chain reaction and histological study.
    Karyotyping and surface immunophenotyping of the cells were performed.
    Results:
    It was found that a population of ligament-derived cells could be
    expanded and subcultured extensively. These cells were able to
    differentiate into osteoblasts, chondrocytes and adipocytes under
    appropriate inductions. Their phenotypic characteristics were similar
    to those of bone marrow mesenchymal stem cells. Karyotyping was normal
    after serial passage.
    Conclusions:
    In summary, our study demonstrates that human multipotent stem cells
    can be isolated and expanded from human ACL and PCL, which are easily
    obtained from patients following total knee or cruciate ligament
    reconstructive surgery. Self-renewal and mesodermal differentiation
    potential of these cells make them a viable alternative source for use
    in regenerative medicine.
 C1 [Lee, O. K-S.] Natl Yang Ming Univ, Inst Clin Med, Taipei Vet Gen Hosp, Dept Orthopaed & Traumatol, Taipei 11217, Taiwan.
    [Cheng, M-T.; Lee, O. K-S.] Natl Yang Ming Univ, Inst Clin Med, Taipei 11217, Taiwan.
    [Cheng, M-T.] Tao Yuan Gen Hosp, Tao Yuan, Taiwan.
 RP Lee, OKS, Natl Yang Ming Univ, Inst Clin Med, Taipei Vet Gen Hosp, Dept
    Orthopaed & Traumatol, 201 Sec 2,Shih Pai Rd, Taipei 11217, Taiwan.
 EM kslee@vghtpe.gov.tw
 FU Ministry of Education, Aim for the Top University Plan, Taiwan 
 FX Grant from Ministry of Education, Aim for the Top University Plan,
    Taiwan.
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 NR 53
 TC 9
 PU WILEY-BLACKWELL PUBLISHING, INC
 PI MALDEN
 PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
 SN 0960-7722
 J9 CELL PROLIFERATION
 JI Cell Prolif.
 PD AUG
 PY 2009
 VL 42
 IS 4
 BP 448
 EP 460
 DI 10.1111/j.1365-2184.2009.00611.x
 PG 13
 SC Cell Biology
 GA 464VZ
 UT ISI:000267538300004
 ER
 
 PT J
 AU Shih, YRV
    Kuo, TK
    Yang, AH
    Lee, OK
    Lee, CH
 AF Shih, Y-R. V.
    Kuo, T. K.
    Yang, A-H.
    Lee, O. K.
    Lee, C-H.
 TI Isolation and characterization of stem cells from the human parathyroid
    gland
 SO CELL PROLIFERATION
 LA English
 DT Article
 ID UMBILICAL-CORD BLOOD; IN-VITRO; TRANSCRIPTIONAL REGULATION;
    ENDOTHELIAL-CELLS; DIFFERENTIATION; EXPRESSION; PERICYTES;
    MICROVASCULATURE; THERAPY; MARKERS
 AB Objectives:
    Somatic stem cells can be obtained from a variety of adult human
    tissues. However, it was not clear whether human parathyroid glands,
    which secrete parathyroid hormones and are essential in maintaining
    homeostasis levels of calcium ions in the circulation, contained stem
    cells. We aimed to investigate the possibility of isolating such
    parathyroid-derived stem cells (PDSC).
    Materials and methods:
    Surgically removed parathyroid glands were obtained with informed
    consent. Cell cytogenetics was used to observe chromosomal
    abnormalities. Surface phenotypes were characterized by flow cytometry.
    Telomerase repeat amplification protocol (TRAP) assay was performed to
    observe the telomerase activity. RT-PCR and real-time PCR was was used
    to detect gene expressions. Real-time calcium uptake imaging was
    performed for extent of calcium uptake and transmission electron
    microscopy and immunofluorecent staining for smooth muscle actin.
    Results:
    After enzymatic digestion and primary culture, plastic-adherent,
    fibroblast-like cells appeared in culture and a morphologically
    homogeneous population was derived from subsequent limiting dilution
    and clonal expansion. Karyotyping was normal and doubling time of
    clonal cell growth was estimated to be 70.7 +/- 14.5 h (mean +/-
    standard deviation). The surface phenotype of the cells was positive
    for CD73, CD166, CD29, CD49a, CD49b, CD49d, CD44, CD105, and MHC class
    I, and negative for CD34, CD133, CD117, CD114, CD31, CD62P, EGF-R,
    ICAM-3, CD26, CXCR4, CD106, CD90 and MHC class II, similar to
    mesenchymal stem cells (MSC). Detectable levels of telomerase activity
    along with pluripotency Sall4 gene expression were observed from the
    isolated PDSCs. Expression of calcium-sensing receptor gene along with
    alpha-smooth muscle actin was induced and cellular uptake of
    extracellular calcium ions was observed. Furthermore, PDSCs possessed
    osteogenic, chondrogenic and adipogenic differentiation potentials.
    Conclusions:
    Our results reveal that PDSCs were similar phenotypically to MSCs and
    further studies are needed to formulate induction conditions to
    differentiate PDSCs into parathyroid hormone-secreting chief cells.
 C1 [Shih, Y-R. V.; Lee, O. K.] Natl Yang Ming Univ, Inst Clin Med, Taipei 112, Taiwan.
    [Kuo, T. K.] Natl Yang Ming Univ, Inst Biopharmaceut Sci, Taipei 112, Taiwan.
    [Yang, A-H.] Taipei Vet Gen Hosp, Dept Pathol, Taipei, Taiwan.
    [Lee, O. K.] Taipei Vet Gen Hosp, Dept Med Res & Educ, Taipei, Taiwan.
    [Lee, O. K.] Natl Taiwan Univ, Stem Cell Res Inst, Taipei 10764, Taiwan.
    [Lee, C-H.] Taipei Vet Gen Hosp, Dept Surg, Taipei, Taiwan.
    [Lee, C-H.] Natl Yang Ming Univ, Sch Med, Taipei 112, Taiwan.
 RP Lee, OK, 201 Shi Pai Rd,Sec 2, Taipei 11221, Taiwan.
 EM kslee@vghtpe.gov.tw
    chlee@vghtpe.gov.tw
 FU Taipei Veterans General Hospital, Taiwan [V95E1-009, V96E1-005]
 FX This work was supported by intramural research grants from Taipei
    Veterans General Hospital, Taiwan (V95E1-009 and V96E1-005).
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 NR 38
 TC 8
 PU WILEY-BLACKWELL PUBLISHING, INC
 PI MALDEN
 PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
 SN 0960-7722
 J9 CELL PROLIFERATION
 JI Cell Prolif.
 PD AUG
 PY 2009
 VL 42
 IS 4
 BP 461
 EP 470
 DI 10.1111/j.1365-2184.2009.00614.x
 PG 10
 SC Cell Biology
 GA 464VZ
 UT ISI:000267538300005
 ER
 
 PT J
 AU Cheng, MT
    Yang, HW
    Chen, TH
    Lee, OKS
 AF Cheng, M-T.
    Yang, H-W.
    Chen, T-H.
    Lee, O. K-S.
 TI Isolation and characterization of multipotent stem cells from human
    cruciate ligaments (vol 42, pg 448, 2009)
 SO CELL PROLIFERATION
 LA English
 DT Correction
 CR CHENG MT, 2009, CELL PROLIFERAT, V42, P448, DOI
    10.1111/j.1365-2184.2009.00611.x
    CHENG MT, 2009, CELL PROLIFERAT, V42, P448, DOI
    10.1111/j.1365-2184.2009.00611.x
    SHIH YRV, 2009, CELL PROLIFERAT, V42, P461, DOI
    10.1111/j.1365-2184.2009.00614.x
 NR 3
 TC 0
 PU WILEY-BLACKWELL PUBLISHING, INC
 PI MALDEN
 PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
 SN 0960-7722
 J9 CELL PROLIFERATION
 JI Cell Prolif.
 PD AUG
 PY 2009
 VL 42
 IS 4
 BP 569
 EP 569
 PG 1
 SC Cell Biology
 GA 464VZ
 UT ISI:000267538300016
 ER
 
 PT J
 AU Shih, YRV
    Kuo, TK
    Yang, AH
    Lee, OK
    Lee, CH
 AF Shih, Y-R. V.
    Kuo, T. K.
    Yang, A-H.
    Lee, O. K.
    Lee, C-H.
 TI Virtual glioblastoma: growth, migration and treatment in a
    three-dimensional mathematical model (vol 42, pg 511, 2009)
 SO CELL PROLIFERATION
 LA English
 DT Correction
 CR CHENG MT, 2009, CELL PROLIFERAT, V42, P448, DOI
    10.1111/j.1365-2184.2009.00611.x
    EIKENBERRY SE, 2009, CELL PROLIFERAT, V42, P511, DOI
    10.1111/j.1365-2184.2009.00613.x
    SHIH YRV, 2009, CELL PROLIFERAT, V42, P461, DOI
    10.1111/j.1365-2184.2009.00614.x
 NR 3
 TC 0
 PU WILEY-BLACKWELL PUBLISHING, INC
 PI MALDEN
 PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
 SN 0960-7722
 J9 CELL PROLIFERATION
 JI Cell Prolif.
 PD AUG
 PY 2009
 VL 42
 IS 4
 BP 570
 EP 570
 DI 10.1111/j.1365-2184.2009.00644.x
 PG 1
 SC Cell Biology
 GA 464VZ
 UT ISI:000267538300017
 ER
 
 PT J
 AU Thao, LB
    Vu, HA
    Yasuda, K
    Taniguchi, S
    Yagasaki, F
    Taguchi, T
    Watanabe, T
    Sato, Y
 AF Thao, Le Ba
    Vu, Hoang Anh
    Yasuda, Kazuki
    Taniguchi, Shigeki
    Yagasaki, Fumiharu
    Taguchi, Takahiro
    Watanabe, Toshiki
    Sato, Yuko
 TI Cas-L was overexpressed in imatinib-resistant gastrointestinal stromal
    tumor cells
 SO CANCER BIOLOGY & THERAPY
 LA English
 DT Article
 DE GISTs; Cas-L; SRC; KIT; imatinib
 ID METASTASIS; MECHANISMS; INHIBITOR; RECEPTORS; INTEGRINS; APOPTOSIS;
    MESYLATE; MUTATION; INSIGHT; KINASE
 AB Gastrointestinal stromal tumors (GISTs) are the most common mesenchymal
    tumors in the gastrointestinal tract. Most GISTs patients respond to
    imatinib, yet will eventually exhibit resistance, and the mechanisms of
    imatinib resistance have not yet been fully elucidated.
    To clarify the mechanisms of secondary imatinib-resistant
    gastrointestinal stromal tumors, we generated resistant cells from the
    imatinib-sensitive GIST-T1 cells by exposing them to increasing
    concentrations of imatinib for 6 m. GIST-T1 IR (imatinib-resistant)
    cells showing an IC50 of imatinib 5-7 mu M were generated. In GIST-T1
    IR cells, KIT and its downstream signaling molecules remained
    phosphorylated with the presence of 1 mu M imatinib, and no new
    mutations were found in KIT, PDGFRA, PKC theta and JAK2. DNA
    micro-array analysis showed the overexpression of Cas-L in the
    resistant cells with 513 fold higher than that in the parental cells.
    Cas-L overexpression and SRC hyper-activation were also observed in the
    resistant cells at protein level and they were markedly decreased in
    KIT siRNA transfected GIST-T1 IR cells. Interestingly, GIST-T1 IR cells
    transfected with Cas-L siRNA turned out to become again sensitive to
    imatinib. Imatinib or PP1, a SRC inhibitor, alone was not enough to
    suppress the activation of KIT and its downstream signaling molecules,
    but the combination of them showed strong inhibitory effects on those
    in the resistant cells.
    We report for the first time that the mechanism of imatinib-resistant
    GISTs, at least in one cell line, involves KIT/Cas-L/SRC signaling.
    Cas-L depletion sensitized the resistant GIST-T1 IR cells to imatinib.
 C1 [Thao, Le Ba; Vu, Hoang Anh; Sato, Yuko] Res Inst Int Med Ctr Japan, Div Ultra Fine Struct, Dept Pathol, Shinjuku Ku, Tokyo 1628655, Japan.
    [Thao, Le Ba; Watanabe, Toshiki] Univ Tokyo, Inst Med Sci, Dept Med Genome Sci, Tokyo, Japan.
    [Yasuda, Kazuki; Taniguchi, Shigeki] Res Inst Int Med Ctr Japan, Dept Metab Disorder, Tokyo 1628655, Japan.
    [Yagasaki, Fumiharu] Saitama Med Sch, Dept Internal Med 1, Saitama, Japan.
    [Taguchi, Takahiro] Kochi Univ, Grad Sch Kuroshio Sci, Div Human Hlth & Med Sci, Nanko Ku, Kochi 780, Japan.
 RP Sato, Y, Res Inst Int Med Ctr Japan, Div Ultra Fine Struct, Dept
    Pathol, Shinjuku Ku, Toyama 1-21-1, Tokyo 1628655, Japan.
 EM ysato@ri.imcj.go.jp
 FU Japan Foundation for Promotion of International Medical Research
    Co-operation (JF-PIMRC) 
 FX This work was supported by The Japan Foundation for Promotion of
    International Medical Research Co-operation (JF-PIMRC). We are grateful
    to Ms. Kazuko Hamada for analyzing gene expression profile.
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 NR 29
 TC 1
 PU LANDES BIOSCIENCE
 PI AUSTIN
 PA 1002 WEST AVENUE, 2ND FLOOR, AUSTIN, TX 78701 USA
 SN 1538-4047
 J9 CANCER BIOL THER
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 PD APR 15
 PY 2009
 VL 8
 IS 8
 BP 683
 EP 688
 PG 6
 SC Oncology
 GA 463CJ
 UT ISI:000267405800015
 ER
 
 PT J
 AU Azhar, M
    Yin, M
    Bommireddy, R
    Duffy, JJ
    Yang, JQ
    Pawlowski, SA
    Boivin, GP
    Engle, SJ
    Sanford, LP
    Grisham, C
    Singh, RR
    Babcock, GF
    Doetschman, T
 AF Azhar, Mohamad
    Yin, Moying
    Bommireddy, Ramireddy
    Duffy, John J.
    Yang, Junqi
    Pawlowski, Sharon A.
    Boivin, Gregory P.
    Engle, Sandra J.
    Sanford, L. P.
    Grisham, Christina
    Singh, Ram R.
    Babcock, George F.
    Doetschman, Thomas
 TI Generation of Mice With a Conditional Allele for Transforming Growth
    Factor beta 1 Gene
 SO GENESIS
 LA English
 DT Article
 DE transforming growth factor beta; conditional knockout mice
 ID TGF-BETA; EXPRESSION PATTERNS; II RECEPTOR; IN-VIVO; TGF-BETA-1;
    GROWTH-FACTOR-BETA-1; CELLS; ACTIVATION; DIFFERENTIATION; LYMPHOCYTES
 AB Transforming growth factor beta 1 (TGF beta 1) is a multifunctional
    growth factor involved in wound healing, tissue fibrosis, and in the
    pathogenesis of many syndromic diseases (e.g., Marfan syndrome,
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    cardiovascular and immunological disorders, and cancer. Since the
    generation of Tgfb1 knockout mice, there has been extraordinary
    progress in understanding its physiological and pathophysiological
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    allele for Tgfb1 in which its exon 6 is flanked with LoxP sites. As
    proof of principle, we crossed these mice to LckCre transgenic mice and
    specifically disrupted Tgfb1 in T cells. The results indicate that
    T-cell-produced TGF beta 1 is required for normal in vivo regulation of
    peripheral T-cell activation, maintenance of T-cell homeostasis, and
    suppression of autoimmunity. genesis 47:423-431, 2009. (C) 2009
    Wiley-Liss, Inc.
 C1 [Azhar, Mohamad; Bommireddy, Ramireddy; Sanford, L. P.; Doetschman, Thomas] Univ Arizona, Inst BIO5, Tucson, AZ USA.
    [Azhar, Mohamad; Doetschman, Thomas] Univ Arizona, Dept Cell Biol, Tucson, AZ USA.
    [Yin, Moying; Duffy, John J.; Pawlowski, Sharon A.; Grisham, Christina] Univ Cincinnati, Dept Mol Genet, Cincinnati, OH USA.
    [Bommireddy, Ramireddy] Univ Arizona, Dept Immunobiol, Tucson, AZ USA.
    [Yang, Junqi] Univ Cincinnati, Dept Canc & Cell Biol, Cincinnati, OH USA.
    [Boivin, Gregory P.] Univ Cincinnati, Dept Pathol & Lab Med, Cincinnati, OH USA.
    [Engle, Sandra J.] Pfizer Inc, Groton, CT 06340 USA.
    [Singh, Ram R.] Univ Calif Los Angeles, David Geffen Sch Med, Los Angeles, CA 90095 USA.
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 RP Azhar, M, 1656 E Mabel St,POB 245217, Tucson, AZ 85724 USA.
 EM azharm@email.arizona.edu
    tdoetsch@u.arizona.edu
 FU National Institutes of Health [CA084291, AI067903]; Arizona Biomedical
    Research Commission [0901]; Steven M. Gootter Foundation ; BIO5
    Institute of the University of Arizona 
 FX Contract grant sponsor: National Institutes of Health Grant, Contract
    grant numbers: CA084291, AI067903; Contract grant sponsor: Arizona
    Biomedical Research Commission, Contract grant number ABRC #0901;
    Contract grant sponsors: Steven M. Gootter Foundation; BIO5 Institute
    of the University of Arizona
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 NR 31
 TC 2
 PU WILEY-LISS
 PI HOBOKEN
 PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA
 SN 1526-954X
 J9 GENESIS
 JI Genesis
 PD JUN
 PY 2009
 VL 47
 IS 6
 BP 423
 EP 431
 DI 10.1002/dvg.20516
 PG 9
 SC Developmental Biology; Genetics & Heredity
 GA 462KW
 UT ISI:000267352400009
 ER
 
 PT J
 AU Ren, FR
    Tanaka, H
    Yang, ZH
 AF Ren, Fengrong
    Tanaka, Hiroshi
    Yang, Ziheng
 TI A likelihood look at the supermatrix-supertree controversy
 SO GENE
 LA English
 DT Article
 DE Bayesian; Combined analysis; Likelihood; Likelihood supertree;
    Supermatrix; Supertree
 ID MAXIMUM-LIKELIHOOD; PHYLOGENETIC ANALYSIS; EVOLUTIONARY RATES; DATA
    SETS; SUBSTITUTION MODELS; MOLECULAR EVOLUTION; DNA-SEQUENCES; TREES;
    PHYLOGENOMICS; SITES
 AB Supermatrix and supertree methods are two strategies advocated for
    phylogenetic analysis of sequence data from multiple gene loci,
    especially when some species are missing at some loci. The supermatrix
    method concatenates sequences from multiple genes into a data
    supermatrix for phylogenetic analysis, and ignores differences in
    evolutionary dynamics among the genes. The supertree method analyzes
    each gene separately and assembles the subtrees estimated from
    individual genes into a supertree for all species. Most algorithms
    suggested for supertree construction lack statistical justifications
    and ignore uncertainties in the subtrees. instead of supermatrix or
    supertree, we advocate the use of likelihood function to combine data
    from multiple genes while accommodating their differences in the
    evolutionary process. This combines the strengths of the supermatrix
    and supertree methods while avoiding their drawbacks. We conduct
    computer simulation to evaluate the performance of the supermatrix,
    supertree, and maximum likelihood methods applied to two phylogenetic
    problems: molecular-clock dating of species divergences and
    reconstruction of species phylogenies. The results confirm the
    theoretical superiority of the likelihood method. Supertree or separate
    analyses of data of multiple genes may be useful in revealing the
    characteristics of the evolutionary process of multiple gene loci, and
    the information may be used to formulate realistic models for combined
    analysis of all genes by likelihood. (C) 2008 Elsevier B.V. All rights
    reserved.
 C1 [Yang, Ziheng] UCL, Dept Biol, London WC1E 6BT, England.
    [Ren, Fengrong; Tanaka, Hiroshi] Tokyo Med & Dent Univ, Ctr Informat Med, Tokyo, Japan.
    [Yang, Ziheng] Univ Tokyo, Grad Sch Agr & Life Sci, Tokyo, Japan.
 RP Yang, ZH, UCL, Dept Biol, Darwin Bldg,Gower St, London WC1E 6BT,
    England.
 EM z.yang@ucl.ac.uk
 FU Ministry of Education, Culture, Sports, and Technology of Japan ;
    Natural Environment Research Council 
 FX We thank David A. Morrison, Andrew Roger, and Ed Susko for comments.
    This study is supported by a Grant-in-Aid for Scientific Research from
    the Ministry of Education, Culture, Sports, and Technology of Japan to
    F.R. and H.T. and by a Natural Environment Research Council grant to
    Z.Y.
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 NR 63
 TC 7
 PU ELSEVIER SCIENCE BV
 PI AMSTERDAM
 PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
 SN 0378-1119
 J9 GENE
 JI Gene
 PD JUL 15
 PY 2009
 VL 441
 IS 1-2
 SI Sp. Iss. SI
 BP 119
 EP 125
 DI 10.1016/j.gene.2008.04.002
 PG 7
 SC Genetics & Heredity
 GA 460YP
 UT ISI:000267229600015
 ER
 
 PT J
 AU Watanabe, G
    Behrns, KE
    Kim, JS
    Kim, RD
 AF Watanabe, Go
    Behrns, Kevin E.
    Kim, Jae-Sung
    Kim, Robin D.
 TI Heat shock protein 90 inhibition abrogates hepatocellular cancer growth
    through cdc2-mediated G(2)/M cell cycle arrest and apoptosis
 SO CANCER CHEMOTHERAPY AND PHARMACOLOGY
 LA English
 DT Article
 DE Hepatocellular cancer; Hsp90; 17-AAG; Xenograft; cdc2
 ID SIGNAL-TRANSDUCTION; DOWN-REGULATION; MOLECULAR CHAPERONE; MITOTIC
    CATASTROPHE; GENE-EXPRESSION; HSP90 FUNCTION; BREAST-CANCER;
    LIVER-CANCER; CDC2; GELDANAMYCIN
 AB 17-(demethoxy), 17-allylamino geldanamycin (17-AAG) suppresses growth
    in some cancers by inhibiting Heat shock protein 90 (Hsp90). We
    examined the effects of 17-AAG-mediated Hsp90 inhibition on human
    hepatocellular carcinoma (HCC) growth in vitro and in vivo.
    Human HCC cell lines, Hep3B and HuH7, were exposed to 17-AAG and cell
    viabilities and apoptosis were determined. Cell cycle profiles were
    analyzed and the G(2)/M cell cycle checkpoint proteins cdc2 and cyclin
    B1 were examined. Studies were performed to determine whether
    17-AAG-mediated cdc2 decrease was due to altered gene expression,
    transcription, or protein degradation. The effects of 17-AAG on Hep3B
    and HuH7 xenograft growth in athymic nude mice were also examined.
    Hep3B and HuH7 treated with 17-AAG versus untreated controls showed
    decreased cell viability and increased apoptosis. Cells treated with
    17-AAG also showed an increased fraction in G(2)/M phase and an
    associated decrease in cdc2 through protein degradation rather than
    through other mechanisms. Hsp90 inhibition by 17-AAG also decreased HCC
    xenograft growth in association with decreased cdc2 expression.
    17-AAG-mediated inhibition of Hsp90 abrogates human HCC cell growth in
    vitro and in vivo through cdc2 decrease, which in turn induces G(2)/M
    cell cycle arrest and apoptosis. Hsp90 is a mediator of HCC growth and
    survival and its inhibition may serve as a potential treatment.
 C1 [Watanabe, Go; Behrns, Kevin E.; Kim, Jae-Sung; Kim, Robin D.] Univ Florida, Dept Surg, Coll Med, Gainesville, FL 32610 USA.
 RP Kim, RD, Univ Florida, Dept Surg, Coll Med, 1600 SW Archer Rd,Room
    6142, Gainesville, FL 32610 USA.
 EM robin.kim@surgery.ufl.edu
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 NR 50
 TC 5
 PU SPRINGER
 PI NEW YORK
 PA 233 SPRING ST, NEW YORK, NY 10013 USA
 SN 0344-5704
 J9 CANCER CHEMOTHER PHARMACOL
 JI Cancer Chemother. Pharmacol.
 PD JUL
 PY 2009
 VL 64
 IS 3
 BP 433
 EP 443
 DI 10.1007/s00280-008-0888-2
 PG 11
 SC Oncology; Pharmacology & Pharmacy
 GA 458QP
 UT ISI:000267038900001
 ER
 
 PT J
 AU Oku, H
    Li, CC
    Shimatani, M
    Iwasaki, H
    Toda, T
    Okabe, T
    Watanabe, H
 AF Oku, Hirosuke
    Li, Changchun
    Shimatani, Masayuki
    Iwasaki, Hironori
    Toda, Takayoshi
    Okabe, Takafumi
    Watanabe, Hisami
 TI Tumor specific cytotoxicity of beta-glucosylceramide:
    structure-cytotoxicity relationship and anti-tumor activity in vivo
 SO CANCER CHEMOTHERAPY AND PHARMACOLOGY
 LA English
 DT Article
 DE Glucosylceramide; Tumor selective; Cytotoxicity; Structure-activity
    relationship; Antitumor immunity
 ID KILLER T-CELLS; ALPHA-GALACTOSYLCERAMIDE; NKT CELLS; SPHINGOSINE
    KINASE; LIVER-INJURY; APOPTOSIS; MICE; SPHINGOLIPIDS; CERAMIDE;
    LYMPHOCYTES
 AB This study describes the structure-cytotoxicity relationship of
    beta-glucosylceramide (beta-GluCer) and its antitumor activity in vivo.
    Unglycosylated ceramide had no selective cytotoxicity which
    demonstrated that the sugar moiety plays a critical role for the
    expression of selective cytotoxicity by beta-GluCer.
    beta-Galactosylceramide also showed tumor specific cytotoxicity
    suggesting that the chemical structure of sugar group is not a factor
    for the selective toxicity. Similarly, unglycosylated ceramides of
    short acyl chain also selectively inhibited the growth of cancer cells.
    These findings in concert point to the importance of the hydrophilicity
    of the ceramide molecule rather than the chemical structure for the
    cyto-selectivity. Treatment of the cells with beta-GluCer increased the
    concentration of reactive oxygen species leading to cell cycle arrest
    and necrosis. Intraperitoneal administration of beta-GluCer
    significantly suppressed the growth of tumor implanted to the back of
    mice. beta-GluCer also induced antitumor immunity via the activation of
    NKT cells in vivo, and decreased the tumor metastasis of lymphoma
    cells. The present study thus demonstrated the antitumor activity of
    beta-GluCer in vivo, and discussed the mechanisms responsible for the
    growth inhibition.
 C1 [Oku, Hirosuke; Li, Changchun; Iwasaki, Hironori; Okabe, Takafumi; Watanabe, Hisami] Univ Ryukyus, Ctr Mol Biosci, Okinawa 9030213, Japan.
    [Shimatani, Masayuki] Univ Ryukyus, Grad Sch Agr, Okinawa 9030213, Japan.
    [Toda, Takayoshi] Univ Ryukyus Hosp, Sch Med, Dept Clin Lab Med, Okinawa 9030125, Japan.
 RP Oku, H, Univ Ryukyus, Ctr Mol Biosci, Okinawa 9030213, Japan.
 EM okuhiros@comb.u-ryukyu.ac.jp
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 NR 40
 TC 2
 PU SPRINGER
 PI NEW YORK
 PA 233 SPRING ST, NEW YORK, NY 10013 USA
 SN 0344-5704
 J9 CANCER CHEMOTHER PHARMACOL
 JI Cancer Chemother. Pharmacol.
 PD JUL
 PY 2009
 VL 64
 IS 3
 BP 485
 EP 496
 DI 10.1007/s00280-008-0896-2
 PG 12
 SC Oncology; Pharmacology & Pharmacy
 GA 458QP
 UT ISI:000267038900006
 ER
 
 PT J
 AU Yang, H
    Cheng, XP
    Li, JW
    Yao, Q
    Ju, G
 AF Yang, Hao
    Cheng, Xi-Ping
    Li, Jing-Wen
    Yao, Qin
    Ju, Gong
 TI De-differentiation Response of Cultured Astrocytes to Injury Induced by
    Scratch or Conditioned Culture Medium of Scratch-Insulted Astrocytes
 SO CELLULAR AND MOLECULAR NEUROBIOLOGY
 LA English
 DT Article
 DE Astrocyte; De-differentiation; Rat; Nestin; GFAP
 ID NEURAL STEM-CELLS; FIBROBLAST-GROWTH-FACTOR; TRAUMATIC BRAIN-INJURY;
    RAT SPINAL-CORD; RADIAL-GLIA; NERVOUS-SYSTEM; SUBVENTRICULAR ZONE;
    REACTIVE ASTROCYTES; PROGENITOR CELLS; MULLER CELLS
 AB Our previous reports indicated that astrocytes (ASTs) in injured adult
    rat spinal cord underwent a process of de-differentiation, and may
    acquire the potential of neural stem cells (NSCs). However, the AST
    de-differentiation and transitional rejuvenation process following
    injury is still largely unclear. The aim of the present study was to
    determine whether injured in vitro ASTs can re-enter the
    multipotential-like stem cell pool and regain NSC characteristics, and
    to further understand the mechanism of AST de-differentiation. We used
    an in vitro scratch-wound model to evoke astrocytic response to
    mechanical injury. GFAP and nestin double-labeled indirect
    immunofluorescence were carried out to characterize these scratched
    cells at various periods. Western-blot analysis was used to determine
    the changes of GFAP and nestin expression following injury.
    Furthermore, the rate of proliferation was determined by
    immunocytochemical detection of BrdU incorporating cells. These
    scratch-wound ASTs were cultured with stem cells medium to explore
    their ability to generate neurospheres and examine the self-renewal and
    multi-potency of such neurospheres. Moreover, scratched AST culture
    supernatant as conditioned cultured medium (ACM) was used to
    investigate if some diffusible factors derived from injured ASTs could
    induce de-differentiation of AST. The results showed: (1) the nestin
    positivity first appeared in GFAP-positive cells at the edge of the
    scratch, subsequently, disseminated into un-insulted zone. The
    expression of nestin in AST was increased with longer culture, while
    that of GFAP was decreased. Furthermore, these nestin-immunoreactive
    ASTs could generate neurospheres, which showed self-renewal and could
    be differentiated into neurons, ASTs and oligodendrocytes. (2)
    Scratched ASTs culture supernatant can induce astrocytic proliferation
    and de-differentiation. These results reveal that the in vitro injured
    ASTs can de-differentiate into nestin-positive stem/precursor cells,
    the process of de-differentiation may arise from direct injury or some
    diffusible factors released from injured ASTs.
 C1 [Yang, Hao; Cheng, Xi-Ping; Li, Jing-Wen; Yao, Qin; Ju, Gong] Fourth Mil Med Univ, Inst Neurosci, Xian 710032, Shaanxi, Peoples R China.
 RP Ju, G, Fourth Mil Med Univ, Inst Neurosci, Xian 710032, Shaanxi,
    Peoples R China.
 EM jugong@fmmu.edu.cn
 FU National Basic Research Program of China [2003CB515301]; Chinese PLA
    national scientific technological project [06G089]
 FX We thank Dr. Gautam Hebbar and Dr. Zhe Liang from Emory University for
    critical reading of the manuscript. This work was supported by the
    National Basic Research Program of China (2003CB515301) and Chinese PLA
    national scientific technological project (06G089).
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 NR 53
 TC 4
 PU SPRINGER/PLENUM PUBLISHERS
 PI NEW YORK
 PA 233 SPRING ST, NEW YORK, NY 10013 USA
 SN 0272-4340
 J9 CELL MOL NEUROBIOL
 JI Cell. Mol. Neurobiol.
 PD JUN
 PY 2009
 VL 29
 IS 4
 BP 455
 EP 473
 DI 10.1007/s10571-008-9337-3
 PG 19
 SC Cell Biology; Neurosciences
 GA 457IH
 UT ISI:000266921200005
 ER
 
 PT J
 AU Yang, XF
    Yang, Y
    Luo, YG
    Li, G
    Wang, JZ
    Yang, ES
 AF Yang, Xifei
    Yang, Ying
    Luo, Yougen
    Li, Geng
    Wang, Jianzhi
    Yang, Edward S.
 TI Hyperphosphorylation and Accumulation of Neurofilament Proteins in
    Transgenic Mice with Alzheimer Presenilin 1 Mutation
 SO CELLULAR AND MOLECULAR NEUROBIOLOGY
 LA English
 DT Article
 DE Neurofilaments; Hyperphosphorylation; JNK; Presenilin-1; Alzheimer's
    disease
 ID PAIRED HELICAL FILAMENTS; AMYOTROPHIC-LATERAL-SCLEROSIS;
    AXONAL-TRANSPORT; IN-VIVO; PHOSPHORYLATION; DISEASE; TAU; APOPTOSIS;
    NEURONS; GENE
 AB Neurofilaments (NFs) are hyperphosphorylated and accumulate in
    Alzheimer's disease (AD) brains. In this study, employing the
    transgenic mouse model, we explored the effect of presenilin 1 (PS-1)
    mutation on the phosphorylation and distribution of NFs. Western blot
    analysis showed that there was a significant increase in the
    phosphorylation of NF-H and NF-M subunits with a concomitant increase
    in phosphorylated c-Jun N-terminal protein kinase 1/2 (JNK1/2)
    mitogen-activated protein kinase (MAPK) in hippocampus of PS-1
    transgenic mice compared to that of wild-type littermates.
    Immunohistochemical analysis revealed that phosphorylated NFs
    accumulated throughout the hippocampal neurons of the transgenic mice.
    These findings suggest that PS-1 mutation may induce
    hyperphosphorylation and accumulation of NFs via a JNK1/2-involved
    mechanism.
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    [Yang, Xifei; Yang, Ying; Luo, Yougen; Wang, Jianzhi] Huazhong Univ Sci & Technol, Dept Pathophysiol, Inst Neurosci, Tongji Med Coll, Wuhan 430074, Peoples R China.
 RP Li, G, Hong Kong Appl Sci & Technol Res Inst Co Ltd, Hong Kong, Hong
    Kong, Peoples R China.
 EM ligenggeng@gmail.com
 FU National Natural Science Foundation of China [30700277]
 FX This study was supported by a grant from National Natural Science
    Foundation of China (30700277).
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 NR 25
 TC 2
 PU SPRINGER/PLENUM PUBLISHERS
 PI NEW YORK
 PA 233 SPRING ST, NEW YORK, NY 10013 USA
 SN 0272-4340
 J9 CELL MOL NEUROBIOL
 JI Cell. Mol. Neurobiol.
 PD JUN
 PY 2009
 VL 29
 IS 4
 BP 497
 EP 501
 DI 10.1007/s10571-008-9341-7
 PG 5
 SC Cell Biology; Neurosciences
 GA 457IH
 UT ISI:000266921200008
 ER
 
 PT J
 AU Yu, KM
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    Zhu, JQ
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    Yang, WX
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    Zhu, Jun-Quan
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    Yang, Wan-Xi
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    sinensis
 SO CELL AND TISSUE RESEARCH
 LA English
 DT Article
 DE Spermatogenesis; Acrosome; KIFC1; Chinese mitten crab; Eriocheir
    sinensis (Crustacea)
 ID KINESIN SUPERFAMILY PROTEINS; EPIDIDYMAL MATURATION; MAMMALIAN
    SPERMATOGENESIS; INTRACELLULAR-TRANSPORT; CANDIDATE MOTORS; GERM-CELLS;
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    spermatogenesis in E. sinensis, KIFC1 probably plays important roles in
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    be essential for the eversion of the acrosome during fertilization.
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    [Zhu, Jun-Quan] Ningbo Univ, Fac Life Sci & Biotechnol, Ningbo 315211, Zhejiang, Peoples R China.
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 RP Yang, WX, Zhejiang Univ, Coll Life Sci, Inst Cell Biol & Genet, Sperm
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 EM wxyang@spermlab.org
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 TC 6
 PU SPRINGER
 PI NEW YORK
 PA 233 SPRING ST, NEW YORK, NY 10013 USA
 SN 0302-766X
 J9 CELL TISSUE RES
 JI Cell Tissue Res.
 PD JUL
 PY 2009
 VL 337
 IS 1
 BP 113
 EP 123
 DI 10.1007/s00441-009-0800-3
 PG 11
 SC Cell Biology
 GA 457EC
 UT ISI:000266910300010
 ER
 
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 AF Kim, Dohoon
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    Kim, Kwang-Soo
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 LA English
 DT Article
 ID HUMAN IMMUNODEFICIENCY VIRUS; HUMAN SOMATIC-CELLS; PARKINSONS-DISEASE;
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 RP Lanza, R, Stern Cell & Regenerat Med Int, 381 Plantat St, Worcester, MA
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 EM rlanza@advancedcell.com
    kskim@mclean.harvard.edu
 FU National Institutes of Health (NIH) [MH48866, DC 006501]; CHA
    University ; Korean Stem Cell Research Center ; Dongyang Corporation
    Co. in Korea 
 FX This work was supported by National Institutes of Health (NIH) grants
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    advisor for Stem Cell and Regenerative Medicine International. K.Y.C.
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 NR 30
 TC 221
 PU CELL PRESS
 PI CAMBRIDGE
 PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
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 J9 CELL STEM CELL
 JI Cell Stem Cell
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 PY 2009
 VL 4
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 BP 472
 EP 476
 DI 10.1016/j.stem.2009.05.005
 PG 5
 SC Cell & Tissue Engineering; Cell Biology
 GA 455UY
 UT ISI:000266793600005
 ER
 
 PT J
 AU Tobinai, K
    Watanabe, T
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    Maruyama, D
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 AF Tobinai, Kensei
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    Ohashi, Yasuo
 TI Phase I/II and pharmacokinetic study of cladribine with 2-h infusion in
    Japanese patients with relapsed indolent B-cell lymphoma mostly
    pretreated with rituximab
 SO CANCER SCIENCE
 LA English
 DT Article
 ID NON-HODGKINS-LYMPHOMA; CHRONIC LYMPHOCYTIC-LEUKEMIA; PREVIOUSLY TREATED
    PATIENTS; ADVANCED LOW-GRADE; 2-CHLORODEOXYADENOSINE CLADRIBINE;
    FOLLICULAR LYMPHOMA; INTRAVENOUS-INFUSION; RESPONSE CRITERIA;
    COMBINATION; CYCLOPHOSPHAMIDE
 AB We conducted a phase I/II study to investigate the toxicity,
    pharmacokinetics, and efficacy profiles of cladribine with 2-h
    intravenous infusion for five consecutive days every four weeks in
    Japanese patients with relapsed indolent B-cell lymphoma. This was a
    dose-escalation study to confirm the safety of the doses which have
    been recommended for Caucasian patients (phase I), and to further
    evaluate the efficacy and safety (phase II). In the phase I portion for
    nine patients, no dose-limiting toxicities were observed at levels 1
    (0.09 mg/kg/day, n = 3) and 2 (0.12 mg/kg/day, n = 6). No appreciable
    accumulation of plasma cladribine concentration was suggested. We
    enrolled a total of 20 patients, and an additional 14 patients in the
    phase II portion at level 2 (0.12 mg/kg/day). Eighteen patients,
    including 13 with follicular lymphoma, were eligible for efficacy
    evaluation, and 15 (83%) were pretreated with rituximab. The overall
    response rate was 50% (9/18; 80% confidence interval, 35-65%), with 11%
    (2/18) complete response. With a median follow-up of 296 days, the
    estimated median time to progression for 18 eligible patients was 382
    days. The most frequent adverse events were hematologic toxicities,
    including grade 4 neutropenia. Non-hematologic toxicities were mild. In
    conclusion, cladribine with 2-h intravenous infusion for five
    consecutive days every four weeks is effective with acceptable
    toxicities for Japanese patients with relapsed indolent B-cell
    lymphoma, including those pretreated with rituximab. (Cancer Sci 2009;
    100: 1344-1350)
 C1 [Tobinai, Kensei; Watanabe, Takashi; Tanimoto, Kazuki; Maruyama, Dai] Natl Canc Ctr, Hematol & Stem Cell Transplantat Div, Chuo Ku, Tokyo 1040045, Japan.
    [Matsuno, Yoshihiro] Natl Canc Ctr, Clin Lab Div, Chuo Ku, Tokyo 1040045, Japan.
    [Nakata, Masanobu; Itoh, Kuniaki] Natl Canc Ctr Hosp E, Div Hematol & Oncol, Kashiwa, Chiba 2778577, Japan.
    [Nawano, Shigeru] Natl Canc Ctr Hosp E, Diagnost Radiol Div, Kashiwa, Chiba 2778577, Japan.
    [Morishima, Yasuo; Ogura, Michinori] Aichi Canc Ctr Hosp, Dept Hematol & Cell Therapy, Chikusa Ku, Nagoya, Aichi 4648681, Japan.
    [Usui, Noriko] Jikei Univ, Sch Med, Dept Internal Med, Div Hematol & Oncol, Tokyo 1058471, Japan.
    [Kasai, Masaharu] Sapporo Hokuyu Hosp, Dept Internal Med, Shiroishi Ku, Sapporo, Hokkaido 0030006, Japan.
    [Terauchi, Takashi] Natl Canc Ctr, Res Ctr Canc Prevent & Screening, Screening Technol & Dev Div, Chuo Ku, Tokyo 1040045, Japan.
    [Matsusako, Masaki] St Lukes Int Hosp, Dept Radiol, Chuo Ku, Tokyo 1048560, Japan.
    [Nakamura, Shigeo] Nagoya Univ Hosp, Pathol & Clin Labs, Showa Ku, Nagoya, Aichi 4668560, Japan.
    [Mori, Shigeo] Teikyo Univ, Sch Med, Dept Pathol, Itabashi Ku, Tokyo 1738606, Japan.
    [Ohashi, Yasuo] Univ Tokyo, Sch Publ Hlth, Dept Biostat, Bunkyo Ku, Tokyo 1138655, Japan.
 RP Tobinai, K, Natl Canc Ctr, Hematol & Stem Cell Transplantat Div, Chuo
    Ku, 5-1-1 Tsukiji, Tokyo 1040045, Japan.
 EM ktobinai@ncc.go.jp
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 NR 37
 TC 3
 PU WILEY-BLACKWELL PUBLISHING, INC
 PI MALDEN
 PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
 SN 1347-9032
 J9 CANCER SCI
 JI Cancer Sci.
 PD JUL
 PY 2009
 VL 100
 IS 7
 BP 1344
 EP 1350
 DI 10.1111/j.1349-7006.2009.01162.x
 PG 7
 SC Oncology
 GA 458AL
 UT ISI:000266982000028
 ER
 
 PT J
 AU Yamada, H
    Takano, T
    Ito, Y
    Matsuzuka, F
    Miya, A
    Kobayashi, K
    Yoshida, H
    Watanabe, M
    Iwatani, Y
    Miyauchi, A
 AF Yamada, Hiroya
    Takano, Toru
    Ito, Yasuhiro
    Matsuzuka, Fumio
    Miya, Akihiro
    Kobayashi, Kaoru
    Yoshida, Hiroshi
    Watanabe, Mikio
    Iwatani, Yoshinori
    Miyauchi, Akira
 TI Expression of nestin mRNA is a differentiation marker in thyroid tumors
 SO CANCER LETTERS
 LA English
 DT Article
 DE Nestin; Cancer stem cell; Anaplastic thyroid carcinoma; Thyroid
    transcription factor-1; Gene expression
 ID INTERMEDIATE-FILAMENT NESTIN; FETAL CELL CARCINOGENESIS; QUANTITATIVE
    MEASUREMENT; ANAPLASTIC CARCINOMA; STEM-CELLS; TRANSCRIPTION; CANCER;
    THYROGLOBULIN; HYPOTHESIS; PAPILLARY
 AB Nestin is a maker that identifies stem cells in some adult tissues, and
    its expression is believed to relate to malignancy in cancer cells. In
    this study, we measured the expression levels of nestin mRNA in various
    kinds of thyroid tumor by the real-time quantitative reverse
    transcription-polymerase chain reaction. Unexpectedly, nestin mRNA was
    detected in almost all differentiated thyroid tumors and normal thyroid
    tissues, whereas extremely decreased expression was observed in
    anaplastic carcinomas, which are the most malignant of the thyroid
    follicular cell-derived tumors. These results suggest that nestin mRNA
    is a differentiation marker, and its expression does not relate to
    malignant characteristics in thyroid tumors. (C) 2009 Elsevier Ireland
    Ltd. All rights reserved.
 C1 [Yamada, Hiroya; Takano, Toru] Osaka Univ, Sch Med, Dept Lab Med, Osaka 5650871, Japan.
    [Yamada, Hiroya; Watanabe, Mikio; Iwatani, Yoshinori] Osaka Univ, Grad Sch Med, Div Hlth Sci, Osaka 5650871, Japan.
    [Ito, Yasuhiro; Matsuzuka, Fumio; Miya, Akihiro; Kobayashi, Kaoru; Yoshida, Hiroshi; Miyauchi, Akira] Kuma Hosp, Chuo Ku, Kobe, Hyogo 6500011, Japan.
 RP Takano, T, Osaka Univ, Sch Med, Dept Lab Med, 2-2 D2, Osaka 5650871,
    Japan.
 EM ttakano@labo.med.osaka-u.ac.jp
 FU Ministry of Education, Culture, Sports, Science and Technology of Japan
    [20590570]; Princess Takamatsu Cancer Research Fund [04-23606]
 FX This research was supported by the Ministry of Education, Culture,
    Sports, Science and Technology of Japan, a Grant-in-Aid for Scientific
    Research C, 2008-2010, No.20590570, and a Research Grant of the
    Princess Takamatsu Cancer Research Fund 04-23606 of Japan.
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 NR 24
 TC 5
 PU ELSEVIER IRELAND LTD
 PI CLARE
 PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
    IRELAND
 SN 0304-3835
 J9 CANCER LETT
 JI Cancer Lett.
 PD JUL 18
 PY 2009
 VL 280
 IS 1
 BP 61
 EP 64
 DI 10.1016/j.canlet.2009.02.006
 PG 4
 SC Oncology
 GA 458GM
 UT ISI:000267003500007
 ER
 
 PT J
 AU Yang, WS
    Tsai, TJ
    Shih, CL
    Huang, JW
    Chuang, HF
    Chen, MH
    Fang, CC
 AF Yang, Wei-Shun
    Tsai, Tun-Jun
    Shih, Chung-Liang
    Huang, Jenq-Wen
    Chuang, Hsueh-Fang
    Chen, Meng-Han
    Fang, Cheng-Chung
 TI Intraperitoneal Vascular Endothelial Growth Factor C Level Is Related
    to Peritoneal Dialysis Ultrafiltration
 SO BLOOD PURIFICATION
 LA English
 DT Article
 DE Interleukin-6; Peritoneal dialysis; Ultrafiltration; Vascular
    endothelial growth factor-C
 ID RESIDUAL RENAL-FUNCTION; ARTERIAL STIFFNESS; MESOTHELIAL CELLS;
    TRANSPORT RATE; EXPRESSION; VEGF; INFLAMMATION; ANGIOGENESIS;
    ASSOCIATION; PREDICTOR
 AB Background: Local inflammation and neovascularization have a negative
    influence on peritoneal dialysis (PD). Patients with higher peritoneal
    transport have higher interleukin-6 (IL-6) and vascular endothelial
    growth factor-A (VEGF-A) levels in their dialysate. However, the
    relationship of other members of the VEGF family, such as VEGF-C, to
    peritoneal transport or ultrafiltration (UF) is yet to be studied.
    Methods: Peritoneal cytokine and growth factor levels were determined
    during the peritoneal equilibration test (PET). Ultrafiltration,
    peritoneal clearance and residual renal function were also considered.
    Results: Forty-two PD patients were enrolled. They had been on PD for
    at least 1 month and free of peritonitis for at least 1 month prior to
    the study. Patients with high or high average PET had higher dialysate
    IL-6 and VEGF-C. Dialysate IL-6 and VEGF-C correlated negatively with
    PET and UF. Conclusions: Dialysate VEGF-C is related to higher
    transport rate and poorer UF. The role of VEGF-C in PD deserves further
    study. Copyright (C) 2009 S. Karger AG, Basel
 C1 [Shih, Chung-Liang; Fang, Cheng-Chung] Natl Taiwan Univ Hosp, Dept Emergency Med, Taipei 100, Taiwan.
    [Chuang, Hsueh-Fang; Chen, Meng-Han] Natl Taiwan Univ Hosp, Dept Nursing, Taipei 100, Taiwan.
    [Tsai, Tun-Jun; Huang, Jenq-Wen] Natl Taiwan Univ Hosp, Dept Internal Med, Taipei 100, Taiwan.
    [Yang, Wei-Shun] Tao Yuan Gen Hosp, Dept Internal Med, Tao Yuan, Taiwan.
 RP Fang, CC, Natl Taiwan Univ Hosp, Dept Emergency Med, 7 Chung Shan S Rd,
    Taipei 100, Taiwan.
 EM conrad@ntu.edu.tw
 FU Tao-Yuan General Hospital Study Found ; Ta-Tung Kidney Foundation ;
    Mrs. Hsiu-Chin Lee Kidney Research Fund. ; Department of Medical
    Research of the National Taiwan University Hospital 
 FX This study was supported by the Tao-Yuan General Hospital Study Found,
    Ta-Tung Kidney Foundation and the Mrs. Hsiu-Chin Lee Kidney Research
    Fund. This work was also supported in part by the Department of Medical
    Research of the National Taiwan University Hospital. The authors wish
    to thank Prof. Wan-Yu Chen, Ms. Shu-Li Hung and Ms. Yuan-Ting Chuang,
    Department of Internal Medicine, National Taiwan University Hospital,
    for their kind assistance.
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 NR 25
 TC 0
 PU KARGER
 PI BASEL
 PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND
 SN 0253-5068
 J9 BLOOD PURIFICAT
 JI Blood Purif.
 PY 2009
 VL 28
 IS 1
 BP 69
 EP 74
 DI 10.1159/000218008
 PG 6
 SC Hematology; Urology & Nephrology
 GA 456WP
 UT ISI:000266883100012
 ER
 
 PT J
 AU Yee, LJ
    Im, K
    Borg, B
    Yang, H
    Liang, TJ
 AF Yee, L. J.
    Im, K.
    Borg, B.
    Yang, H.
    Liang, T. J.
 CA Virahep C Study
 TI Interleukin-6 haplotypes and the response to therapy of chronic
    hepatitis C virus infection
 SO GENES AND IMMUNITY
 LA English
 DT Article
 DE hepatitis C; race; therapy; response; African American
 ID PEGINTERFERON ALPHA-2B; AMERICAN PATIENTS; RIBAVIRIN; ASSOCIATION;
    POLYMORPHISMS; GENOTYPE-1; GENE
 AB Chronic hepatitis C virus (HCV) infection affects nearly 170 million
    individuals worldwide. Treatment of HCV with pegylated
    interferon-alpha-2a is successful in eradicating virus from only 30 to
    80% of those treated. Interleukin-6 (IL-6) is an important cytokine
    involved in the immune response to infectious agents and in vitro
    studies suggest that host genetic variation, particularly haplotypes,
    may affect IL-6 expression. We examined the contribution of haplotypes
    in the IL-6 gene on sustained viral response (SVR) to the therapy for
    chronic HCV infection. We observed the IL-6 T-T-G-G-G-G-C-A-G-A
    haplotype to be associated with a lower risk of achieving SVR among
    Caucasian Americans (CAs) ((relative risk) RR = 0.80; 95% CI:
    0.66-0.98; P = 0.0261). Using a sliding window approach, the
    rs1800797-(G)-rs1800796-(G)-rs1800795-( G) haplotype was associated
    with a reduced chance of SVR (RR = 0.79; 95% CI: 0.66-0.94; P =
    0.0081), as was the rs1800796-(G)-rs1800795-(G)-rs2069830-(C) haplotype
    (RR = 0.78; 95% CI: 0.66-0.94; P = 0.0065) among CAs. Overall, the
    rs1800797-(G)-rs1800796(G)-rs1800795-(G) haplotype was independently
    associated with a reduced chance of SVR (RR 0.78; 95% CI: 0.62-1.0; P =
    0.0489) after adjustment for potential confounding factors. Our
    findings further illustrate the complexity of IL-6 genetic regulation
    and the potential importance of haplotypes on IL-6 expression. Our
    findings provide additional support for the potential importance of
    genetic variation in the IL-6 gene and the response to HCV therapy.
    Genes and Immunity (2009) 10, 365-372; doi:10.1038/gene.2009.26;
    published online 23 April 2009
 C1 [Yee, L. J.; Im, K.] Univ Pittsburgh, Dept Epidemiol, Pittsburgh, PA 15261 USA.
    [Im, K.] Univ Pittsburgh, Dept Biostat, Pittsburgh, PA 15261 USA.
    [Borg, B.; Liang, T. J.] NIDDK, Liver Dis Branch, NIH, Bethesda, MD USA.
    [Yang, H.] Cedars Sinai Med Ctr, Inst Med Genet, Los Angeles, CA 90048 USA.
 RP Yee, LJ, Univ Pittsburgh, Dept Epidemiol, A511 Crabtree Hall,
    Pittsburgh, PA 15261 USA.
 EM YeeL@edc.pitt.edu
    JakeL@bdg10.niddk.nih.gov
 FU National Center on Minority Health and Health Disparities (NCMHD) [U01
    DK60329, U01 DK60340, U01 DK60324, U01 DK60344, U01 DK60327, U01
    DK60335, U01 DK60352, U01 DK60342, U01 DK60345, U01 DK60309, U01
    DK60346, U01 DK60349, U01 DK60341]; NIDDKNational Center for Research
    Resources (NCRR) ; NIH ; Center for Cancer Research ; New York
    Presbyterian [M01 RR00645]; University of California, San Francisco
    [M02 RR000079]; University of Maryland [M01 RR16500]; University of
    Michigan [M01 RR000042]; University of North Carolina [M01 RR00046];
    National Institutes of Health Clinical Research Career Development
    [1KL2 RR024154-02]
 FX This clinical study was a co-operative agreement funded by the NIDDK
    and co-funded by the National Center on Minority Health and Health
    Disparities (NCMHD), with a Co-operative Research and Development
    Agreement (CRADA) with Roche Laboratories Inc., Grant numbers: U01
    DK60329, U01 DK60340, U01 DK60324, U01 DK60344, U01 DK60327, U01
    DK60335, U01 DK60352, U01 DK60342, U01 DK60345, U01 DK60309, U01
    DK60346, U01 DK60349 and U01 DK60341. Other support: National Center
    for Research Resources (NCRR), Intramural Research Program of the NIH,
    NIDDK, Center for Cancer Research, General Clinical Research Centers
    Program Grants: M01 RR00645 (New York Presbyterian), M02 RR000079
    (University of California, San Francisco), M01 RR16500 (University of
    Maryland), M01 RR000042 (University of Michigan) and M01 RR00046
    (University of North Carolina). In addition support for Dr Leland J Yee
    was provided by a National Institutes of Health Clinical Research
    Career Development Award Grant (1KL2 RR024154-02).
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 NR 18
 TC 3
 PU NATURE PUBLISHING GROUP
 PI LONDON
 PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
 SN 1466-4879
 J9 GENES IMMUN
 JI Genes Immun.
 PD JUN
 PY 2009
 VL 10
 IS 4
 BP 365
 EP 372
 DI 10.1038/gene.2009.26
 PG 8
 SC Genetics & Heredity; Immunology
 GA 452UO
 UT ISI:000266566900009
 ER
 
 PT J
 AU Xu, HM
    Wang, WC
    Li, CL
    Yu, HY
    Yang, AC
    Wang, BB
    Jin, Y
 AF Xu, Huiming
    Wang, Weicheng
    Li, Chunliang
    Yu, Hongyao
    Yang, Acong
    Wang, Beibei
    Jin, Ying
 TI WWP2 promotes degradation of transcription factor OCT4 in human
    embryonic stem cells
 SO CELL RESEARCH
 LA English
 DT Article
 DE transcription factor OCT4; WWP2; protein degradation; embryonic stem
    cells
 ID DOMAIN-CONTAINING PROTEINS; UBIQUITIN LIGASE; HUMAN BLASTOCYSTS; RNA
    INTERFERENCE; MAMMALIAN EMBRYO; GENE-EXPRESSION; DIFFERENTIATION;
    IDENTIFICATION; UBIQUITYLATION; PLURIPOTENCY
 AB POU transcription factor OCT4 not only plays an essential role in
    maintaining the pluripotent and self-renewing state of embryonic stem
    (ES) cells but also acts as a cell fate determinant through a gene
    dosage effect. However, the molecular mechanisms that control the
    intracellular OCT4 protein level remain elusive. Here, we report that
    human WWP2, an E3 ubiquitin (Ub)-protein ligase, interacts with OCT4
    specifically through its WW domain and enhances Ub modification of OCT4
    both in vitro and in vivo. We first demonstrated that endogenous OCT4
    in human ES cells can be post-translationally modified by Ub.
    Furthermore, we found that WWP2 promoted degradation of OCT4 through
    the 26S proteasome in a dosage-dependent manner, and the active site
    cysteine residue of WWP2 was required for both its enzymatic activity
    and proteolytic effect on OCT4. Remarkably, our data show that the
    endogenous OCT4 protein level was significantly elevated when WWP2
    expression was downregulated by specific RNA interference (RNAi),
    suggesting that WWP2 is an important regulator for maintaining a proper
    OCT4 protein level in human ES cells. Moreover, northern blot analysis
    showed that the WWP2 transcript was widely present in diverse human
    tissues/organs and highly expressed in undifferentiated human ES cells.
    However, its expression level was quickly decreased after human ES
    cells differentiated, indicating that WWP2 expression might be
    developmentally regulated. Our findings demonstrate that WWP2 is an
    important regulator of the OCT4 protein level in human ES cells.
 C1 [Xu, Huiming; Wang, Weicheng; Yang, Acong; Jin, Ying] Shanghai Jiao Tong Univ, Sch Med, Shanghai Stem Cell Inst, Shanghai 200025, Peoples R China.
    [Xu, Huiming; Wang, Weicheng; Li, Chunliang; Yu, Hongyao; Yang, Acong; Wang, Beibei; Jin, Ying] Chinese Acad Sci, Shanghai Jiao Tong Univ, Sch Med,Shanghai Inst Biol Sci, Key Lab Stem Cell Biol,Inst Hlth Sci, Shanghai 200031, Peoples R China.
    [Jin, Ying] Shanghai Jiao Tong Univ, Sch Med, Chinese Minist Educ, Key Lab Cell Differentiat & Apoptosis, Shanghai 200025, Peoples R China.
 RP Jin, Y, Shanghai Jiao Tong Univ, Sch Med, Shanghai Stem Cell Inst, 225
    S Chongqing Rd, Shanghai 200025, Peoples R China.
 EM yjin@sibs.ac.cn
 FU National High Technology Research and Development Program of China
    [2006CB943900]; National Natural Science Foundation of China
    [30500088]; Shanghai Jiao Tong University School of Medicine ; Shanghai
    Institutes for Biological Sciences, Chinese Academy of Sciences ;
    Shanghai Leading Academic Deciline [S30201]
 FX We are grateful to Dr DA Melton (Harvard University) for sharing his
    human ES cells with us. The study was supported by grants from the
    National High Technology Research and Development Program of China
    (2006CB943900), the National Natural Science Foundation of China
    (General Program, 30500088), the Shanghai Jiao Tong University School
    of Medicine, and the Shanghai Institutes for Biological Sciences,
    Chinese Academy of Sciences. The study was also supported by the
    Shanghai Leading Academic Deciline Project (S30201).
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 NR 45
 TC 5
 PU NATURE PUBLISHING GROUP
 PI NEW YORK
 PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
 SN 1001-0602
 J9 CELL RES
 JI Cell Res.
 PD MAY
 PY 2009
 VL 19
 IS 5
 BP 561
 EP 573
 DI 10.1038/cr.2009.31
 PG 13
 SC Cell Biology
 GA 452GG
 UT ISI:000266527600006
 ER
 
 PT J
 AU Wang, LP
    Yin, HF
    Qian, Q
    Yang, J
    Huang, CF
    Hu, XH
    Luo, D
 AF Wang, Liping
    Yin, Hengfu
    Qian, Qian
    Yang, Jun
    Huang, Chaofeng
    Hu, Xiaohe
    Luo, Da
 TI NECK LEAF 1, a GATA type transcription factor, modulates organogenesis
    by regulating the expression of multiple regulatory genes during
    reproductive development in rice
 SO CELL RESEARCH
 LA English
 DT Article
 DE elongation of upper internodes; organogenesis; panicle development;
    phase transition; NECK LEAF 1; GATA-like transcription factor
 ID PHASE-CHANGE; CYTOCHROME-P450 MONOOXYGENASE; INTERNODE ELONGATION;
    PLANT ARCHITECTURE; FLOWER DEVELOPMENT; LEAF INITIATION; ARABIDOPSIS;
    MUTANT; PLASTOCHRON1; HOMOLOG
 AB In the monocot rice species Oryza sativa L., one of the most striking
    morphological processes during reproductive development is the
    concurrence of panicle development with the sequential elongation of
    upper internodes (UPIs). To elucidate the underlying molecular
    mechanisms, we cloned the rice gene NECK LEAF 1 (NL1), which when
    mutated results in delays in flowering time, smaller panicles with
    overgrown bracts and abnormal UPI elongation patterns. The NL1 gene
    encodes a GATA-type transcription factor with a single zinc finger
    domain, and its transcripts are detected predominantly in the bract
    primordia, which normally degenerate in the wild-type plants.
    Overexpression of NL1 in transgenic plants often gives rise to severe
    growth retardation, less vegetative phytomers and smaller leaves,
    suggesting that NL1 plays an important role in organ differentiation. A
    novel mutant allele of PLASTOCHRON1 (PLA1), a gene known to play a key
    role in regulating leaf initiation, was identified in this study.
    Genetic analysis demonstrated an interaction between nl1 and pla1, with
    NL1 acting upstream of PLA1. The expression level and spatial pattern
    of PLA1 were found to be altered in the nl1 mutant. Furthermore, the
    expression of two regulators of flowering, Hd3a and OsMADS1, was also
    affected in the nl1 mutant. On the basis of these findings, we propose
    that NL1 is an intrinsic factor that modulates and coordinates
    organogenesis through regulating the expression of PLA1 and other
    regulatory genes during reproductive development in rice.
 C1 [Wang, Liping; Yin, Hengfu; Yang, Jun; Huang, Chaofeng; Hu, Xiaohe; Luo, Da] Chinese Acad Sci, Grad Sch, Natl Key Lab Plant Mol Genet, Inst Plant Physiol & Ecol,Shanghai Inst Biol Sci, Shanghai 200032, Peoples R China.
    [Qian, Qian] Chinese Acad Agr Sci, China Natl Rice Res Inst, Hangzhou 310006, Zhejiang, Peoples R China.
 RP Luo, D, Chinese Acad Sci, Grad Sch, Natl Key Lab Plant Mol Genet, Inst
    Plant Physiol & Ecol,Shanghai Inst Biol Sci, Shanghai 200032, Peoples R
    China.
 EM dluo@sibs.ac.cn
 FU Ministry of Science and Technology of China [2006AA10A102]
 FX We thank Dr Hongxuan Lin at the Institute of Plant Physiology and
    Ecology for the kind support on NL1 mapping. We are grateful to Shuping
    Xu (Institute of Plant Physiology and Ecology, Chinese Academy of
    Sciences) and Meixian Yan (China National Rice Research Institute) for
    the help of transgenic work, and we acknowledge financial support of
    National High-Tech Projects from the Ministry of Science and Technology
    of China (grant number: 2006AA10A102).
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 NR 37
 TC 4
 PU NATURE PUBLISHING GROUP
 PI NEW YORK
 PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
 SN 1001-0602
 J9 CELL RES
 JI Cell Res.
 PD MAY
 PY 2009
 VL 19
 IS 5
 BP 598
 EP 611
 DI 10.1038/cr.2009.36
 PG 14
 SC Cell Biology
 GA 452GG
 UT ISI:000266527600009
 ER
 
 PT J
 AU Li, XQ
    Yang, XM
    Xu, YL
    Jiang, XJ
    Li, X
    Nan, FJ
    Tang, H
 AF Li, Xiaoqi
    Yang, Xuanming
    Xu, Youli
    Jiang, Xuejun
    Li, Xin
    Nan, Fajun
    Tang, Hong
 TI Troglitazone inhibits cell proliferation by attenuation of epidermal
    growth factor receptor signaling independent of peroxisome
    proliferator-activated receptor gamma
 SO CELL RESEARCH
 LA English
 DT Article
 DE EGFR; PPAR gamma; troglitazone; endocytosis; growth arrest
 ID BREAST-CANCER CELLS; PPAR-GAMMA; ENDOTHELIAL-CELLS; PROTEIN-KINASE;
    IN-VITRO; PROSTATE-CANCER; LUNG-CANCER; APOPTOSIS; ENDOCYTOSIS; LIGAND
 AB Peroxisome proliferator-activated receptors (PPAR) belong to the
    nuclear hormone receptor superfamily of ligand-dependent transcription
    factors. Recent results have shown that agonists of PPAR gamma, such as
    troglitazone (TGZ), can inhibit cell proliferation and promote cell
    differentiation independent of PPAR gamma. In the present study, we
    provide evidence that TGZ may bind directly to EGFR and trigger its
    signaling and internalization independent of PPAR gamma. Detailed
    studies revealed that prolonged incubation with TGZ effectively
    attenuated EGFR signaling by targeting the receptor to the
    endo-lysosomal degradation machinery. Although the extracellular
    signal-regulated kinase-signaling pathway was transiently activated by
    TGZ in EGFR overexpressing cancer cells, inhibition of EGF-induced Akt
    phosphorylation most likely accounted for the growth arrest of tumor
    cells caused by TGZ at pharmacologically achievable concentrations.
    Therefore, we have provided a new line of evidence indicating that TGZ
    inhibits cell proliferation by promoting EGFR degradation and
    attenuating Akt phosphorylation.
 C1 [Li, Xiaoqi; Yang, Xuanming; Xu, Youli; Tang, Hong] Chinese Acad Sci, Inst Biophys, Ctr Infect & Immun, Beijing 100101, Peoples R China.
    [Li, Xiaoqi; Yang, Xuanming; Xu, Youli; Tang, Hong] Chinese Acad Sci, Inst Biophys, Natl Lab Biomacromol, Beijing 100101, Peoples R China.
    [Li, Xin; Nan, Fajun] Chinese Acad Sci, Shanghai Inst Mat Med, Shanghai 201203, Peoples R China.
    [Jiang, Xuejun] Chinese Acad Sci, Inst Microbiol, Beijing 100080, Peoples R China.
 RP Tang, H, Chinese Acad Sci, Inst Biophys, Ctr Infect & Immun, Beijing
    100101, Peoples R China.
 EM tanghong@moon.ibp.ac.cn
 FU Ministry of Science and Technology, China [2007DFC30190]; Chinese
    Academy of Sciences [kscx-1-YW-10]
 FX We thank Dr Yongfeng Shang (Beijing University, Health Science Center)
    for the PPAR gamma. reporter plasmid and Dr Youyong Lu (Beijing
    University, School of Oncology) for Du145 cells. We especially thank Mr
    Chunchun Liu of Institute of Biophysics, Chinese Academy of Sciences
    for expert technical assistance. This work was supported in part by
    grants to Hong Tang from the National Basic Research Program of the
    Ministry of Science and Technology, China (2007DFC30190) and Chinese
    Academy of Sciences (kscx-1-YW-10).
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 NR 51
 TC 6
 PU NATURE PUBLISHING GROUP
 PI NEW YORK
 PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
 SN 1001-0602
 J9 CELL RES
 JI Cell Res.
 PD JUN
 PY 2009
 VL 19
 IS 6
 BP 720
 EP 732
 DI 10.1038/cr.2009.53
 PG 13
 SC Cell Biology
 GA 452GJ
 UT ISI:000266528000006
 ER
 
 PT J
 AU Zhang, J
    Zheng, XD
    Yang, X
    Liao, K
 AF Zhang, Jing
    Zheng, Xiudan
    Yang, Xiao
    Liao, Kan
 TI CIN85 associates with endosomal membrane and binds phosphatidic acid
 SO CELL RESEARCH
 LA English
 DT Article
 DE CIN85; the coiled-coil domain; phosphatidic acid; EGFR endocytosis;
    ESCRT assembly
 ID RECEPTOR DOWN-REGULATION; GROWTH-FACTOR RECEPTORS; PHOSPHOLIPASE-D;
    TYROSINE KINASES; MAMMALIAN-CELLS; EGF RECEPTORS; C-CBL; PROTEIN;
    COMPLEX; TRAFFICKING
 AB CIN85 (Cbl-interacting protein of 85 kDa) is an important molecule
    involved in receptor tyrosine kinase endocytosis. Here we report that
    through its positively charged C-terminus, CIN85 associates with a
    fusogenic lipid - phosphatidic acid. Its coiled-coil domain plays an
    important role in mediating this protein-lipid interaction. Deletion of
    the coiled-coil domain results in loss of membrane association, and
    reduced interaction with c-cbl, finally causing the blockage of
    epidermal growth factor receptor downregulation. In addition, a
    significant portion of CIN85 is located on the endosomal compartment
    and is related to endocytic cargo sorting, characterized by CIN85's
    localization on the "E class" compartment and EGF degradation blockage
    in CIN85 knockdown cells. Taken together, our results suggest that
    CIN85 may function as a scaffold molecule in both the internalization
    and endocytic cargo sorting processes through its association with the
    endosomal membrane.
 C1 [Zhang, Jing; Zheng, Xiudan; Yang, Xiao; Liao, Kan] Chinese Acad Sci, Inst Biochem & Cell Biol, Shanghai Inst Biol Sci, State Key Lab Mol Biol, Shanghai 200031, Peoples R China.
 RP Liao, K, Chinese Acad Sci, Inst Biochem & Cell Biol, Shanghai Inst Biol
    Sci, State Key Lab Mol Biol, Shanghai 200031, Peoples R China.
 EM kliao@sibs.ac.cn
 FU National Nature Sciences Foundation of China [90208007, 30521005,
    30623002]; Ministry of Sciences and Technology of China [2002CB513000,
    2006CB910700]
 FX We thank Dr Margo Myers (UCSF, USA) for providing the plasmid of c-Cbl,
    Dr Remy Sadoul (Universite Joseph Fourier, France) for providing the
    plasmids of Alix and truncated forms of Alix, and Dr Uta von Schwedler
    (University of Utah, USA) for providing the plasmids of Vps4 and Vps4
    M, and CHMP4B. This work was supported by grants 90208007, 30521005 and
    30623002 from the National Nature Sciences Foundation of China, and
    grants 2002CB513000 and 2006CB910700 from the Ministry of Sciences and
    Technology of China.
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 NR 40
 TC 4
 PU NATURE PUBLISHING GROUP
 PI NEW YORK
 PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
 SN 1001-0602
 J9 CELL RES
 JI Cell Res.
 PD JUN
 PY 2009
 VL 19
 IS 6
 BP 733
 EP 746
 DI 10.1038/cr.2009.51
 PG 14
 SC Cell Biology
 GA 452GJ
 UT ISI:000266528000007
 ER
 
 PT J
 AU Xu, HM
    Wang, WC
    Li, CL
    Yu, HY
    Yang, AC
    Wang, BB
    Jin, Y
 AF Xu, Huiming
    Wang, Weicheng
    Li, Chunliang
    Yu, Hongyao
    Yang, Acong
    Wang, Beibei
    Jin, Ying
 TI WWP2 promotes degradation of transcription factor OCT4 in human
    embryonic stem cells (vol 19, pg 561, 2009)
 SO CELL RESEARCH
 LA English
 DT Correction
 C1 [Xu, Huiming; Wang, Weicheng; Yu, Hongyao; Yang, Acong; Jin, Ying] Shanghai Jiao Tong Univ, Sch Med, Inst Hlth Sci, Key Lab Stem Cell Biol, Shanghai 200025, Peoples R China.
    [Xu, Huiming; Wang, Weicheng; Yu, Hongyao; Yang, Acong; Jin, Ying] Chinese Acad Sci, Shanghai Inst Biol Sci, Shanghai 200025, Peoples R China.
    [Xu, Huiming; Wang, Weicheng; Li, Chunliang; Yang, Acong; Wang, Beibei; Jin, Ying] Shanghai Jiao Tong Univ, Sch Med, Shanghai Stem Cell Inst, Shanghai 200025, Peoples R China.
    [Jin, Ying] Shanghai Jiao Tong Univ, Sch Med, Key Lab Cell Differentiat & Apoptosis, Chinese Minist Educ, Shanghai 200025, Peoples R China.
 RP Xu, HM, Shanghai Jiao Tong Univ, Sch Med, Inst Hlth Sci, Key Lab Stem
    Cell Biol, 225 S Chongqing Rd, Shanghai 200025, Peoples R China.
 CR XU HM, 2009, CELL RES, V19, P561, DOI 10.1038/cr.2009.31
 NR 1
 TC 0
 PU NATURE PUBLISHING GROUP
 PI NEW YORK
 PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
 SN 1001-0602
 J9 CELL RES
 JI Cell Res.
 PD JUN
 PY 2009
 VL 19
 IS 6
 BP 796
 EP 796
 DI 10.1038/cr.2009.63
 PG 1
 SC Cell Biology
 GA 452GJ
 UT ISI:000266528000013
 ER
 
 PT J
 AU Sha, HB
    He, Y
    Chen, H
    Wang, C
    Zenno, A
    Shi, H
    Yang, XY
    Zhang, XM
    Qi, L
 AF Sha, Haibo
    He, Yin
    Chen, Hui
    Wang, Cindy
    Zenno, Anna
    Shi, Hang
    Yang, Xiaoyong
    Zhang, Xinmin
    Qi, Ling
 TI The IRE1 alpha-XBP1 Pathway of the Unfolded Protein Response Is
    Required for Adipogenesis
 SO CELL METABOLISM
 LA English
 DT Article
 ID PLASMA-CELL DIFFERENTIATION; TRANSCRIPTION FACTOR XBP-1;
    ENDOPLASMIC-RETICULUM; TRANSMEMBRANE PROTEIN; KINASE-ACTIVITY;
    PPAR-GAMMA; BINDING; IRE1; REVEALS; BIOLOGY
 AB Signaling cascades during adipogenesis culminate in the expression of
    two essential adipogenic factors, PPAR gamma and C/EBP alpha. Here we
    demonstrate that the IRE1 alpha-XBP1 pathway, the most conserved branch
    of the unfolded protein response (UPR), is indispensable for
    adipogenesis. Indeed, XBP1-deficient mouse embryonic fibroblasts and
    3T3-L1 cells with XBP1 or IRE1 alpha knockdown exhibit profound defects
    in adipogenesis. Intriguingly, C/EBP beta, a key early adipogenic
    factor, induces Xbp1 expression by directly binding to its proximal
    promoter region. Subsequently, XBP1 binds to the promoter of Cebpa and
    activates its gene expression. The posttranscriptional splicing of Xbp1
    mRNA by IRE1 alpha is required as only the spliced form of XBP1 (XBP1s)
    rescues the adipogenic defect exhibited by XBP1-deficient cells. Taken
    together, our data show that the IRE1 alpha-XBP1 pathway plays a key
    role in adipocyte differentiation by acting as a critical regulator of
    the morphological and functional transformations during adipogenesis.
 C1 [Sha, Haibo; Chen, Hui; Wang, Cindy; Zenno, Anna; Qi, Ling] Cornell Univ, Div Nutr Sci, Ithaca, NY 14853 USA.
    [Qi, Ling] Cornell Univ, Grad Program Genet & Dev, Ithaca, NY 14853 USA.
    [Shi, Hang] Wake Forest Univ, Dept Internal Med, Winston Salem, NC 27157 USA.
    [Yang, Xiaoyong] Yale Univ, Sch Med, Comparat Med Sect, New Haven, CT 06519 USA.
    [Zhang, Xinmin] Roche Nimblegen Inc, Madison, WI 53719 USA.
 RP Qi, L, Cornell Univ, Div Nutr Sci, Ithaca, NY 14853 USA.
 EM lq35@cornell.edu
 FU Cornell start-up package ; American Federation for Aging Research
    [RAG08061]; American Diabetes Association (ADA) [7-08-JF-47]; National
    Institutes of Health [R01DK082582]; 2008 Rosalinde and Arthur
    Foundation/American Federation for Aging Research New Investigator
    Award in Alzheimer's Diseases ; ADA Junior Faculty Award ; ADA grant
    [7-08-JF-47]
 FX We thank Drs. L. Glimcher, L. Kraus, and J. Pleiss for reagents; Drs.
    K. L. Guan, S. Lee, M. Montminy, and three anonymous reviewers for
    insightful comments and suggestions. The Qi laboratory is supported by
    the Cornell start-up package and grants from American Federation for
    Aging Research (RAG08061), American Diabetes Association (ADA)
    (7-08-JF-47), and National Institutes of Health (R01DK082582). L.Q. is
    the recipient of the 2008 Rosalinde and Arthur Foundation/American
    Federation for Aging Research New Investigator Award in Alzheimer's
    Diseases and the ADA Junior Faculty Award. The study was funded by the
    Cornell start-up package and an ADA grant (7-08-JF-47).
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 NR 34
 TC 24
 PU CELL PRESS
 PI CAMBRIDGE
 PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
 SN 1550-4131
 J9 CELL METAB
 JI Cell Metab.
 PD JUN 3
 PY 2009
 VL 9
 IS 6
 BP 556
 EP 564
 DI 10.1016/j.cmet.2009.04.009
 PG 9
 SC Cell Biology; Endocrinology & Metabolism
 GA 453ZU
 UT ISI:000266652200010
 ER
 
 PT J
 AU Dixit, VD
    Yang, HW
    Cooper-Jenkins, A
    Giri, BB
    Patel, K
    Taub, DD
 AF Dixit, Vishwa D.
    Yang, Hyunwon
    Cooper-Jenkins, Anthony
    Giri, Banabihari B.
    Patel, Kalpesh
    Taub, Dennis D.
 TI Reduction of T cell-derived ghrelin enhances proinflammatory cytokine
    expression: implications for age-associated increases in inflammation
 SO BLOOD
 LA English
 DT Article
 ID SECRETAGOGUE RECEPTOR; LEPTIN; PROLIFERATION; ACTIVATION; SECRETION
 AB Ghrelin (Grln) is a peptide hormone that is predominantly produced in
    the stomach and stimulates appetite and induces growth hormone (GH)
    release. We have previously reported that ghrelin is also expressed in
    T cells and exerts prothymic and anti-inflammatory effects. However,
    the biologic relevance of T cell-derived ghrelin remains to be
    determined. Here, we report that acylated-bioactive ghrelin is
    expressed in human T cells and preferentially segregates within the
    lipid raft domains upon TCR ligation. The RNA interference
    (RNAi)-mediated down-regulation of ghrelin in primary human T cells
    activates IkB, and increases Th1 cytokines and IL-17 secretion. Ghrelin
    expression declines with increasing age in spleen and T cells and
    exogenous ghrelin administration in old mice reduces proinflammatory
    cytokines. These findings demonstrate that ghrelin functions in an
    autocrine and paracrine capacity to regulate proinflammatory cytokine
    expression in human and murine T cells and may contribute in regulating
    "inflamm-aging." (Blood. 2009; 113: 5202-5205)
 C1 [Taub, Dennis D.] NIA, Clin Immunol Sect, Immunol Lab, Intramural Res Program,NIH, Baltimore, MD 21224 USA.
 RP Taub, DD, NIA, Clin Immunol Sect, Immunol Lab, Intramural Res
    Program,NIH, 5600 Nathan Shock Dr, Baltimore, MD 21224 USA.
 EM taubd@grc.nia.nih.gov
 FU NIA, National Institutes of Health 
 FX This research was entirely supported by the Intramural Research Program
    of the NIA, National Institutes of Health.
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 NR 21
 TC 12
 PU AMER SOC HEMATOLOGY
 PI WASHINGTON
 PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
 SN 0006-4971
 J9 BLOOD
 JI Blood
 PD MAY 21
 PY 2009
 VL 113
 IS 21
 BP 5202
 EP 5205
 DI 10.1182/blood-2008-09-181255
 PG 4
 SC Hematology
 GA 450ML
 UT ISI:000266404500026
 ER
 
 PT J
 AU Banno, F
    Chauhan, AK
    Kokame, K
    Yang, J
    Miyata, S
    Wagner, DD
    Miyata, T
 AF Banno, Fumiaki
    Chauhan, Anil K.
    Kokame, Koichi
    Yang, Jin
    Miyata, Shigeki
    Wagner, Denisa D.
    Miyata, Toshiyuki
 TI The distal carboxyl-terminal domains of ADAMTS13 are required for
    regulation of in vivo thrombus formation
 SO BLOOD
 LA English
 DT Article
 ID VON-WILLEBRAND-FACTOR; GLYCOPROTEIN-IB-ALPHA; THROMBOCYTOPENIC PURPURA;
    ADAMTS13-DEFICIENT MICE; PLATELET-AGGREGATION; FLOW CONDITIONS; MOUSE
    MODEL; CLEAVAGE; DEFICIENCY; SUBSTRATE
 AB ADAMTS13 is a multidomain protease that limits platelet thrombogenesis
    through the cleavage of von Willebrand factor (VWF). We previously
    identified 2 types of mouse Adamts13 gene: the 129/Sv-strain Adamts13
    gene encodes the long-form ADAMTS13 having the same domains as human
    ADAMTS13, whereas the C57BL/6-strain Adamts13 gene encodes the
    short-form ADAMTS13 lacking the distal C-terminal domains. To assess
    the physiologic significance of the distal C-terminal domains of
    ADAMTS13, we generated and analyzed 129/Sv-genetic background congenic
    mice (Adamts13(S/S)) that carry the short-form ADAMTS13. Similar to
    wild-type 129/Sv mice (Adamts13(L/L)), Adamts13S/S did not have
    ultralarge VWF multimers in plasma, in contrast to 129/Sv-genetic
    background ADAMTS13-deficient mice (Adamts13(-/-)). However, in vitro
    thrombogenesis under flow at a shear rate of 5000 s(-1) was accelerated
    in Adamts13(S/S) compared with Adamts13(L/L). Both in vivo thrombus
    formation in ferric chloride-injured arterioles and thrombocytopenia
    induced by collagen plus epinephrine challenge were more dramatic in
    Adamts13(S/S) than in Adamts13(L/L) but less than in Adamts13(-/-).
    These results suggested that the C-terminally truncated ADAMTS13
    exhibited decreased activity in the cleavage of VWF under high shear
    rate. Role of the C-terminal domains may become increasingly important
    under prothrombotic conditions. (Blood. 2009; 113: 5323-5329)
 C1 [Banno, Fumiaki; Kokame, Koichi; Yang, Jin; Miyata, Toshiyuki] Natl Cardiovasc Ctr, Res Inst, Osaka 5658565, Japan.
    [Chauhan, Anil K.; Wagner, Denisa D.] Harvard Univ, Sch Med, Dept Pathol, Boston, MA 02115 USA.
    [Chauhan, Anil K.; Wagner, Denisa D.] Harvard Univ, Sch Med, Immune Dis Inst, Boston, MA USA.
    [Miyata, Shigeki] Natl Cardiovasc Ctr, Div Transfus Med, Suita, Osaka 565, Japan.
 RP Miyata, T, Natl Cardiovasc Ctr, Res Inst, 5-7-1 Fujishirodai, Osaka
    5658565, Japan.
 EM miyata@ri.ncvc.go.jp
 FU Ministry of Health, Labor, and Welfare of Japan, Tokyo, Japan ;
    Ministry of Education, Culture, Sports, Science, and Technology of
    Japan, Tokyo, Japan ; Japan Society for the Promotion of Science,
    Tokyo, Japan ; Program for Promotion of Fundamental Studies in Health
    Sciences of the National Institute of Biochemical Innovation of Japan,
    Ibaraki, Japan ; Baxter Bioscience, Vienna, Austria ; National Heart,
    Lung, and Blood Institute of the National Institutes of Health
    [P01-HL066105]
 FX This work was supported in part by grants-in-aid from the Ministry of
    Health, Labor, and Welfare of Japan, Tokyo, Japan (T. M.); the Ministry
    of Education, Culture, Sports, Science, and Technology of Japan, Tokyo,
    Japan (F. B., K. K., and T. M.); the Japan Society for the Promotion of
    Science, Tokyo, Japan (K. K. and T. M.); and from the Program for
    Promotion of Fundamental Studies in Health Sciences of the National
    Institute of Biochemical Innovation of Japan, Ibaraki, Japan (T. M.); a
    Sponsored Research Agreement from Baxter Bioscience, Vienna, Austria
    (A. K. C. and D. D. W.) and a National Heart, Lung, and Blood Institute
    of the National Institutes of Health grant P01-HL066105 (D. D. W.).
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 NR 38
 TC 15
 PU AMER SOC HEMATOLOGY
 PI WASHINGTON
 PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
 SN 0006-4971
 J9 BLOOD
 JI Blood
 PD MAY 21
 PY 2009
 VL 113
 IS 21
 BP 5323
 EP 5329
 DI 10.1182/blood-2008-07-169359
 PG 7
 SC Hematology
 GA 450ML
 UT ISI:000266404500040
 ER
 
 PT J
 AU Horkheimer, I
    Quigley, M
    Zhu, JG
    Huang, XP
    Chao, NJ
    Yang, YP
 AF Horkheimer, Ian
    Quigley, Michael
    Zhu, Jiangao
    Huang, Xiaopei
    Chao, Nelson J.
    Yang, Yiping
 TI Induction of type I IFN is required for overcoming tumor-specific
    T-cell tolerance after stem cell transplantation
 SO BLOOD
 LA English
 DT Article
 ID BONE-MARROW-TRANSPLANTATION; DENDRITIC CELLS; TRANSGENIC MICE;
    PERIPHERAL TOLERANCE; METASTATIC MELANOMA; ANTIGEN-4 BLOCKADE;
    IMMUNE-RESPONSES; REGULATORY CELLS; CANCER VACCINES; TGF-BETA
 AB Tumor-specific T-cell tolerance represents one major mechanism of
    tumor-induced immune evasion. Myeloablative chemotherapy with stem cell
    transplantation may offer the best chance of achieving a state of
    minimal residual disease and, thus, minimize tumor-induced immune
    evasion. However, studies have shown that tumor-specific T-cell
    tolerance persists after transplantation. Here, we showed that
    CD4(+)CD25(+) regulatory T (T-Reg) cells play a critical role in
    tumor-specific CD8(+) T-cell tolerance after trans-plantation. Removal
    of T-Reg cells from the donor lymphocyte graft did not overcome this
    tolerance because of rapid conversion of donor CD4(+)CD25(-) T cells
    into CD4(+)CD25(+)Foxp3(+) T-Reg cells in recipients after
    transplantation, and depletion of T-Reg cells in recipients was
    necessary for the reversal of tumor-specific tolerance. These results
    suggest that strategies capable of overcoming T-cell tolerance in
    recipients are required to promote antitumor immunity after
    transplantation. Toward this goal, we showed that dendritic cell (DC)
    vaccines coadministered with the TLR9 ligand, CpG could effectively
    overcome tumor-specific tolerance, leading to significant prolongation
    of tumor-free survival after transplantation. We further showed that
    CpG-induced type I interferon was critical for the reversal of
    tumor-specific tolerance in vivo. Collectively, these results may
    suggest effective immunotherapeutic strategies for treating cancer
    after stem cell transplantation. (Blood. 2009; 113: 5330-5339)
 C1 [Horkheimer, Ian; Zhu, Jiangao; Huang, Xiaopei; Chao, Nelson J.; Yang, Yiping] Duke Univ, Med Ctr, Dept Med, Durham, NC 27710 USA.
    [Quigley, Michael; Chao, Nelson J.; Yang, Yiping] Duke Univ, Med Ctr, Div Immunol, Durham, NC 27710 USA.
 RP Yang, YP, Duke Univ, Med Ctr, Dept Med, Box 103005, Durham, NC 27710
    USA.
 EM yang0029@mc.duke.edu
 FU National Institutes of Health (Bethesda, MD) [CA111807, CA047741,
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 FX This work was supported by grants CA111807 (Y. Y.), CA047741 (N. J.
    C.), and CA136934 (Y. Y.) from the National Institutes of Health
    (Bethesda, MD) and by a grant from the Alliance for Cancer Gene Therapy
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 NR 57
 TC 3
 PU AMER SOC HEMATOLOGY
 PI WASHINGTON
 PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
 SN 0006-4971
 J9 BLOOD
 JI Blood
 PD MAY 21
 PY 2009
 VL 113
 IS 21
 BP 5330
 EP 5339
 DI 10.1182/blood-2008-05-155150
 PG 10
 SC Hematology
 GA 450ML
 UT ISI:000266404500041
 ER
 
 PT J
 AU Kataru, RP
    Jung, K
    Jang, C
    Yang, H
    Schwendener, RA
    Baik, JE
    Han, SH
    Alitalo, K
    Koh, GY
 AF Kataru, Raghu P.
    Jung, Keehoon
    Jang, Cholsoon
    Yang, Hanseul
    Schwendener, Reto A.
    Baik, Jung Eun
    Han, Seung Hyun
    Alitalo, Kari
    Koh, Gou Young
 TI Critical role of CD11b(+) macrophages and VEGF in inflammatory
    lymphangiogenesis, antigen clearance, and inflammation resolution
 SO BLOOD
 LA English
 DT Article
 ID HIGH ENDOTHELIAL VENULES; DRAINING LYMPH-NODES; MONOCYTE RECRUITMENT/;
    LIPOTEICHOIC ACID; TRANSGENIC MICE; IN-VIVO; CELLS; GROWTH; VESSELS;
    EXPRESSION
 AB Using a bacterial pathogen-induced acute inflammation model in the
    skin, we defined the roles of local lymphatic vessels and draining
    lymph nodes (DLNs) in antigen clearance and inflammation resolution. At
    the peak day of inflammation, robust expansion of lymphatic vessels and
    profound infiltration of CD11b(+)/Gr-1(+) macrophages into the inflamed
    skin and DLN were observed. Moreover, lymph flow and inflammatory cell
    migration from the inflamed skin to DLNs were enhanced. Concomitantly,
    the expression of lymphangiogenic growth factors such as vascular
    endothelial growth factor C (VEGF-C), VEGF-D, and VEGF-A were
    significantly up-regulated in the inflamed skin, DLNs, and particularly
    in enriched CD11b(+) macrophages from the DLNs. Depletion of
    macrophages, or blockade of VEGF-C/D or VEGF-A, largely attenuated
    these phenomena, and produced notably delayed antigen clearance and
    inflammation resolution. Conversely, keratin 14 (K14)-VEGF-C transgenic
    mice, which have dense and enlarged lymphatic vessels in the skin
    dermis, exhibited accelerated migration of inflammatory cells from the
    inflamed skin to the DLNs and faster antigen clearance and inflammation
    resolution. Taken together, these results indicate that VEGF-C,-D,
    and-A derived from the CD11b(+)/Gr-1(+) macrophages and local inflamed
    tissues play a critical role in promoting antigen clearance and
    inflammation resolution. (Blood. 2009; 113: 5650-5659)
 C1 [Kataru, Raghu P.; Jung, Keehoon; Jang, Cholsoon; Yang, Hanseul; Koh, Gou Young] Korea Adv Inst Sci & Technol, Dept Biol Sci, Taejon 305701, South Korea.
    [Kataru, Raghu P.; Jung, Keehoon; Jang, Cholsoon; Yang, Hanseul; Koh, Gou Young] Korea Adv Inst Sci & Technol, Natl Res Lab Vasc Biol, Taejon 305701, South Korea.
    [Schwendener, Reto A.] Univ Zurich, Lab Liposome Res, Inst Mol Canc Res, Zurich, Switzerland.
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    [Han, Seung Hyun] Int Vaccine Inst, Seoul, South Korea.
    [Alitalo, Kari] Univ Helsinki, Biomedicum Helsinki, Lab Mol Canc Biol, Helsinki, Finland.
 RP Koh, GY, Korea Adv Inst Sci & Technol, Dept Biol Sci, 373-1 Guseong
    Dong, Taejon 305701, South Korea.
 EM gykoh@kaist.ac.kr
 FU Korea Science and Engineering Foundation (KOSEF) [2004-02376]; Ministry
    of Science and Technology [20080401034061]
 FX This work was supported by the Korea Science and Engineering Foundation
    (KOSEF) through the National Research Laboratory Program (2004-02376,
    G.Y.K.) funded by the Ministry of Science and Technology and BioGreen
    21 Program, Rural Development Administration (20080401034061, S. H.
    H.), Republic of Korea.
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 NR 49
 TC 28
 PU AMER SOC HEMATOLOGY
 PI WASHINGTON
 PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
 SN 0006-4971
 J9 BLOOD
 JI Blood
 PD MAY 28
 PY 2009
 VL 113
 IS 22
 BP 5650
 EP 5659
 DI 10.1182/blood-2008-09-176776
 PG 10
 SC Hematology
 GA 453TD
 UT ISI:000266634700038
 ER
 
 PT J
 AU Punj, V
    Matta, H
    Schamus, S
    Yang, TB
    Chang, Y
    Chaudhary, PM
 AF Punj, Vasu
    Matta, Hittu
    Schamus, Sandra
    Yang, Tianbing
    Chang, Yuan
    Chaudhary, Preet M.
 TI Induction of CCL20 production by Kaposi sarcoma-associated herpesvirus:
    role of viral FLICE inhibitory protein K13-induced NF-kappa B activation
 SO BLOOD
 LA English
 DT Article
 ID MICROVASCULAR ENDOTHELIAL-CELLS; PRIMARY EFFUSION LYMPHOMA;
    GENE-EXPRESSION; HUMAN-HERPESVIRUS-8 INFECTION; INDUCED APOPTOSIS;
    CHEMOKINE LARC; KINASE COMPLEX; SPINDLE CELLS; K13; TRANSFORMATION
 AB Kaposi sarcoma-associated herpesvirus (KSHV), also known as human
    herpesvirus 8, is the etiologic agent of Kaposi sarcoma (KS), an
    angioproliferative lesion characterized by dramatic angiogenesis and
    inflammatory infiltration. In this study, we report that expression of
    chemokine CCL20, a potent chemoattractant of dendritic cells and
    lymphocytes, is strongly induced in cultured cells either by KSHV
    infection or on ectopic expression of viral FLICE inhibitory protein
    K13. This induction is caused by transcriptional activation of CCL20
    gene, which is mediated by binding of the p65, p50, and c-Rel subunits
    of the transcription factor nuclear factor-kappa B (NF-kappa B) to an
    atypical NF-kappa B-binding site present in the CCL20 gene promoter.
    The CCL20 gene induction is defective in K13 mutants that lack NF-kappa
    B activity, and can be blocked by specific genetic and pharmacologic
    inhibitors of the NF-kappa B pathway. CCR6, the specific receptor for
    CCL20, is also induced in cultured cells either by KSHV infection or on
    K13 expression. Finally, expression of CCL20 and CCR6 is increased in
    clinical samples of KS. These results suggest that KSHV and
    K13-mediated induction of CCL20 and CCR6 may contribute to the
    recruitment of dendritic cells and lymphocytes into the KS lesions, and
    to tumor growth and metastases. (Blood. 2009; 113: 5660-5668)
 C1 [Chaudhary, Preet M.] Univ Pittsburgh, Hillman Canc Ctr, Inst Canc, Dept Med,Div Hematol Oncol, Pittsburgh, PA 15213 USA.
    [Yang, Tianbing] Univ Pittsburgh, Spang Translat Res Core Facil, Inst Canc, Pittsburgh, PA 15213 USA.
    [Chang, Yuan] Univ Pittsburgh, Dept Pathol, Inst Canc, Pittsburgh, PA 15213 USA.
 RP Chaudhary, PM, Univ Pittsburgh, Hillman Canc Ctr, Inst Canc, Dept
    Med,Div Hematol Oncol, 5117 Ctr Ave,Suite 1-19A, Pittsburgh, PA 15213
    USA.
 EM chaudharypm@upmc.edu
 FU National Institutes of Health (Bethesda, MD) [CA85177, CA124621,
    HL085189]; Leukemia & Lymphoma Society (White Plains, NY) ; Mario
    Lemieux Foundation (Pittsburgh, PA) 
 FX The authors thank Dr Hiroyasu Nakano and Dr Gutian Xiao for providing
    MEFs lacking the NF-kappa B p65 and p50 subunits, respectively; Dr
    Tomoko Kohno for pGL2-CCL20/MIP-alpha (CCL20 WT-Luc) and
    pGL2-CCL20/MIP-3 alpha/kappa BM (CCL20 Delta NF-kappa B-Luc) for
    luciferase reporter constructs; the National Cancer Research
    Institute-sponsored AIDS and Cancer Specimen Resources at University of
    California, San Francisco, CA, and George Washington University,
    Washington, DC, for providing patient samples; Marie Acquafondata
    (Tissue and Research Pathology Services) for help with
    immunohistochemistry; and Dr Siddhartha Kar and Aletheia Tamewitz for
    critical reading of the manuscript.
    This work was supported by the National Institutes of Health (Bethesda,
    MD; grants CA85177, CA124621, and HL085189), the Leukemia & Lymphoma
    Society (White Plains, NY), and the Mario Lemieux Foundation
    (Pittsburgh, PA).
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 NR 64
 TC 4
 PU AMER SOC HEMATOLOGY
 PI WASHINGTON
 PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
 SN 0006-4971
 J9 BLOOD
 JI Blood
 PD MAY 28
 PY 2009
 VL 113
 IS 22
 BP 5660
 EP 5668
 DI 10.1182/blood-2008-10-186403
 PG 9
 SC Hematology
 GA 453TD
 UT ISI:000266634700039
 ER
 
 PT J
 AU Mosnier, LO
    Zampolli, A
    Kerschen, EJ
    Schuepbach, RA
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 AF Mosnier, Laurent O.
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 TI Hyperantithrombotic, noncytoprotective Glu149Ala-activated protein C
    mutant
 SO BLOOD
 LA English
 DT Article
 ID COAGULATION-FACTOR VA; RANDOMIZED CONTROLLED-TRIAL; SEVERE SEPSIS;
    ACTIVATED RECEPTOR-1; ANTICOAGULANT ACTIVITY; CRYSTAL-STRUCTURE;
    BLOOD-COAGULATION; ENDOTHELIAL-CELLS; ANTITHROMBIN-III; CLOTTING FACTORS
 AB Activated protein C (APC) reduces mortality in severe sepsis patients.
    APC exerts anticoagulant activities via inactivation of factors Va and
    VIIIa and cytoprotective activities via endothelial protein C receptor
    and protease activated receptor-1. APC mutants with selectively altered
    and opposite activity profiles, that is, greatly reduced anticoagulant
    activity or greatly reduced cytoprotective activities, are compared
    here. Glu149Ala-APC exhibited enhanced in vitro anticoagulant and in
    vivo antithrombotic activity, but greatly diminished in vitro
    cytoprotective effects and in vivo reduction of endotoxin-induced
    murine mortality. Thus, residue Glu149 and the C-terminal region of
    APC's light chain are identified as functionally important for
    expression of multiple APC activities. In contrast to Glu149Ala-APC,
    5A-APC (Lys191-193Ala + Arg229/230Ala) with protease domain mutations
    lacked in vivo antithrombotic activity, although it was potent in
    reducing endotoxin-induced mortality, as previously shown. These data
    imply that APC molecular species with potent antithrombotic activity,
    but without robust cyto-protective activity, are not sufficient to
    reduce mortality in endotoxemia, emphasizing the need for APC's
    cytoprotective actions, but not anticoagulant actions, to reduce
    endotoxin-induced mortality. Protein engineering can provide APC
    mutants that permit definitive mechanism of action studies for APC's
    multiple activities, and may also provide safer and more effective
    second generation APC mutants with reduced bleeding risk. (Blood. 2009;
    113: 5970-5978)
 C1 [Mosnier, Laurent O.; Zampolli, Antonella; Banerjee, Yajnavalka; Fernandez, Jose A.; Yang, Xia V.; Ruggeri, Zaverio M.; Griffin, John H.] Scripps Res Inst, Dept Mol & Expt Med, La Jolla, CA 92037 USA.
    [Kerschen, Edward J.; Weiler, Hartmut] Blood Res Inst, Milwaukee, WI USA.
    [Schuepbach, Reto A.; Riewald, Matthias] Scripps Res Inst, Dept Immunol & Microbial Sci, La Jolla, CA 92037 USA.
 RP Griffin, JH, Scripps Res Inst, Dept Mol & Expt Med MEM 180, 10550 N
    Torrey Pines Rd, La Jolla, CA 92037 USA.
 EM jgriffin@scripps.edu
 FU National Heart, Lung, and Blood Institute [HL087618, HL073318,
    HL060655, HL093388, HL031950, HL31950, HL52246]
 FX This work was supported in part by National Heart, Lung, and Blood
    Institute grants HL087618 (to L. O. M.), HL073318 (to M. R.), HL060655
    and HL093388 (to H. W.), HL031950 (to Z. M. R.), and HL31950 and
    HL52246 (to J. H. G.).
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 NR 52
 TC 20
 PU AMER SOC HEMATOLOGY
 PI WASHINGTON
 PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
 SN 0006-4971
 J9 BLOOD
 JI Blood
 PD JUN 4
 PY 2009
 VL 113
 IS 23
 BP 5970
 EP 5978
 DI 10.1182/blood-2008-10-183327
 PG 9
 SC Hematology
 GA 454BH
 UT ISI:000266656100040
 ER
 
 PT J
 AU Yang, LJ
    Shen, L
    Shao, YH
    Zhao, Q
    Zhang, W
 AF Yang, Lijun
    Shen, Lian
    Shao, Yuehu
    Zhao, Qing
    Zhang, Wei
 TI Cytoplasmic domain of human Fcalpha/mu receptor is required for ligand
    internalization
 SO CELLULAR IMMUNOLOGY
 LA English
 DT Article
 DE Fcalpha/mu receptor; Igm; IgA; Internalization
 ID FC-ALPHA/MU-R; NATURAL-KILLER-CELLS; MU-RECEPTOR; EPSILON-RI; T-CELLS;
    IGM; BINDING; EXPRESSION; SPECIFICITY; TISSUES
 AB The Fcalpha/mu receptor (Fc alpha/mu R), a type I tramsmembrane
    protein, is an immunoglobulin Fc receptor for both IgA and IgM. Its
    functions in immune defense are not clear at present. In this work,
    human Fc alpha/mu R was expressed in CHO, 293T, and COS-7 cells to
    study its biochemical functions. Fc alpha/mu R expressed by CHO and
    293T was only in monomer form in cytoplasma and the monomeric receptor
    could not bind IgA or IgM. In comparison, Fc alpha/mu R expressed by
    COS-7 cells had both monomer and dimer forms. The binding assay showed
    that Fc alpha/mu R expressed by COS-7 cells could bind IgM strongly and
    IgA weakly, implying that dimeric receptor could be expressed on cell
    membrane and functioned. The bound IgM could be internalized and the
    internalization was abolished when the cytoplasmic domain of Fc
    alpha/mu R was truncated. Therefore, the cytoplasmic portion of human
    Fc alpha/mu R is required in the internalization. (C) 2009 Elsevier
    Inc. All rights reserved
 C1 [Yang, Lijun; Shen, Lian; Shao, Yuehu; Zhao, Qing; Zhang, Wei] Chinese Acad Med Sci, Inst Basic Med Sci, Peking Union Med Coll, Sch Basic Med, Beijing, Peoples R China.
 RP Zhang, W, Inst Basic Med Sci, Dept Immunol, 5 Dong Dan San Tiao,
    Beijing 100005, Peoples R China.
 EM wzhang@pumc.edu.cn
 FU National Natural Science Foundation of China [30571693]; Glasgow
    University, UK 
 FX This work is supported by a grant (No. 30571693) from the National
    Natural Science Foundation of China. The authors thank Dr. Alan Jardine
    (Glasgow University, UK) for donating human Fcot/ pR cDNA.
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 NR 31
 TC 4
 PU ACADEMIC PRESS INC ELSEVIER SCIENCE
 PI SAN DIEGO
 PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
 SN 0008-8749
 J9 CELL IMMUNOL
 JI Cell. Immunol.
 PY 2009
 VL 258
 IS 1
 BP 78
 EP 82
 DI 10.1016/j.cellimm.2009.03.015
 PG 5
 SC Cell Biology; Immunology
 GA 451CU
 UT ISI:000266449100010
 ER
 
 PT J
 AU Cai, G
    Yang, JH
    Wang, HZ
    Cai, Q
    Zhao, DB
    Shen, Q
 AF Cai Gang
    Yang Jiahui
    Wang Huaizhou
    Cai Qing
    Zhao Dongbao
    Shen Qian
 TI Defects of mitogen-activated protein kinase in ICOS signaling pathway
    lead to CD4(+) and CD8(+) T-cell dysfunction in patients with active SLE
 SO CELLULAR IMMUNOLOGY
 LA English
 DT Article
 DE Systemic lupus erythematosus; MAP kinase; IL-2; Inducible costimulator
 ID SYSTEMIC-LUPUS-ERYTHEMATOSUS; INDUCIBLE COSTIMULATOR; B-CELL;
    EXPRESSION; MOLECULE; CD28; PROLIFERATION; INVOLVEMENT; AILIM/ICOS;
    CRITERIA
 AB in this study, hypoproliferation and defects of effectors and cytokines
    in CD4(+) and CD8(+) T-cells via ICOS costimulation were found in
    active SLE patients, relative to normal individuals and RA patient
    controls. Exogenous IL-2 can partially reverse those defects. In
    addition, low level of ERK phosphorylation in ICOS-mediated signaling
    pathway was discovered in lupus CD4(+) and CD8(+) T-cells. When blocked
    with ERK-specific chemical inhibitor PD98059, cell proliferation and
    IL-2 production via ICOS costimulation from both CD4(+) and CD8(+)
    T-cells will be severely inhibited. These findings confirmed the
    dysfunction of both CD4(+) and CD8(+) T-cells after ICOS costimulation
    in lupus patients and most importantly pointed out that impairment of
    ERK activation might be one of the critical factors involved in
    ICOS-mediated IL-2 and T-cell hypoproliferation in active SLE. (C) 2009
    Elsevier Inc. All rights reserved.
 C1 [Cai Gang; Yang Jiahui; Wang Huaizhou; Shen Qian] Shanghai Changhai Hosp, Dept Expt Diag, Shanghai 200433, Peoples R China.
    [Cai Qing; Zhao Dongbao] Shanghai Changhai Hosp, Dept Rheumatol, Shanghai, Peoples R China.
 RP Shen, Q, Shanghai Changhai Hosp, Dept Expt Diag, 168 Changhai Rd,
    Shanghai 200433, Peoples R China.
 EM laoshenqch@yahoo.cn
 FU Cancer Research Institution, The Second Military Medical University
    [CD3 (12-176]; Hi-tech Research and Development Program of China
    [2002AA214091]; Shanghai Natural Science foundation [3ZR14026]
 FX We are grateful to Prof. Yajun Guo (Cancer Research Institution, The
    Second Military Medical University) for providing the mAb specific for
    human CD3 (12-176).
    This work was supported by a grant from the Hi-tech Research and
    Development Program of China 2002AA214091 and Shanghai Natural Science
    foundation Grant 3ZR14026.
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 NR 25
 TC 0
 PU ACADEMIC PRESS INC ELSEVIER SCIENCE
 PI SAN DIEGO
 PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
 SN 0008-8749
 J9 CELL IMMUNOL
 JI Cell. Immunol.
 PY 2009
 VL 258
 IS 1
 BP 83
 EP 89
 DI 10.1016/j.cellimm.2009.03.016
 PG 7
 SC Cell Biology; Immunology
 GA 451CU
 UT ISI:000266449100011
 ER
 
 PT J
 AU Gu, WY
    Cochrane, M
    Leggatt, GR
    Payne, E
    Choyce, A
    Zhou, F
    Tindle, R
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 AF Gu, Wenyi
    Cochrane, Melanie
    Leggatt, Graham R.
    Payne, Elizabeth
    Choyce, Allison
    Zhou, Fang
    Tindle, Robert
    McMillan, Nigel A. J.
 TI Both treated and untreated tumors are eliminated by short hairpin
    RNA-based induction of target-specific immune responses
 SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
    AMERICA
 LA English
 DT Article
 DE antigen presentation; cancer; CTL epitope; RNAi
 ID SMALL INTERFERING RNA; DOUBLE-STRANDED-RNA; DEFECTIVE RIBOSOMAL
    PRODUCTS; HUMAN-PAPILLOMAVIRUS TYPE-16; DENDRITIC CELLS;
    CROSS-PRESENTATION; MAMMALIAN-CELLS; T-CELLS; IN-VIVO; ANTIGEN
 AB RNA interference (RNAi) for cancer treatment relies on the ability to
    directly kill cancer cells via down-regulation of target genes, but
    issues of delivery and efficacy have limited clinical adoption.
    Furthermore, current studies using immune-deficient animal models
    disregard potential interactions with the adaptive immune system. It
    has previously been observed that certain viral antigens appear to be
    more rapidly presented to the immune system than normal proteins due to
    the production of defective ribosomal products by the virus. Given that
    RNAi could potentially result in the generation of truncated mRNAs, we
    wondered whether a similar mechanism of immune presentation of a target
    gene was possible. Here we show that RNAi-cleaved mRNAs can be
    translated into incomplete protein, and if cleavage was downstream of
    cytotoxic T cell epitopes, resulted in increased presentation of target
    protein and the generation of a tumor-protective immune response. We
    show that mice inoculated with tumor cells treated with such short
    hairpin RNAs (shRNAs) were protected from subsequent challenge with
    untreated tumors. However, protection was only found if shRNAs were
    targeted downstream of the dominant cytotoxic T cell (CTL) epitope. Our
    work suggests that RNAi can alter immunity to targets and shows that
    not all tumor cells require direct RNAi exposure for treatment to be
    effective in vivo, pointing the way to a new class of RNAi-based
    therapy.
 C1 [Gu, Wenyi; Leggatt, Graham R.; Payne, Elizabeth; Choyce, Allison; Zhou, Fang; McMillan, Nigel A. J.] Univ Queensland Diamantina, Inst Canc Immunol & Metab Med, Brisbane, Qld 4072, Australia.
    [Cochrane, Melanie; Tindle, Robert] Royal Childrens Hosp, Sir Albert Sakzewski Virus Res Ctr, Brisbane, Qld 4072, Australia.
    [Cochrane, Melanie; Tindle, Robert] Univ Queensland, Clin Med Virol Ctr, Brisbane, Qld 4072, Australia.
 RP McMillan, NAJ, Univ Queensland Diamantina, Inst Canc Immunol & Metab
    Med, Brisbane, Qld 4072, Australia.
 EM n.mcmillan@uq.edu.au
 FU National Health and Medical Research Council of Australia ; The Cancer
    Council of Queensland 
 FX This work was funded by grants from the National Health and Medical
    Research Council of Australia and The Cancer Council of Queensland.
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 NR 35
 TC 6
 PU NATL ACAD SCIENCES
 PI WASHINGTON
 PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA
 SN 0027-8424
 J9 PROC NAT ACAD SCI USA
 JI Proc. Natl. Acad. Sci. U. S. A.
 PD MAY 19
 PY 2009
 VL 106
 IS 20
 BP 8314
 EP 8319
 DI 10.1073/pnas.0812085106
 PG 6
 SC Multidisciplinary Sciences
 GA 447RH
 UT ISI:000266209000042
 ER
 
 PT J
 AU Li, XY
    Liu, HZ
    Yang, SL
    Tang, ZL
    Ma, YH
    Chu, MX
    Li, K
 AF Li, Xinyun
    Liu, Huazhen
    Yang, Shulin
    Tang, Zhonglin
    Ma, Yuehui
    Chu, Mingxing
    Li, Kui
 TI Characterization analysis and polymorphism detection of the porcine
    Myd88 gene
 SO GENETICS AND MOLECULAR BIOLOGY
 LA English
 DT Article
 DE Myd88; TLR; polymorphism; pig; chromosome mapping
 ID ENDOTOXIN-TOLERANT CELLS; TOLL-LIKE RECEPTORS; INNATE IMMUNITY; IL-1;
    RECOGNITION; CLONING; FAMILY; PIGS
 AB The myeloid differentiation primary response protein 88 (Myd88) is an
    essential adaptor protein, which mediates in all Toll-like receptor
    (TLR) members signal transduction, except for TLR3. In this study, the
    4464 bp genomic sequence of porcine Myd88 was first isolated, whereupon
    tissue distribution, chromosome mapping and single nucleotide
    polymorphism (SNP) were analyzed. Our results revealed that porcine
    Myd88 gene, which was located at chromosome 13 linked with marker S0288
    (distance = 40 cR; LOD = 8.66), was widely expressed in all the
    examined tissues. There were 16 potential SNPs in the isolated genome
    fragment. SNP 797T/C in the first intron was studied, with no
    significant association being found between the genotype and immune
    traits in pigs (p > 0.05). The porcine Myd88 protein contained both the
    death domain (DD) and the Toll/IL-1 receptor domain (TIR). Leu
    residues, essential for its structure, were the most abundant
    encountered in the DD. The TIR contained two conserved motifs which may
    play important roles in the Myd88 function.
 C1 [Li, Xinyun; Yang, Shulin; Tang, Zhonglin; Ma, Yuehui; Chu, Mingxing; Li, Kui] Chinese Acad Agr Sci, Inst Anim Sci, Key Lab Farm Anim Genet Resources & Utlizat, Minist Agr China, Beijing 100094, Peoples R China.
    [Li, Xinyun; Liu, Huazhen] Huazhong Agr Univ, Key Lab Anim Genet Breeding & Reprod, Minist Educ China, Wuhan, Peoples R China.
 RP Li, K, Chinese Acad Agr Sci, Inst Anim Sci, Key Lab Farm Anim Genet
    Resources & Utlizat, Minist Agr China, Beijing 100094, Peoples R China.
 EM kuili@iascaas.net.cn
 FU State Platform of Technology Infrastructure [2005DKA21101]; Key Project
    of National Basic Research and Developmental Plan of China
    [G2006CB102105]; National High Science and Technology Foundation of
    China [20060110Z1039]; National Natural Science Foundation of China
    [30571300]; National Scientific and Technology Mainstay Project
    [2006BDA13B08]; Project of Science and Technology Innovation Team 
 FX We are grateful to Dr. Yerle for supplying the RH panel. This research
    was supported by the State Platform of Technology Infrastructure
    (2005DKA21101), the Key Project of National Basic Research and
    Developmental Plan of China (G2006CB102105), the National High Science
    and Technology Foundation of China (20060110Z1039), the National
    Natural Science Foundation of China (30571300), the National Scientific
    and Technology Mainstay Project (2006BDA13B08) and the Project of
    Science and Technology Innovation Team for "Research and Improvement of
    Domestic Animal Germplasm" of IAS, CAAS.
 CR 3DJIGSAW PROGRAM
    CLUSTAL W PROGRAM
    IMPRH MAPPING TOOL
    NETPHOS PROGRAM
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 NR 26
 TC 0
 PU SOC BRASIL GENETICA
 PI RIBEIRAO PRET
 PA RUA CAP ADELMIO NORBET DA SILVA, 736, ALTO DA BOA VISTA, 14025-670
    RIBEIRAO PRET, BRAZIL
 SN 1415-4757
 J9 GENET MOL BIOL
 JI Genet. Mol. Biol.
 PY 2009
 VL 32
 IS 2
 BP 295
 EP 300
 PG 6
 SC Biochemistry & Molecular Biology; Genetics & Heredity
 GA 448SC
 UT ISI:000266281300015
 ER
 
 PT J
 AU Chen, YF
    Kao, CH
    Chen, YT
    Wang, CH
    Wu, CY
    Tsai, CY
    Liu, FC
    Yang, CW
    Wei, YH
    Hsu, MT
    Tsai, SF
    Tsai, TF
 AF Chen, Yi-Fan
    Kao, Cheng-Heng
    Chen, Ya-Ting
    Wang, Chih-Hao
    Wu, Chia-Yu
    Tsai, Ching-Yen
    Liu, Fu-Chin
    Yang, Chu-Wen
    Wei, Yau-Huei
    Hsu, Ming-Ta
    Tsai, Shih-Feng
    Tsai, Ting-Fen
 TI Cisd2 deficiency drives premature aging and causes
    mitochondria-mediated defects in mice
 SO GENES & DEVELOPMENT
 LA English
 DT Article
 DE Cisd2; Wolfram syndrome 2; autophagy; knockout mice; mitochondria;
    premature aging
 ID WOLFRAM DIDMOAD SYNDROME; PANCREATIC BETA-CELLS; ENDOPLASMIC-RETICULUM
    STRESS; OPTIC ATROPHY; PROGEROID SYNDROME; DIABETES-MELLITUS;
    TRANSMEMBRANE PROTEIN; INSULIN-SECRETION; DEAFNESS DIDMOAD; MOUSE MODELS
 AB CISD2, the causative gene for Wolfram syndrome 2 (WFS2), is a
    previously uncharacterized novel gene. Significantly, the CISD2 gene is
    located on human chromosome 4q, where a genetic component for longevity
    maps. Here we show for the first time that CISD2 is involved in
    mammalian life-span control. Cisd2 deficiency in mice causes
    mitochondrial breakdown and dysfunction accompanied by autophagic cell
    death, and these events precede the two earliest manifestations of
    nerve and muscle degeneration; together, they lead to a panel of
    phenotypic features suggestive of premature aging. Our study also
    reveals that Cisd2 is primarily localized in the mitochondria and that
    mitochondrial degeneration appears to have a direct phenotypic
    consequence that triggers the accelerated aging process in Cisd2
    knockout mice; furthermore, mitochondrial degeneration exacerbates with
    age, and the autophagy increases in parallel to the development of the
    premature aging phenotype. Additionally, our Cisd2 knockout mouse work
    provides strong evidence supporting an earlier clinical hypothesis that
    WFS is in part a mitochondria-mediated disorder; specifically, we
    propose that mutation of CISD2 causes the mitochondria-mediated
    disorder WFS2 in humans. Thus, this mutant mouse provides an animal
    model for mechanistic investigation of Cisd2 protein function and help
    with a pathophysiological understanding of WFS2.
 C1 [Chen, Yi-Fan; Chen, Ya-Ting; Wu, Chia-Yu; Tsai, Ching-Yen; Tsai, Shih-Feng; Tsai, Ting-Fen] Natl Yang Ming Univ, Dept Life Sci, Taipei 112, Taiwan.
    [Kao, Cheng-Heng] Chang Gung Univ, Ctr Gen Educ, Tao Yuan 333, Taiwan.
    [Chen, Ya-Ting; Tsai, Shih-Feng; Tsai, Ting-Fen] Natl Hlth Res Inst, Div Mol & Genom Med, Zhunan 350, Miaoli County, Taiwan.
    [Wang, Chih-Hao; Wei, Yau-Huei; Hsu, Ming-Ta] Natl Yang Ming Univ, Inst Biochem & Mol Biol, Taipei 112, Taiwan.
    [Liu, Fu-Chin] Natl Yang Ming Univ, Inst Neurosci, Taipei 112, Taiwan.
    [Yang, Chu-Wen] Soochow Univ, Dept Microbiol, Taipei 111, Taiwan.
 RP Tsai, TF, Natl Yang Ming Univ, Dept Life Sci, Taipei 112, Taiwan.
 EM tftsai@ym.edu.tw
 FU National Research Program for Genomic Medicine (NRPGM) ; National
    Science Council ; National Science Council [NRPGM 95HC007,
    NSC96-2752-B-010004-PAE, NSC97-2320-B-010-015-MY3]; Ministry of
    Education 
 FX We thank Dr. Lian-Fu Deng (Affiliated Ruijin Hospital of Shanghai
    Second Medical University, Shanghai Institute of Traumatology and
    Orthopeadics); Dr. An-Guor Wang (Taipei Veterans General Hospital); Dr.
    Ming-Ling Kuo (Chang Gung University); Dr. Chih-Cheng Chen (Academia
    Sinica); and Dr. Alan M. Lin, Dr. Hen-Li Chen, Dr. Chun-Ming Chen, Dr.
    ChiChang Juan, Yi-Shin Lai, Ching-Wen Cheng, and Hui-Wen Zhuang
    (National Yang-Ming University) for their insight and technical
    assistance. We thank the Microarray and Gene Expression Analysis Core
    Facility of the National Yang-Ming University Genome Research Center.
    The Core Facility is supported by the National Research Program for
    Genomic Medicine (NRPGM), National Science Council. We acknowledge
    support from the National Science Council (NRPGM 95HC007,
    NSC96-2752-B-010004-PAE, and NSC97-2320-B-010-015-MY3) and a grant from
    the Ministry of Education, Aim for the Top University Plan.
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 NR 57
 TC 15
 PU COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT
 PI WOODBURY
 PA 500 SUNNYSIDE BLVD, WOODBURY, NY 11797-2924 USA
 SN 0890-9369
 J9 GENE DEVELOP
 JI Genes Dev.
 PD MAY 15
 PY 2009
 VL 23
 IS 10
 BP 1183
 EP 1194
 DI 10.1101/gad.1779509
 PG 12
 SC Cell Biology; Developmental Biology; Genetics & Heredity
 GA 447QD
 UT ISI:000266205300006
 ER
 
 PT J
 AU Yang, J
    Ahmed, A
    Ashcroft, M
 AF Yang, Jun
    Ahmed, Afshan
    Ashcroft, Margaret
 TI Activation of a unique p53-dependent DNA damage response
 SO CELL CYCLE
 LA English
 DT Letter
 DE small molecule activator; DNA damage response; hypoxia
 ID CANCER-THERAPY; P53; ANTAGONISTS; PATHWAY; MDM2
 C1 [Ahmed, Afshan; Ashcroft, Margaret] UCL, Ctr Cell Signalling & Mol Genet, Div Med, Hypoxia Signalling & Angiogenesis Lab, London WC1E 6JJ, England.
    [Yang, Jun; Ashcroft, Margaret] Canc Res UK Ctr Canc Therapeut, Inst Canc Res, Cell Growth Regulat & Angiogenesis Team, Sutton, Surrey, England.
 RP Ashcroft, M, UCL, Ctr Cell Signalling & Mol Genet, Div Med, Hypoxia
    Signalling & Angiogenesis Lab, Rayne Bldg,5 Univ St, London WC1E 6JJ,
    England.
 EM m.ashcroft@ucl.ac.uk
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 NR 9
 TC 4
 PU LANDES BIOSCIENCE
 PI AUSTIN
 PA 1002 WEST AVENUE, 2ND FLOOR, AUSTIN, TX 78701 USA
 SN 1538-4101
 J9 CELL CYCLE
 JI Cell Cycle
 PD MAY 15
 PY 2009
 VL 8
 IS 10
 BP 1630
 EP 1632
 PG 3
 SC Cell Biology
 GA 446IP
 UT ISI:000266115600031
 ER
 
 PT J
 AU Yang, Q
    Mao, ZX
 AF Yang, Qian
    Mao, Zixu
 TI Regulation of MEF2s by chaperone-mediated autophagy
 SO CELL CYCLE
 LA English
 DT Editorial Material
 ID SURVIVAL
 C1 [Mao, Zixu] Emory Univ, Sch Med, Dept Pharmacol, Atlanta, GA 30322 USA.
    Emory Univ, Sch Med, Dept Neurol, Atlanta, GA 30322 USA.
 RP Mao, ZX, Emory Univ, Sch Med, Dept Pharmacol, Atlanta, GA 30322 USA.
 EM zmao@pharm.emory.edu
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 NR 8
 TC 0
 PU LANDES BIOSCIENCE
 PI AUSTIN
 PA 1002 WEST AVENUE, 2ND FLOOR, AUSTIN, TX 78701 USA
 SN 1538-4101
 J9 CELL CYCLE
 JI Cell Cycle
 PD MAY 1
 PY 2009
 VL 8
 IS 9
 BP 1304
 EP 1304
 PG 1
 SC Cell Biology
 GA 446IF
 UT ISI:000266114600004
 ER
 
 PT J
 AU Yuan, K
    Li, N
    Huo, Y
    Yan, F
    Yang, Y
    Ward, T
    Jin, CJ
    Yao, XB
 AF Yuan, Kai
    Li, Na
    Huo, Yuda
    Yan, Feng
    Yang, Yong
    Ward, Tarsha
    Jin, Changjiang
    Yao, Xuebiao
 TI Recruitment of separase to mitotic chromosomes is regulated by Aurora B
 SO CELL CYCLE
 LA English
 DT Article
 DE chromosome segregation; chromosome arm; separase; cohesin; aurora B
 ID SISTER-CHROMATID SEPARATION; SPINDLE-ASSEMBLY CHECKPOINT; HUMAN-CELLS;
    CENTROSOME DUPLICATION; ANAPHASE; COHESIN; CLEAVAGE; KINETOCHORE;
    INHIBITION; METAPHASE
 AB Accurate segregation of chromosome, initiated by abrupt and
    irreversible dissolution of sister-chromatid cohesion at anaphase, is
    crucial for the faithful inheritance of parental genomes during
    eukaryotic cell division. The dissolution of sister-chromatid cohesion
    is catalyzed by separase after the destruction of securin by the
    anaphase-promoting complex/cyclosome (APC/C). However, separase was
    localized to the mitotic centrosome, raising the question as how
    separase hydrolyzes sister-chromatid cohesion of centromere at the
    anaphase onset. Here we show that separase is associated with mitotic
    chromosomes and this association is regulated by Aurora B kinase. Using
    a panel of separase antibodies, we found that separase protein was
    accumulated in mitosis and degraded at the end of telophase. To study
    the spatiotemporal distribution of separase in mitosis, we carried out
    immunofluorescence microscopic analyses. Surprisingly, separase was
    found to be associated with mitotic chromosomes from prophase to
    metaphase and dissociated from the chromosomes in anaphase right after
    sister chromatids separation. Staining of isolated mitotic chromosomes
    from Nocodazole-arrested cells revealed that separase is concentrated
    at the centromeric cohesion. To examine if any mitotic kinases are
    responsible for chromosomal localization of separase in mitosis, we
    carried out RNAi-mediated knockdown and found that association of
    separase with mitotic chromosomes was a function of Aurora B.
    Consistent with the phenotype seen in the Aurora B-repressed cells,
    inhibition of Aurora B kinase by hersperadin prevents the association
    of separase with chromosomes. Our results suggest that Aurora B kinase
    activity helps coordinate the association of separase with chromosome
    and the initiation of sister-chromatid separation.
 C1 [Yuan, Kai; Li, Na; Huo, Yuda; Yan, Feng; Yang, Yong; Jin, Changjiang; Yao, Xuebiao] Univ Sci & Technol China, Sch Life Sci, Hefei 230027, Anhui, Peoples R China.
    [Yuan, Kai; Li, Na; Huo, Yuda; Yan, Feng; Yang, Yong; Jin, Changjiang; Yao, Xuebiao] Univ Sci & Technol China, Anhui Lab Cellular Dynam & Chem Biol, Hefei 230027, Anhui, Peoples R China.
    [Yuan, Kai; Yan, Feng; Yang, Yong; Ward, Tarsha] Morehouse Sch Med, Dept Physiol, Atlanta, GA 30310 USA.
 RP Jin, CJ, Univ Sci & Technol China, Lab Cellular Dynam, 96 Jinzhai Rd,
    Hefei 230027, Anhui, Peoples R China.
 EM jincj@ustc.edu.cn
    yaoxb@ustc.edu.cn
 FU Chinese Academy of Science [KSCX1-YW-R65, KSCX2YW- H10]; Chinese 973
    project [2002CB713700, 2007CB914503, 2006CB943600]; Chinese Natural
    Science Foundation [30270654, 30070349, 90508002, 30121001]; American
    Cancer Society [RPG-99-173-01]; Georgia Cancer Coalition Breast Cancer
    Research ; University of Science and Technology of China USTC 
 FX We thank Dr. Zou Hui for generously providing the separase antibody. We
    thank the anonymous reviewers for comments on the manuscript. This work
    is supported by grants from the Chinese Academy of Science
    KSCX1-YW-R65, KSCX2YW- H10), Chinese 973 project 2002CB713700,
    2007CB914503 and 2006CB943600), Chinese Natural Science Foundation
    30270654, 30070349, 90508002 and 30121001), American Cancer Society
    RPG-99-173-01) and a Georgia Cancer Coalition Breast Cancer Research
    grant to X. Y.). K. Y. is supported by the innovation foundation from
    University of Science and Technology of China USTC).
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 NR 38
 TC 8
 PU LANDES BIOSCIENCE
 PI AUSTIN
 PA 1002 WEST AVENUE, 2ND FLOOR, AUSTIN, TX 78701 USA
 SN 1538-4101
 J9 CELL CYCLE
 JI Cell Cycle
 PD MAY 1
 PY 2009
 VL 8
 IS 9
 BP 1433
 EP 1443
 PG 11
 SC Cell Biology
 GA 446IF
 UT ISI:000266114600031
 ER
 
 PT J
 AU Yang, W
    Ng, P
    Zhao, M
    Hirankarn, N
    Lau, CS
    Mok, CC
    Chan, TM
    Wong, RWS
    Lee, KW
    Mok, MY
    Wong, SN
    Avihingsanon, Y
    Lee, TL
    Ho, MHK
    Lee, PPW
    Wong, WHS
    Lau, YL
 AF Yang, W.
    Ng, P.
    Zhao, M.
    Hirankarn, N.
    Lau, C. S.
    Mok, C. C.
    Chan, T. M.
    Wong, R. W. S.
    Lee, K. W.
    Mok, M. Y.
    Wong, S. N.
    Avihingsanon, Y.
    Lee, T. L.
    Ho, M. H. K.
    Lee, P. P. W.
    Wong, W. H. S.
    Lau, Y. L.
 TI Population differences in SLE susceptibility genes: STAT4 and BLK, but
    not PXK, are associated with systemic lupus erythematosus in Hong Kong
    Chinese
 SO GENES AND IMMUNITY
 LA English
 DT Article
 DE systemic lupus erythematosus; STAT4; PXK; BLK; population difference
 ID GENOME-WIDE ASSOCIATION; RHEUMATOID-ARTHRITIS; JAPANESE POPULATION;
    DISEASE; ITGAM; RISK; HAPLOTYPE; VARIANTS
 AB In this study, we compared the association of several newly discovered
    susceptibility genes for systemic lupus erythematosus (SLE) between
    populations of European origin and two Asian populations. Using 910 SLE
    patients and 1440 healthy controls from Chinese living in Hong Kong,
    and 278 SLE patients and 383 controls in Thailand, we studied
    association of STAT4, BLK and PXK with the disease. Our data confirmed
    association of STAT4 (rs7574865, odds ratio (OR) 1.71, P = 3.55 x
    10(-23)) and BLK (rs13277113, OR = 0.77, P = 1.34 x 10(-5)) with SLE.
    It was showed that rs7574865 of STAT4 is also linked to hematologic
    disorders and potentially some other subphenotypes of the disease. More
    than one genetic variant in STAT4 were found to be associated with the
    disease independently in our populations (rs7601754, OR = 0.59, P =
    1.39 x 10(-9), and P = 0.00034 when controlling the effect of
    rs7574865). With the same set of samples, however, our study did not
    detect any significant disease association for PXK, a risk factor for
    populations of European origin (rs6445975, joint P = 0.36, OR = 1.06,
    95% confidence interval: 0.93-1.21). Our study indicates that some of
    the susceptibility genes for this disease may be population specific.
    Genes and Immunity (2009) 10, 219-226; doi:10.1038/gene.2009.1;
    published online 19 February 2009
 C1 [Yang, W.; Ng, P.; Zhao, M.; Lee, T. L.; Ho, M. H. K.; Lee, P. P. W.; Wong, W. H. S.; Lau, Y. L.] Univ Hong Kong, Queen Mary Hosp, Dept Paediat & Adolescent Med, Li Ka Shing Fac Med, Hong Kong, Hong Kong, Peoples R China.
    [Hirankarn, N.] Chulalongkorn Univ, Fac Med, Dept Microbiol, Lupus Res Unit, Bangkok 10330, Thailand.
    [Lau, C. S.; Chan, T. M.; Wong, R. W. S.; Mok, M. Y.] Univ Hong Kong, Li Ka Shing Fac Med, Dept Med, Hong Kong, Hong Kong, Peoples R China.
    [Mok, C. C.] Tuen Mun Hosp, Dept Med, Hong Kong, Hong Kong, Peoples R China.
    [Lee, K. W.] Pamela Youde Nethersole Eastern Hosp, Dept Med, Hong Kong, Hong Kong, Peoples R China.
    [Wong, S. N.] Tuen Mun Hosp, Dept Paediat & Adolescent Med, Hong Kong, Hong Kong, Peoples R China.
    [Avihingsanon, Y.] Chulalongkorn Univ, Fac Med, Dept Med, Lupus Res Unit, Bangkok 10330, Thailand.
 RP Lau, YL, Univ Hong Kong, Queen Mary Hosp, Dept Paediat & Adolescent
    Med, Li Ka Shing Fac Med, Hong Kong, Hong Kong, Peoples R China.
 EM lauylung@hkucc.hku.hk
 FU Shun Tak District Min Yuen Tong of Hong Kong ; Edward Sai Kim Hotung
    Paediatric Education and Research Fund ; University Postgraduate
    Studentship ; UGC ; UHK [200711159155]
 FX This study was partially supported by the Shun Tak District Min Yuen
    Tong of Hong Kong. PN and MZ were supported by Edward Sai Kim Hotung
    Paediatric Education and Research Fund, and University Postgraduate
    Studentship. WY acknowledges support from UGC, UHK (200711159155).
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 NR 22
 TC 20
 PU NATURE PUBLISHING GROUP
 PI LONDON
 PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
 SN 1466-4879
 J9 GENES IMMUN
 JI Genes Immun.
 PD APR
 PY 2009
 VL 10
 IS 3
 BP 219
 EP 226
 DI 10.1038/gene.2009.1
 PG 8
 SC Genetics & Heredity; Immunology
 GA 444DS
 UT ISI:000265961300003
 ER
 
 PT J
 AU Chu, X
    Dong, C
    Lei, R
    Sun, L
    Wang, Z
    Dong, Y
    Shen, M
    Wang, Y
    Wang, B
    Zhang, K
    Yang, L
    Li, Y
    Yuan, W
    Wang, Y
    Song, H
    Jin, L
    Xiong, M
    Huang, W
 AF Chu, X.
    Dong, C.
    Lei, R.
    Sun, L.
    Wang, Z.
    Dong, Y.
    Shen, M.
    Wang, Y.
    Wang, B.
    Zhang, K.
    Yang, L.
    Li, Y.
    Yuan, W.
    Wang, Y.
    Song, H.
    Jin, L.
    Xiong, M.
    Huang, W.
 TI Polymorphisms in the interleukin 3 gene show strong association with
    susceptibility to Graves' disease in Chinese population
 SO GENES AND IMMUNITY
 LA English
 DT Article
 DE Graves' disease; IL3; single-nucleotide polymorphism
 ID AUTOIMMUNE THYROID-DISEASE; RHEUMATOID-ARTHRITIS; CATION TRANSPORTER;
    JAPANESE PATIENTS; HUMAN IL-3; LINKAGE; GENOME; LOCI; VARIANTS; PROMOTER
 AB Graves' disease (GD) is a common organ-specific autoimmune disorder,
    which is multifactorial and develops in genetically susceptible
    individuals. We had earlier mapped a susceptibility locus for GD to
    chromosome 5q31-33 in a linkage study. Here we used tag
    single-nucleotide polymorphisms (SNPs) to search for genetic variants
    associated with GD, and examined 19 functional candidate genes in this
    chromosomal region. We identified 192 polymorphisms by re-sequencing
    the candidate genes, and selected 51 tagSNPs to genotype in a
    case-control collection of 1118 south Han Chinese subjects (428 cases
    and 690 controls). Initial analysis suggested that a non-synonymous SNP
    rs40401 (P27S) of interleukin 3 (IL3) was associated with GD, and
    further fine-mapping showed that rs40401, or its perfect proxy SNP
    rs31480 in the 50 flanking region of IL3, fully accounted for the
    association signal at this locus. We replicated significant association
    of rs40401 with GD in an independent sample collection of 839 north Han
    Chinese subjects. A combined analysis revealed strong validation of
    this association (odds ratio (ORcommon) 1.63, combined P (P-comb) = 4 x
    10(-6) in the Recessive disease model). This study provides convincing
    evidence that the IL3 gene is a susceptibility locus for GD in the
    Chinese population. Genes and Immunity (2009) 10, 260-266;
    doi:10.1038/gene.2009.3; published online 5 March 2009
 C1 [Chu, X.; Lei, R.; Song, H.; Huang, W.] Shanghai Jiao Tong Univ, Ruijin Hosp, Sch Med, Shanghai 200025, Peoples R China.
    [Chu, X.; Dong, C.; Sun, L.; Wang, Z.; Shen, M.; Wang, Y.; Wang, B.; Zhang, K.; Yang, L.; Li, Y.; Yuan, W.; Wang, Y.; Jin, L.; Huang, W.] Chinese Natl Human Genome Ctr, Dept Genet, Shanghai MOST Key Lab Hlth & Dis Genom, Shanghai, Peoples R China.
    [Dong, Y.] Shanghai Jiao Tong Univ, Xinhua Hosp, Sch Med, Dept Endocrinol, Shanghai 200025, Peoples R China.
    [Jin, L.] Fudan Univ, Sch Life Sci, State Key Lab Genet Engn, Shanghai 200433, Peoples R China.
    [Xiong, M.] Univ Texas Houston Hlth Sci Ctr, Ctr Human Genet, Houston, TX USA.
 RP Huang, W, Shanghai Jiao Tong Univ, Ruijin Hosp, Sch Med, 197 Rui Jin II
    Rd, Shanghai 200025, Peoples R China.
 EM huangwei@chgc.sh.cn
 FU Chinese High-Tech Program [2006AA020706, 2006AA02A406]; National Key
    Project for Basic Research [2004CB518605]; Chinese National Natural
    Science Fund for Distinguished Young Scholars [30625019]; Shanghai
    Science and Technology Committee [06XD14015]; Chinese National Natural
    Science Fund [30771029]
 FX We gratefully acknowledge Prof Zhu Chen for insightful instruction.
    This work was supported by the grants from Chinese High-Tech Program
    (2006AA020706, 2006AA02A406), National Key Project for Basic Research
    (2004CB518605), Chinese National Natural Science Fund for Distinguished
    Young Scholars (30625019), Shanghai Science and Technology Committee
    (06XD14015) and Chinese National Natural Science Fund (30771029).
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 NR 36
 TC 6
 PU NATURE PUBLISHING GROUP
 PI LONDON
 PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
 SN 1466-4879
 J9 GENES IMMUN
 JI Genes Immun.
 PD APR
 PY 2009
 VL 10
 IS 3
 BP 260
 EP 266
 DI 10.1038/gene.2009.3
 PG 7
 SC Genetics & Heredity; Immunology
 GA 444DS
 UT ISI:000265961300008
 ER
 
 PT J
 AU Zeng, YW
    Yang, SM
    Cui, H
    Yang, XJ
    Xu, LM
    Du, J
    Pu, XY
    Li, ZC
    Cheng, ZQ
    Huang, XQ
 AF Zeng, Yawen
    Yang, Shuming
    Cui, Hong
    Yang, Xiaojuan
    Xu, Liming
    Du, Juan
    Pu, Xiaoying
    Li, Zichao
    Cheng, Zaiquan
    Huang, Xingqi
 TI QTLs of Cold Tolerance-Related Traits at the Booting Stage for NIL-RILs
    in Rice Revealed by SSR
 SO GENES & GENOMICS
 LA English
 DT Article
 DE cold tolerance-related traits; near-isogenic line at booting stage;
    quantitative trait loci (QTL); rice (Oryza sativa L.)
 ID ORYZA-SATIVA L.; NEAR-ISOGENIC LINES; JAPONICA RICE; LOCUS;
    IDENTIFICATION; POPULATION; YUNNAN; CHINA; YIELD; CROSS
 AB QTLs for cold tolerance-related traits at the booting stage using
    balanced population for 1525 recombinant inbred lines of near-isogenic
    lines (viz-NIL-RILs for BC5F3 and BC5F4 and BC5F5) over 3 years and two
    locations by backcrossing the strongly cold-tolerant landrace
    (Kunmingxiaobaigu) and a cold-sensitive cultivar (Towada) was analyzed.
    In this study, 676 microsatellite markers were employed to identify
    QTLs conferring cold tolerance at booting stage. Single marker analysis
    revealed that 12 markers associated with cold tolerance on chromosome
    1, 4 and 5. Using a LOD significance threshold of 3.0,compositive
    interval mapping based on a mixed linear model revealed eight QTLs for
    10 cold tolerance-related traits on chromosomes 1, 4, and 5. They were
    tentatively designated qCTB-1-1, qCTB-4-1, qCTB-4-2, qCTB-4-3,
    qCTB-4-4, qCTB4-5, qCTB-4-6, and qCTB-5-1. The marker intervals of them
    were narrowed to 0.3-6.8 cM. Genetic distances between the peaks of the
    QTL and nearest markers varied from 0 to 0.04 cM. We were noticed in
    some traits associated cold tolerance, such as qCTB-1-1 for 5 traits
    (plant height, panicle exsertion, spike length, blighted grains per
    spike and spikelet fertility), qCTB-4-1 for 8 traits (plant height,
    node length under spike, leaf length, leaf width, spike length, full
    grains per spike, total grains per spike and spikelet fertility),
    qCTB-4-2 for 3 traits (spike length, full grains per spike and spikelet
    fertility), qCTB5-1 for 5 traits (plant height, particle exsertion,
    blighted grains per spike, full grains per spike and spikelet
    fertility). The variance explained by a single QTL ranged from 0.80 to
    16.80%. Three QTLs (qCTB-1-1, qCTB-4-1, qCTB-4-2 were detected in two
    or more trials. Our study sets a foundation for cloning cold-tolerance
    genes and provides opportunities to understand the mechanism of cold
    tolerance at the booting stage.
 C1 [Zeng, Yawen; Yang, Shuming; Du, Juan; Pu, Xiaoying; Cheng, Zaiquan; Huang, Xingqi] Yunnan Acad Agr Sci, Biotechnol & Genet Resources Inst, Kunming 650205, Peoples R China.
    [Cui, Hong] Yunnan Univ, Sch Life Sci, Kunming 650001, Peoples R China.
    [Zeng, Yawen; Yang, Xiaojuan] Yunnan Agr Univ, Sch Agron & Biotechnol, Kunming 650201, Peoples R China.
    [Xu, Liming; Li, Zichao] China Agr Univ, Beijing 100094, Peoples R China.
 RP Zeng, YW, Yunnan Acad Agr Sci, Biotechnol & Genet Resources Inst,
    Kunming 650205, Peoples R China.
 EM zengyw1967@126.com
 FU National Natural Science Foundation of China [30571140, 39760042,
    30660092]; Yunnan Province Natural Science Foundation [2004CO01OZ];
    Cooperation Program between Province and Zhejiang Umiversty [2006YX
    12]; Yunnan Introduction and Foster Talent [2005PY01-14]
 FX This work was funded by the National Natural Science Foundation of
    China (Nos. 30571140, 39760042 and 30660092), and Yunnan Province
    Natural Science Foundation (No. 2004CO01OZ), Cooperation Program
    between Province and Zhejiang Umiversty from Yunnan provincial
    Scientific and Technology Department (2006YX 12) and Yunnan
    Introduction and Foster Talent (No. 2005PY01-14).
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 NR 30
 TC 2
 PU KOREAN SOC GENETICS
 PI SEOUL
 PA KOREAN SCIENCE & TECHNOLOGY CENTER, RM 1002, 635-4 YEOKSAM-DONG,
    KANGNAM, SEOUL, 135-703, SOUTH KOREA
 SN 1976-9571
 J9 GENES GENOM
 JI Genes Genom.
 PD APR
 PY 2009
 VL 31
 IS 2
 BP 143
 EP 154
 PG 12
 SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology;
    Genetics & Heredity
 GA 445DH
 UT ISI:000266029400004
 ER
 
 PT J
 AU Du, P
    Ling, YH
    Sang, XC
    Zhao, FM
    Xie, R
    Yang, ZL
    He, GH
 AF Du, Peng
    Ling, Ying-Hua
    Sang, Xian-Chun
    Zhao, Fang-Ming
    Xie, Rong
    Yang, Zheng-Lin
    He, Guang-Hua
 TI Gene Mapping Related to Yellow Green Leaf in a Mutant Line in Rice
    (Oryza sadva L.)
 SO GENES & GENOMICS
 LA English
 DT Article
 DE rice (Oryza sadva L.); yellow green leaf mutant; chlorophyll;
    fluorescence kinetic parameters; gene mapping
 ID CHLOROPHYLL SYNTHESIS; MG-CHELATASE; BIOSYNTHESIS; REGULATOR; MARKER;
    SYSTEM; SERIES; MAIZE; GUN4; DNA
 AB A mutant, which derived from the restorer line Jinhui10 treated with
    EMS, showed completely yellow green leaves, and it had low chlorophyll
    content and poor agronomic characteristics during the growing stage.
    The F, plants from the cross between normal x the mutant showed normal
    green leaves, and the segregation ratio of normal to yellow green
    leaves was 3: 1 in F-2 population. It indicated that the trait was
    controlled by a single recessive nuclear gene, temporarily designated
    as ygl3. The gene ygl3 was mapped between RM468 and RM3684 with genetic
    distances 8.4 cM and 1.8 cM on chromosome 3. This result would be used
    as genetic information for fine mapping and map-based cloning of ygl3
    gene.
 C1 [Du, Peng; Ling, Ying-Hua; Sang, Xian-Chun; Zhao, Fang-Ming; Yang, Zheng-Lin; He, Guang-Hua] Southwest Univ, Rice Res Inst, Key Lab Biotechnol & Crop Qual Improvement, Minist Agr, Chongqing 400715, Peoples R China.
    [Xie, Rong] Sichuan Acad Agr Sci, Rice & Sorghum Inst, Luzhou 646000, Sichuan, Peoples R China.
 RP He, GH, Southwest Univ, Rice Res Inst, Key Lab Biotechnol & Crop Qual
    Improvement, Minist Agr, Chongqing 400715, Peoples R China.
 EM hegh1968@yahoo.com.cn
 FU National Natural Sciences Foundation [30800598]; Excellent Youth
    Foundation Project of Chongqing [2008BA1033]; Natural Sciences
    Foundation Project of Chongqing [2008BB1258]; Fine Animals and Plants
    Breeding Project of Chongqing [2007AA1019]
 FX This research was supported by the National Natural Sciences Foundation
    (30800598), the Excellent Youth Foundation Project of Chongqing (CSTC,
    2008BA1033), the Natural Sciences Foundation Project of Chongqing
    (CSTC, 2008BB1258) and the Fine Animals and Plants Breeding Project of
    Chongqing (CSTC, 2007AA1019).
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 NR 32
 TC 1
 PU KOREAN SOC GENETICS
 PI SEOUL
 PA KOREAN SCIENCE & TECHNOLOGY CENTER, RM 1002, 635-4 YEOKSAM-DONG,
    KANGNAM, SEOUL, 135-703, SOUTH KOREA
 SN 1976-9571
 J9 GENES GENOM
 JI Genes Genom.
 PD APR
 PY 2009
 VL 31
 IS 2
 BP 165
 EP 171
 PG 7
 SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology;
    Genetics & Heredity
 GA 445DH
 UT ISI:000266029400006
 ER
 
 PT J
 AU French, D
    Yang, WJ
    Cheng, C
    Raimondi, SC
    Mullighan, CG
    Downing, JR
    Evans, WE
    Pui, CH
    Relling, MV
 AF French, Deborah
    Yang, Wenjian
    Cheng, Cheng
    Raimondi, Susana C.
    Mullighan, Charles G.
    Downing, James R.
    Evans, William E.
    Pui, Ching-Hon
    Relling, Mary V.
 TI Acquired variation outweighs inherited variation in whole genome
    analysis of methotrexate polyglutamate accumulation in leukemia
 SO BLOOD
 LA English
 DT Article
 ID ACUTE LYMPHOBLASTIC-LEUKEMIA; PEDIATRIC-ONCOLOGY-GROUP; ACUTE
    LYMPHOCYTIC-LEUKEMIA; FOLATE CARRIER EXPRESSION; HIGH-DOSE
    METHOTREXATE; CANCER-GROUP CCG; GENE-EXPRESSION; IN-VIVO;
    FOLYLPOLYGLUTAMATE SYNTHETASE; DIHYDROFOLATE-REDUCTASE
 AB Methotrexate polyglutamates (MTXPGs) determine in vivo efficacy in
    acute lymphoblastic leukemia (ALL). MTXPG accumulation differs by
    leukemic subtypes, but genomic determinants of MTXPG variation in ALL
    remain unclear. We analyzed 3 types of whole genome variation: leukemia
    cell gene expression and somatic copy number variation, and inherited
    single nucleotide polymorphism (SNP) genotypes and determined their
    association with MTXPGs in leukemia cells. Seven genes (FHOD3, IMPA2,
    ME2, RASSF4, SLC39A6, SMAD2, and SMAD4) displayed all 3 types of
    genomic variation associated with MTXPGs (P < .05 for gene expression,
    P < .01 for copy number variation and SNPs): 6 on chromosome 18 and 1
    on chromosome 10. Increased chromosome 18 (P = .002) or 10 (P = .036)
    copy number was associated with MTXPGs even after adjusting for ALL
    subtype. The expression of the top 7 genes in leukemia cells accounted
    for more variation in MTXPGs (46%) than did the expression of the top 7
    genes in normal HapMap cell lines (20%). The top 7 inherited SNPs in
    patients accounted for approximately the same degree of variation (17%)
    in MTXPGs as did the top 7 SNP genotypes in HapMap cell lines (20%). We
    conclude that acquired genetic variation in leukemia cells has a
    stronger influence on MTXPG accumulation than inherited genetic
    variation. (Blood. 2009;113:4512-4520)
 C1 [French, Deborah; Yang, Wenjian; Evans, William E.; Relling, Mary V.] St Jude Childrens Hosp, Dept Pharmaceut Sci, Memphis, TN 38105 USA.
    [Cheng, Cheng] St Jude Childrens Hosp, Dept Biostat, Memphis, TN 38105 USA.
    [Cheng, Cheng; Raimondi, Susana C.; Mullighan, Charles G.; Downing, James R.; Evans, William E.; Pui, Ching-Hon; Relling, Mary V.] St Jude Childrens Hosp, Hematol Malignancies Program, Memphis, TN 38105 USA.
    [Raimondi, Susana C.; Mullighan, Charles G.; Downing, James R.] St Jude Childrens Hosp, Dept Pathol, Memphis, TN 38105 USA.
    [Raimondi, Susana C.; Evans, William E.; Pui, Ching-Hon; Relling, Mary V.] Univ Tennessee, Memphis, TN USA.
    [Pui, Ching-Hon] St Jude Childrens Hosp, Dept Oncol, Memphis, TN 38105 USA.
 RP Relling, MV, St Jude Childrens Hosp, Dept Pharmaceut Sci, 262 Danny
    Thomas Pl, Memphis, TN 38105 USA.
 EM mary.relling@stjude.org
 FU National Cancer Institute [CA51001, CA78224, CA21765]; National
    Institutes of Health/National Institute of General Medical Sciences
    Pharmacogenetics Research Network and Database [U01GM61393, UO1GM61374,
    PS207998, PS207999]; Phelan Foundation ; State of Tennessee ; American
    Lebanese Syrian Associated Charities 
 FX We thank the patients and their families, and our research faculty and
    staff for participating; Dr J. Carl Panetta for the pharmacokinetic
    analysis; Nancy Kornegay, Diana Chan, and MarkWilkinson for database
    and computer expertise; and Yaqin Chu, May Chung, Natalya Lenchik,
    Margaret Needham, Emily Melton, and Siamac Salehy for outstanding
    technical assistance.
    This work was supported by National Cancer Institute (CA51001, CA78224,
    CA21765), the National Institutes of Health/National Institute of
    General Medical Sciences Pharmacogenetics Research Network and Database
    (U01GM61393, UO1GM61374; www. pharmgkb. org PS207998 and PS207999), the
    Phelan Foundation, a Center of Excellence grant from the State of
    Tennessee, and the American Lebanese Syrian Associated Charities.
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 NR 59
 TC 10
 PU AMER SOC HEMATOLOGY
 PI WASHINGTON
 PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
 SN 0006-4971
 J9 BLOOD
 JI Blood
 PD MAY 7
 PY 2009
 VL 113
 IS 19
 BP 4512
 EP 4520
 DI 10.1182/blood-2008-07-172106
 PG 9
 SC Hematology
 GA 443LC
 UT ISI:000265910300012
 ER
 
 PT J
 AU Liu, CY
    Yang, Q
    Cupples, LA
    Melgs, JB
    Dupuis, J
 AF Liu, Chunyu
    Yang, Qiong
    Cupples, L. Adrienne
    Melgs, James B.
    Dupuis, Josee
 TI Selection of the Most Informative Individuals From Families With
    Multiple Siblings for Association Studies
 SO GENETIC EPIDEMIOLOGY
 LA English
 DT Article
 DE linkage analysis; association study; linkage disequilibrium;
    identity-by-descent (IBD)
 ID QUANTITATIVE-TRAIT LOCI; LINKAGE DISEQUILIBRIUM; POWER; PAIRS
 AB Association analyses may follow an initial linkage analysis for mapping
    and identifying genes underlying complex quantitative traits and may be
    conducted on unrelated subsets of individuals where only one member of
    a family is included. We evaluate two methods to select one sibling per
    sibship when multiple siblings are available: (1) one sibling with the
    most extreme trait value; and (2) one sibling using a combination score
    statistic based on extreme trait values and identity-by-descent sharing
    information. We compare the type 1 error and power. Furthermore, we
    compare these selection strategies with a strategy that randomly
    selects one sibling per sibship and with an approach that includes all
    siblings, using both simulation Study and an application to fasting
    blood glucose in the Framingham Heart Study. When genetic effect is
    homogeneous, we find that using the combination score call increase
    power by 30-40% compared to a random selection strategy, and loses only
    8-13% of power compared to the full sibship analysis, across all
    additive models considered, but offers at least 50% genotyping cost
    saving. In the presence of genetic heterogeneity, the score of fers a
    50% increase in power over a random selection strategy, but there is
    substantial loss compared to the full sibship analysis. In application
    to fasting blood sample, two SNPs are found in common for the selection
    strategies and the full sample among the 10 highest ranked single
    nucleotide polymorphisms. The EV strategy tends to agree with the
    IBD-EV strategy and the analysis of the full sample. Genet. Epidemiol.
    33:299-307, 2009. (C) 2008 Wiley-Liss, Inc.
 C1 [Liu, Chunyu] Biogen Idec, Dept Drug Discovery, Genet & Genom, Cambridge, MA USA.
    [Yang, Qiong; Cupples, L. Adrienne; Dupuis, Josee] Boston Univ, Dept Biostat, Boston, MA 02215 USA.
    [Melgs, James B.] Massachusetts Gen Hosp, Div Gen Med, Boston, MA 02114 USA.
    [Melgs, James B.] Harvard Univ, Sch Med, Boston, MA USA.
 RP Liu, CY, Biogen Idec, Dept Drug Discovery, Genet & Genom, 12 Cambridge
    Ctr, Cambridge, MA USA.
 EM chunyu.liu@biogenidec.com
 FU NIH NCRR [1S10RR163736-01A1]; National Heart, Lung and Blood
    Institute's Framingham Heart Study [N01-HC-25195]; American Diabetes
    Association 
 FX Contract grant sponsor: NIH NCRR; Contract grant number:
    1S10RR163736-01A1; Contract grant sponsor: National Heart, Lung and
    Blood Institute's Framingham Heart Study; Contract grant number:
    N01-HC-25195; Contract grant sponsor: American Diabetes Association.
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 NR 18
 TC 0
 PU WILEY-LISS
 PI HOBOKEN
 PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA
 SN 0741-0395
 J9 GENET EPIDEMIOL
 JI Genet. Epidemiol.
 PD MAY
 PY 2009
 VL 33
 IS 4
 BP 299
 EP 307
 DI 10.1002/gepi.20380
 PG 9
 SC Genetics & Heredity; Public, Environmental & Occupational Health
 GA 440UJ
 UT ISI:000265724900003
 ER
 
 PT J
 AU Wang, L
    Sun, LH
    Zhang, YL
    Wu, HW
    Li, C
    Pan, ZW
    Lu, YJ
    Yang, BF
 AF Wang, Ling
    Sun, Lihua
    Zhang, Yanli
    Wu, Huiwei
    Li, Chao
    Pan, Zhenwei
    Lu, Yanjie
    Yang, Baofeng
 TI Ionic Mechanisms Underlying Action Potential Prolongation by Focal
    Cerebral Ischemia in Rat Ventricular Myocytes
 SO CELLULAR PHYSIOLOGY AND BIOCHEMISTRY
 LA English
 DT Article
 DE Cerebral ischemia; Arrhythmia; QT prolongation; Ion currents
 ID OUTWARD POTASSIUM CURRENT; CARDIAC AUTONOMIC DERANGEMENT; CURRENT I-TO;
    MOLECULAR-BASIS; MESSENGER-RNA; QT INTERVAL; K+ CURRENT; STROKE;
    CHANNEL; REPOLARIZATION
 AB Despite prolongation of the QTc interval in humans during cerebral
    ischemia, little is known about the mechanisms that underlie these
    actions. Cerebral ischemic model was established by middle cerebral
    artery occlusion (MCAO) for 24 h. In rat ventricular myocytes, the
    effect of cerebral ischemia on action potential duration (APD) and
    underlying electrophysiologic mechanisms were investigated by
    whole-cell patch clamp. We demonstrated that heart rate-corrected QT
    interval and APD were prolonged with frequent occurrence of ventricular
    tachyarrhythmias in a rat model of MCAO. The I-Na density was overall
    smaller in cerebral ischemic myocytes relative to sham myocytes (P <
    0.01). The Nav1.5 protein and mRNA levels (pore-forming subunit for
    I-Na) were decreased by about 20% (P < 0.01) in cerebral ischemic rat
    hearts than those in sham-operated rat hearts. Peak transient outward
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    < 0.01) in cerebral ischemic rats. The peak amplitude of L-type Ca2+
    current (I-Ca,I-L) was increased and the inactivation kinetics were
    slowed (P < 0.01). Protein level of the pore-forming subunit for I-to
    was decreased, but that for I-Ca,I-L was increased. The inward
    rectifier K+ current (I-K1) at -120 mV and its protein level were
    unaffected. Our study represents the first documentation of I-Na, I-to
    and I-Ca,I-L channelopathy as the major ionic mechanism for cerebral
    ischemic QT prolongation. Copyright (C) 2009 S. Karger AG, Basel
 C1 [Wang, Ling] Harbin Med Coll, Dept Physiol, Harbin 150081, Heilongjiang, Peoples R China.
    [Lu, Yanjie; Yang, Baofeng] Harbin Med Coll, Inst Cardiovasc Res, Harbin 150081, Heilongjiang, Peoples R China.
    [Wang, Ling; Sun, Lihua; Zhang, Yanli; Wu, Huiwei; Li, Chao; Pan, Zhenwei; Lu, Yanjie; Yang, Baofeng] Harbin Med Coll, Dept Pharmacol, State Prov Key Lab China, Harbin 150081, Heilongjiang, Peoples R China.
 RP Wang, L, Harbin Med Coll, Dept Pharmacol, State Prov Key Lab China,
    Harbin 150081, Heilongjiang, Peoples R China.
 EM wangling66@yahoo.com.cn
 FU National Basic Research Program of China Foundation (973 Program)
    [2007CB512000, 2007CB512006]; Department of Education of Heilongjiang
    province of China Foundation [11521081]; Specialized Research Fund for
    the Doctoral Program of Higher Education [20060226019]
 FX This work was supported by the National Basic Research Program of China
    Foundation (973 Program) (NO 2007CB512000, 2007CB512006), the
    Department of Education of Heilongjiang province of China Foundation
    (NO 11521081), and the Specialized Research Fund for the Doctoral
    Program of Higher Education (20060226019).
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 NR 37
 TC 2
 PU KARGER
 PI BASEL
 PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND
 SN 1015-8987
 J9 CELL PHYSIOL BIOCHEM
 JI Cell. Physiol. Biochem.
 PY 2009
 VL 23
 IS 4-6
 BP 305
 EP 316
 DI 10.1159/000218177
 PG 12
 SC Cell Biology; Physiology
 GA 442TY
 UT ISI:000265864700009
 ER
 
 PT J
 AU Decker, WK
    Xing, D
    Li, S
    Robinson, SN
    Yang, H
    Steiner, D
    Komanduri, KV
    Shpall, EJ
 AF Decker, William K.
    Xing, Dongxia
    Li, Sufang
    Robinson, Simon N.
    Yang, Hong
    Steiner, David
    Komanduri, Krishna V.
    Shpall, Elizabeth J.
 TI Th-1 polarization is regulated by dendritic-cell comparison of MHC
    class I and class II antigens
 SO BLOOD
 LA English
 DT Article
 ID TRANSFER-RNA-SYNTHETASE; HELPER T-CELLS; LINKED RECOGNITION;
    IMMUNE-RESPONSES; CUTTING EDGE; CD83; AUTOANTIBODIES; MYOSITIS;
    INDUCTION; EXPRESSION
 AB In the control of T-helper type I (Th-1) polarization, dendritic cells
    (DCs) must interpret a complex array of stimuli, many of which are
    poorly understood. Here we demonstrate that Th-1 polarization is
    heavily influenced by DC-autonomous phenomena triggered by the loading
    of DCs with antigenically matched major histocompatibility complex
    (MHC) class I and class II determinants, that is, class I and II
    peptide epitopes exhibiting significant amino acid sequence overlap (
    such as would be physiologically present during infectious processes
    requiring Th-1 immunity for clearance). Data were derived from 13
    independent antigenic models including whole-cell systems,
    single-protein systems, and 3 different pairs of overlapping class I
    and II binding epitopes. Once loaded with matched class I and II
    antigens, these "Th-1 DCs" exhibited differential cytokine secretion
    and surface marker expression, a distinct transcriptional signature,
    and acquired the ability to enhance generation of CD8(+) T lymphocytes.
    Mechanistically, tRNA-synthetases were implicated as components of a
    putative sensor complex involved in the comparison of class I and II
    epitopes. These data provide rigorous conceptual explanations for the
    process of Th-1 polarization and the antigenic specificity of cognate
    T-cell help, enhance the understanding of Th-1 responses, and should
    contribute to the formulation of more effective vaccination strategies.
    ( Blood. 2009; 113: 4213-4223)
 C1 [Decker, William K.; Xing, Dongxia; Li, Sufang; Robinson, Simon N.; Yang, Hong; Steiner, David; Komanduri, Krishna V.; Shpall, Elizabeth J.] Univ Texas MD Anderson Canc Ctr, Dept Stem Cell Transplantat & Cellular Therapy, Houston, TX 77030 USA.
 RP Decker, WK, Univ Texas MD Anderson Canc Ctr, Dept Stem Cell
    Transplantat & Cellular Therapy, Unit 065,1515 Holcombe Blvd, Houston,
    TX 77030 USA.
 EM wkdecker@mdanderson.org
 FU National Institutes of Health [5-R01 CA061508-13]
 FX This work was supported in part by National Institutes of Health (NIH,
    Bethesda, MD) grant no. 5-R01 CA061508-13 ( to E.J.S.).
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 NR 49
 TC 1
 PU AMER SOC HEMATOLOGY
 PI WASHINGTON
 PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
 SN 0006-4971
 J9 BLOOD
 JI Blood
 PD APR 30
 PY 2009
 VL 113
 IS 18
 BP 4213
 EP 4223
 DI 10.1182/blood-2008-10-185470
 PG 11
 SC Hematology
 GA 442MW
 UT ISI:000265846300017
 ER
 
 PT J
 AU Beriou, G
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    Ashley, CW
    Yang, L
    Kuchroo, VK
    Baecher-Allan, C
    Hafler, DA
 AF Beriou, Gaelle
    Costantino, Cristina M.
    Ashley, Charles W.
    Yang, Li
    Kuchroo, Vijay K.
    Baecher-Allan, Clare
    Hafler, David A.
 TI IL-17-producing human peripheral regulatory T cells retain suppressive
    function
 SO BLOOD
 LA English
 DT Article
 ID GROWTH-FACTOR-BETA; ROR-GAMMA-T; TH17 CELLS; TGF-BETA; IN-VITRO;
    AUTOIMMUNE INFLAMMATION; RHEUMATOID-ARTHRITIS; HELPER-CELLS;
    DIFFERENTIATION; FOXP3
 AB Although implicated in antagonistic functions, both regulatory T cells
    (Tregs) and Th17 effector cells play an important role in controlling
    autoimmune pathogenesis. Paradoxically, recent studies indicate that
    Tregs have the capacity to produce interleukin-17 (IL-17), although the
    ability of these cells to retain their suppressive function remains
    unknown. Here we report that human Tregs within the CD4(+) CD45RA(-)
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    activated in the presence of the proinflammatory cytokines IL-1 beta
    and IL-6, whereas IL-17 secretion was inhibited by TGF beta. To assess
    the ability of a single Treg to secrete IL-17 and to suppress in vitro
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    IL-17(+)/FoxP3(+) Treg clones retain suppressive function and exhibit
    the plasticity to secrete IL-17 or suppress depending on the nature of
    the stimulus provided. IL-17 production by these Treg clones was
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 C1 [Beriou, Gaelle; Costantino, Cristina M.; Ashley, Charles W.; Yang, Li; Kuchroo, Vijay K.; Baecher-Allan, Clare; Hafler, David A.] Harvard Univ, Sch Med, Brigham & Womens Hosp, Div Mol Immunol,Ctr Neurol Dis, Boston, MA USA.
 RP Baecher-Allan, C, NRB 641,77 Ave Louis Pasteur, Boston, MA 02115 USA.
 EM callan@rics.bwh.harvard.edu
 FU National Multiple Sclerosis Society [FG1744A1, RG3825A1]; National
    Institutes of Health [U19AI070352, R01NS024247, P01AI03971,
    P01NS038037]; National Institute of Neurological Disorders and Stroke 
 FX This work was supported by the National Multiple Sclerosis Society
    grants FG1744A1 ( G. B.) and RG3825A1 ( C. B. A.) and by the National
    Institutes of Health grants U19AI070352, R01NS024247, P01AI03971, and
    P01NS038037 ( D. A. H.). D. A. H. is a Jacob Javits Scholar of the
    National Institute of Neurological Disorders and Stroke.
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 NR 35
 TC 72
 PU AMER SOC HEMATOLOGY
 PI WASHINGTON
 PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
 SN 0006-4971
 J9 BLOOD
 JI Blood
 PD APR 30
 PY 2009
 VL 113
 IS 18
 BP 4240
 EP 4249
 DI 10.1182/blood-2008-10-183251
 PG 10
 SC Hematology
 GA 442MW
 UT ISI:000265846300020
 ER
 
 PT J
 AU Chan, G
    Kalaitzidis, D
    Usenko, T
    Kutok, JL
    Yang, WT
    Mohi, MG
    Neel, BG
 AF Chan, Gordon
    Kalaitzidis, Demetrios
    Usenko, Tatiana
    Kutok, Jeffery L.
    Yang, Wentian
    Mohi, M. Golam
    Neel, Benjamin G.
 TI Leukemogenic Ptpn11 causes fatal myeloproliferative disorder via
    cell-autonomous effects on multiple stages of hematopoiesis
 SO BLOOD
 LA English
 DT Article
 ID TYROSINE-PHOSPHATASE SHP-2; COLONY-STIMULATING FACTOR; ONCOGENIC K-RAS;
    ERYTHROID-DIFFERENTIATION; NOONAN-SYNDROME; MOUSE MODEL; STEM-CELLS;
    IN-VIVO; STEM/PROGENITOR CELLS; FUNCTIONAL-ANALYSIS
 AB PTPN11, which encodes the tyrosine phosphatase SHP2, is mutated in
    approximately 35% of patients with juvenile myelomonocytic leukemia
    (JMML) and at a lower incidence in other neoplasms. To model JMML
    pathogenesis, we generated knockin mice that conditionally express the
    leukemia-associated mutant Ptpn11(D61Y). Expression of Ptpn11(D61Y) in
    all hematopoietic cells evokes a fatal myeloproliferative disorder
    (MPD), featuring leukocytosis, anemia, hepatosplenomegaly, and
    factor-independent colony formation by bone marrow (BM) and spleen
    cells. The Lin(-)Sca1(+)cKit(+) (LSK) compartment is expanded and
    "right-shifted," accompanied by increased stem cell factor (SCF)-evoked
    colony formation and Erk and Akt activation. However, repopulating
    activity is decreased in diseased mice, and mice that do engraft with
    Ptpn11(D61Y) stem cells fail to develop MPD. Ptpn11(D61Y) common
    myeloid progenitors (CMPs) and granulocyte-monocyte progenitors (GMPs)
    produce cytokine-independent colonies in a cell-autonomous manner and
    demonstrate elevated Erk and Stat5 activation in response to
    granulocyte-macrophage colony-stimulating factor (GM-CSF) stimulation.
    Ptpn11(D61Y) megakaryocyte-erythrocyte progenitors (MEPs) yield
    increased numbers of erythrocyte burst-forming units (BFU-Es), but MEPs
    and erythrocyte-committed progenitors (EPs) produce fewer erythrocyte
    colony-forming units (CFU-Es), indicating defective erythroid
    differentiation. Our studies provide a mouse model for Ptpn11-evoked
    MPD and show that this disease results from cell-autonomous and
    distinct lineage-specific effects of mutant Ptpn11 on multiple stages
    of hematopoiesis. (Blood. 2009; 113: 4414-4424)
 C1 [Chan, Gordon; Usenko, Tatiana; Neel, Benjamin G.] Ontario Canc Inst, Dept Stem Cell & Dev Biol, Toronto, ON M5G 1L7, Canada.
    [Chan, Gordon; Kalaitzidis, Demetrios; Yang, Wentian; Mohi, M. Golam; Neel, Benjamin G.] Harvard Univ, Sch Med, Beth Israel Deaconess Med Ctr, Boston, MA USA.
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 RP Chan, G, Ontario Canc Inst, Dept Stem Cell & Dev Biol, 101 Coll St,TMDT
    Rm 8-301, Toronto, ON M5G 1L7, Canada.
 EM gordon.chan@uhnresearch.ca
 FU National Institutes of Health (NIH; Bethesda, MD) [5T32-HL07623-20, RO1
    CA114945]; Deutsche Jose Carreras Leukamie-Stiftung e. V. (Munchen,
    Germany) ; American Society of Hematology (Washington, DC) 
 FX We thank Dr Norman Iscove (Ontario Cancer Institute [OCI]) for critical
    reading of this paper; John Daley (Dana-Farber Cancer Institute
    [DFCI]), Susan Lazo-Kallanian (DFCI), Michelle Tseng (Hospital for Sick
    Children, [HSC], Toronto, ON) Leanne Jamieson (HSC), and Pier-Andre
    Pentilla (HSC) for expert assistance with flow cytometry; and Jason
    Gilliland (Beth Israel Deaconess Medical Center, [BIDMC]) Sonja
    Boet-Whitaker (BIDMC), Tarun Sharma (OCI), and Ashley Sanders (OCI) for
    technical assistance.
    D. K. was supported by a National Institutes of Health (NIH; Bethesda,
    MD) postdoctoral institutional training grant in hematology
    (5T32-HL07623-20). M. G. M. was supported by a fellowship from the
    Deutsche Jose Carreras Leukamie-Stiftung e. V. (Munchen, Germany; and a
    scholar award from the American Society of Hematology (Washington, DC).
    This work was supported by NIH RO1 CA114945 awarded to B. G. N.
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 NR 42
 TC 13
 PU AMER SOC HEMATOLOGY
 PI WASHINGTON
 PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
 SN 0006-4971
 J9 BLOOD
 JI Blood
 PD APR 30
 PY 2009
 VL 113
 IS 18
 BP 4414
 EP 4424
 DI 10.1182/blood-2008-10-182626
 PG 11
 SC Hematology
 GA 442MW
 UT ISI:000265846300037
 ER
 
 PT J
 AU Huang, CW
    Cheng, YS
    Rouvier, R
    Yang, KT
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 AF Huang, Chang-Wen
    Cheng, Yu-Shin
    Rouvier, Roger
    Yang, Kuo-Tai
    Wu, Chean-Ping
    Huang, Hsiu-Lin
    Huang, Mu-Chiou
 TI Duck (Anas platyrhynchos) linkage mapping by AFLP fingerprinting
 SO GENETICS SELECTION EVOLUTION
 LA English
 DT Article
 ID QUAIL COTURNIX-JAPONICA; GENETIC-LINKAGE; SELECTION RESPONSES;
    DNA-SEQUENCES; MARKERS; GENOME; MAP; MICROSATELLITES; POULTRY; CATTLE
 AB Amplified fragment length polymorphism (AFLP) with multicolored
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 C1 [Huang, Chang-Wen; Yang, Kuo-Tai; Wu, Chean-Ping; Huang, Hsiu-Lin; Huang, Mu-Chiou] Natl Chung Hsing Univ, Dept Anim Sci, Taichung 402, Taiwan.
    [Huang, Chang-Wen] Acad Sinica, Inst Cellular & Organism Biol, Taipei 115, Taiwan.
    [Cheng, Yu-Shin] Council Agr, Livestock Res Inst, Tainan 712, Taiwan.
    [Rouvier, Roger] INRA, Stn Ameliorat Genet Anim, Ctr Rech Toulouse, F-31326 Castanet Tolosan, France.
    [Yang, Kuo-Tai] Acad Sinica, Inst Biomed Sci, Taipei 115, Taiwan.
    [Wu, Chean-Ping] Natl Chiayi Univ, Dept Anim Sci, Chiayi 600, Taiwan.
 RP Huang, MC, Natl Chung Hsing Univ, Dept Anim Sci, 250 Kuo Kung Rd,
    Taichung 402, Taiwan.
 EM amino0116@yahoo.com.tw
    yushin@mail.tlri.gov.tw
    rouvier@germinal.toulouse.inra.fr
    ktyang@ibms.sinica.edu.tw
    wucheanp@yahoo.com.tw
    hlhuang2001@yahoo.com
    mchuang@mail.nchu.edu.tw
 FU National Science Council, Executive Yuan, Taiwan [NSC92-2313-B005-106]
 FX This study was funded by a grant awarded by the National Science
    Council, Executive Yuan, Taiwan (Grant No. NSC92-2313-B005-106).
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 TC 3
 PU BIOMED CENTRAL LTD
 PI LONDON
 PA CURRENT SCIENCE GROUP, MIDDLESEX HOUSE, 34-42 CLEVELAND ST, LONDON W1T
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 SN 0999-193X
 J9 GENET SEL EVOL
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 PD MAR 17
 PY 2009
 VL 41
 AR 28
 DI 10.1186/1297-9686-41-28
 PG 8
 SC Agriculture, Dairy & Animal Science; Genetics & Heredity
 GA 438LC
 UT ISI:000265555900001
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    Wei, W
    Wang, ZZ
 AF Yang, Jian-She
    Jing, Xigang
    Li, Wen-Jian
    Hu, Xiang-Kai
    Wei, Wei
    Wang, Zhuan-Zi
 TI A new potential radiosensitizer- multi-walled carbon nanotubes modified
    by ammonium persulfate
 SO GENE THERAPY AND MOLECULAR BIOLOGY
 LA English
 DT Article
 DE ammonium persulfate; multi-walled carbon nanotubes
 ID ENDOCYTOSIS; PEPTIDES; GROWTH
 AB Here we prepare carbon nanotubes modified with ammonium persulfate,
    very short carbon nanotubes with 50-100 nanometer length was obtained,
    and the higher Z potential of 52 mV was detected, these supporting the
    successful modification. HeLa cells were irradiated with gamma rays via
    adding or absent above functionalized carbon nanotubes (f-WCNTs) into
    cell culture medium with different concentration and radiation dosage.
    Confocal microscopy images and fluorescence-labeled DNA detection
    verified the successfully pure multi-wailed carbon nanotubes (p-WCNTs)
    and f-WCNTs penetrated into cells. Compared with pure radiation, by MTT
    test, f-WCNTs induced cell death markedly with about 8.7 times higher
    than former one under little dose of radiation; meanwhile, no obvious
    toxicity was observed both in p-WCNTs and f-WCNTs without of radiation
    exposure. We hypothesized that large amount of hydroxyl and carbonyl
    organs on the surface of very short f-WCNTs changed into free radicals
    result from radiations led cell damage. These implied that f-WCNTs
    could be regarded as a new radiosensitizer.
 C1 [Yang, Jian-She] NW Normal Univ, Sch Life Sci, Lanzhou 730070, Peoples R China.
    [Yang, Jian-She; Jing, Xigang; Li, Wen-Jian; Hu, Xiang-Kai; Wei, Wei; Wang, Zhuan-Zi] Chinese Acad Sci, Inst Modern Phys, Lanzhou 730000, Peoples R China.
 RP Yang, JS, NW Normal Univ, Sch Life Sci, Lanzhou 730070, Peoples R China.
 EM yangjs@impcas.ac.cn
 FU MOST [2006CB705600]; National Natural Science Foundation [10475109]; K.
    C. Wong Education Foundation, Hong Kong [20060037]; China Postdoctoral
    Science Foundation [20060400686]
 FX Financial support from the 973 program of MOST (Grant No.
    2006CB705600). National Natural Science Foundation (Grant No.
    10475109), K. C. Wong Education Foundation, Hong Kong (Grant No.
    20060037) and China Postdoctoral Science Foundation (Grant No.
    20060400686) are greatly acknowledged.
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 TC 1
 PU GENE THERAPY PRESS
 PI ATHENS
 PA GREGORIOU AFXENTIOU 7, ALIMOS, ATHENS, 17455, GREECE
 SN 1529-9120
 J9 GENE THER MOL BIOL
 JI Gene Ther. Mol. Biol.
 PY 2008
 VL 12B
 BP 247
 EP 252
 PG 6
 SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology;
    Medicine, Research & Experimental
 GA 439JM
 UT ISI:000265623400010
 ER
 
 PT J
 AU Xu, Y
    Zheng, FQ
    Fang, J
    Zhang, QW
    Qin, YD
    Liu, Y
    Yang, RJ
    Wu, B
 AF Xu, Yin
    Zheng, Fei-qun
    Fang, Jia
    Zhang, Qun-wei
    Qin, Yi-de
    Liu, Yang
    Yang, Ren-jie
    Wu, Bin
 TI Attenuation of experimental liver fibrosis by hepatocyte growth factor
    gene delivery mediated by adenovirus
 SO GENE THERAPY AND MOLECULAR BIOLOGY
 LA English
 DT Article
 DE Liver fibrosis; Hepatocyte growth factor; Transforming growth factor;
    Gene therapy; Adenovirus
 ID ENDOTHELIAL-CELL MOTILITY; SCATTER FACTOR-RECEPTOR;
    CARBON-TETRACHLORIDE; MICE; RATS; REGENERATION; IDENTIFICATION;
    ACTIVATION; CIRRHOSIS; THERAPY
 AB The hepatocyte growth factor (HGF), originally identified and cloned as
    a potent mitogen for hepatocytes, has an essential part in the
    development and regeneration of the liver. In this study, HGF
    expression in vitro and in vivo was determined using ELISA. Rats were
    injected subcutaneously with CCl4 for eight weeks to induce liver
    fibrosis, and then divided randomly into groups for administration of
    various doses of adenovirus HGF (Ad-HGF) or vehicle. All rats were
    sacrificed 8 weeks after obtaining samples of serum and hepatic tissue.
    The results showed that glutamic oxaloacetic transaminase (GOT),
    glutamate pyruvate transaminase (GPT), total protein (TP), albumin
    (ALB), and total bilirubin (TBil) in serum were significantly recovered
    after gene therapy (P<0.05). Ad-HGF also attenuated the expression of
    TGF-beta 1 and the deposition of collagen. We conclude that intravenous
    administration of Ad-HGF may be useful for the treatment of fibrotic
    liver by promoting liver function recovery and collagenolytic
    capacities.
 C1 [Xu, Yin; Zheng, Fei-qun; Fang, Jia; Zhang, Qun-wei; Liu, Yang; Wu, Bin] Beijing Inst Radiat Med, Dept Expt Hematol, Beijing 100850, Peoples R China.
    [Xu, Yin; Fang, Jia; Qin, Yi-de] Anhui Med Univ, Basic Med Sci Sch, Hefei 230032, Anhui, Peoples R China.
    [Zheng, Fei-qun; Yang, Ren-jie] Peking Univ, Key Lab Carcinogenesis & Translat Res, Dept Intervent Therapy, Beijing Canc Hosp & Inst,Sch Oncol,Dept Intervent, Beijing 100036, Peoples R China.
 RP Wu, B, Beijing Inst Radiat Med, Dept Expt Hematol, 27 Taiping Rd,
    Beijing 100850, Peoples R China.
 EM renjieyang2007@163.com
    wubin63@yahoo.com.cn
 FU Chinese National High-Tech RD Program [2003AA216081]
 FX This project was supported by Chinese National High-Tech R&D Program,
    No. 2003AA216081.
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 NR 41
 TC 0
 PU GENE THERAPY PRESS
 PI ATHENS
 PA GREGORIOU AFXENTIOU 7, ALIMOS, ATHENS, 17455, GREECE
 SN 1529-9120
 J9 GENE THER MOL BIOL
 JI Gene Ther. Mol. Biol.
 PY 2008
 VL 12B
 BP 387
 EP 394
 PG 8
 SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology;
    Medicine, Research & Experimental
 GA 439JM
 UT ISI:000265623400021
 ER
 
 PT J
 AU Ding, KK
    Yang, CJ
    Shen, JJ
    Xu, LL
    Li, YL
    Zhou, PK
    Zeng, YJ
 AF Ding, Kuke
    Yang, Chunjie
    Shen, Jingjing
    Xu, Lili
    Li, Yanling
    Zhou, Pinkun
    Zeng, Yanjun
 TI Gamma-ray Up-regulated Holocarboxylase Synthetase Gene
 SO CELLULAR AND MOLECULAR NEUROBIOLOGY
 LA English
 DT Article
 DE Radiation effect; Gene expression; Holocarboxylase synthetase
 ID MULTIPLE CARBOXYLASE DEFICIENCY; DROSOPHILA-MELANOGASTER; HISTONE
    BIOTINYLATION; BIOTIN DEFICIENCY; EXPRESSION; MICE; PATTERNS
 AB Purpose: To investigate the effects of holocarboxylase synthetase (HCS)
    gene to irradiation in a time- and dose-dependent manner. Materials and
    methods: AHH-1 cells, Hela cells, and the nude mice inoculated with
    tumor cells were exposed to gamma-ray of cobalt 60. The mRNA level of
    HCS was detected using real-time PCR. The profiles of mRNA of HCS after
    radiation were analyzed and described. Results: The expression of HCS
    gene was higher in AHH-1 cells than that in Hela cells. Furthermore,
    both AHH-1 and Hela displayed similar time-dependent transcriptional
    levels of HCS gene to radiations at the dose of 2 and 10 Gy. We set the
    parameters of D, V, R, F, N to quantitatively analyze HCS gene
    regulation in response to irradiation. We also observed that
    irradiation resulted in higher levels of HCS in human hepatocyte
    xenografts, compared with three other types of human tumor xenografts.
    2 and 4 Gy radiation had little influence on the HCS gene of human lung
    cancer and brain cancer, mammary gland cancer was more sensitive to the
    4 Gy gamma-ray dose compared with the 2 Gy gamma-ray dose. Conclusion:
    HCS is a good radiation-responsive gene. It may be used as a candidate
    for developing novel biomarkers of radiation damage and it has a great
    potential to be used in radiation-therapy of liver tumors.
 C1 [Zeng, Yanjun] Beijing Univ Technol, Biomed Engn Sch, Beijing 100124, Peoples R China.
    [Ding, Kuke; Shen, Jingjing; Xu, Lili; Li, Yanling] Capital Med Univ, Biomed Engn Sch, Beijing 100069, Peoples R China.
    [Ding, Kuke; Zhou, Pinkun] Beijing Inst Radiat Med, Dept Radiat Toxicol & Oncol, Beijing 100850, Peoples R China.
    [Yang, Chunjie] Hebei Med Univ, Hosp 2, Shijiazhuang 050000, Hebei Province, Peoples R China.
 RP Zeng, YJ, Beijing Univ Technol, Biomed Engn Sch, 100 Pingleyuan Rd,
    Beijing 100124, Peoples R China.
 EM yjzeng@bjut.edu.cn
 FU National Natural Science Foundation of China [30770533]; Chinese
    National High Technology "863'' Programs [2004AA221160]; foundation of
    Beijing municipal education commission [Km200710025007]
 FX This study was supported by the grants from National Natural Science
    Foundation of China (No. 30770533) and Chinese National High Technology
    "863'' Programs (No. 2004AA221160), and the foundation of Beijing
    municipal education commission (No. Km200710025007).
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 NR 17
 TC 0
 PU SPRINGER/PLENUM PUBLISHERS
 PI NEW YORK
 PA 233 SPRING ST, NEW YORK, NY 10013 USA
 SN 0272-4340
 J9 CELL MOL NEUROBIOL
 JI Cell. Mol. Neurobiol.
 PD MAY
 PY 2009
 VL 29
 IS 3
 BP 383
 EP 389
 DI 10.1007/s10571-008-9330-x
 PG 7
 SC Cell Biology; Neurosciences
 GA 438SI
 UT ISI:000265575300010
 ER
 
 PT J
 AU Wang, DD
    Weng, QJ
    Zhang, L
    He, QJ
    Yang, B
 AF Wang, Duoduo
    Weng, Qinjie
    Zhang, Lei
    He, Qiaojun
    Yang, Bo
 TI VEGF and Bcl-2 Interact Via MAPKs Signaling Pathway in the Response to
    Hypoxia in Neuroblastoma
 SO CELLULAR AND MOLECULAR NEUROBIOLOGY
 LA English
 DT Article
 DE Hypoxia; VEGF; Bcl-2; MAPKs
 ID ACTIVATED PROTEIN-KINASE; GROWTH-FACTOR VEGF; P38 MAPK; C-JUN;
    GENE-TRANSCRIPTION; PROSTATE CARCINOMA; INDUCED APOPTOSIS; OXIDATIVE
    STRESS; CANCER-CELLS; IN-VIVO
 AB Tumor hypoxia has been reported to be a negative prognostic factor in a
    number of tumor sites, which suggests a positive correlation between
    tumor hypoxia and increased metastatic efficiency. Evidence shows that
    vascular endothelial growth factor (VEGF) stimulates angiogenesis in
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    death. Human neuroblastoma cells (CHP126) were exposed to moderate
    hypoxia for different time spans to explore the molecular stress
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    but these effects were reversed with the extension of hypoxic
    treatment. Hypoxia also activated MAPKs signaling pathways in a
    time-relative manner, which were involved in the regulation of
    hypoxia-related resistance of CHP126 cells. Meanwhile, VEGF and its
    receptor KDR were found to interact with MAPKs signaling pathways
    except the effect of hypoxia. Furthermore, rhVEGF(165) was utilized to
    discern that VEGF increased Bcl-2 and procaspase 3 expressions,
    contributing to a synergistic relationship of an angiogenic response
    with Bcl-2 in hypoxia via a cross talk, while the activation of ERK
    MAPK is important for both productions. These altered signals may be
    critical to predict a poor outcome; therefore, our knowledge provides
    new insight into apoptosis and angiogenesis control of tumor cells and
    suggests a strategy based on the blockade of hypoxia-induced VEGF
    signaling under hypoxia in neuroblastoma.
 C1 [Wang, Duoduo; Weng, Qinjie; Zhang, Lei; He, Qiaojun; Yang, Bo] Zhejiang Univ, Coll Pharmaceut Sci, Inst Pharmacol & Toxicol, Hangzhou 310058, Zhejiang, Peoples R China.
 RP He, QJ, Zhejiang Univ, Coll Pharmaceut Sci, Inst Pharmacol & Toxicol,
    388 Yuhangtang Rd, Hangzhou 310058, Zhejiang, Peoples R China.
 EM qiaojunhe@zju.edu.cn
    yang924@zju.edu.cn
 FU National Natural Science Foundation [30672484]; Natural Science
    Foundation of Zhejiang Province [R20512]; Zhejiang Provincial Program 
 FX The authors thank the grant sponsors. Grant information: This study
    received financial support from the National Natural Science Foundation
    (30672484), the Natural Science Foundation of Zhejiang Province
    (R20512), and Zhejiang Provincial Program for the cultivation of
    High-level Innovative Health talents.
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 NR 48
 TC 4
 PU SPRINGER/PLENUM PUBLISHERS
 PI NEW YORK
 PA 233 SPRING ST, NEW YORK, NY 10013 USA
 SN 0272-4340
 J9 CELL MOL NEUROBIOL
 JI Cell. Mol. Neurobiol.
 PD MAY
 PY 2009
 VL 29
 IS 3
 BP 391
 EP 401
 DI 10.1007/s10571-008-9331-9
 PG 11
 SC Cell Biology; Neurosciences
 GA 438SI
 UT ISI:000265575300011
 ER
 
 PT J
 AU Huang, Y
    Liu, YH
    Chen, Y
    Yu, XW
    Yang, JL
    Lu, MD
    Lu, QY
    Ke, Q
    Shen, AG
    Yan, MJ
 AF Huang, Ye
    Liu, Yonghua
    Chen, Ying
    Yu, Xiaowei
    Yang, Junling
    Lu, Mudan
    Lu, Qiuyan
    Ke, Qing
    Shen, Aiguo
    Yan, Meijuan
 TI Peripheral Nerve Lesion Induces an Up-regulation of Spy1 in Rat Spinal
    Cord
 SO CELLULAR AND MOLECULAR NEUROBIOLOGY
 LA English
 DT Article
 DE Glial cells; Proliferation; Sciatic nerve injury; Spinal cord; Spy1
 ID CELL-CYCLE REGULATOR; CDK INHIBITORS; DNA-DAMAGE; PROGRESSION;
    ACTIVATION; PHOSPHORYLATION; REGENERATION; EXPRESSION; P27(KIP1);
    PROTEINS
 AB Spy1, as a member of the Speedy/RINGO family and a novel activator of
    cyclin-dependent kinases, was shown to promote cell cycle progression
    and cell survival in response to DNA damage. While its expression and
    roles in nervous system lesion and repair were still unknown. Here, we
    performed an acute sciatic nerve injury model in adult rats and studied
    the dynamic changes of Spy1 expression in lumbar spinal cord.
    Temporally, Spy1 expression was increased shortly after sciatic nerve
    crush and peaked at day 2. Spatially, Spy1 was widely expressed in the
    lumbar spinal cord including neurons and glial cells. While after
    injury, Spy1 expression was increased predominantly in astrocytes and
    microglia, which were largely proliferated. Moreover, there was a
    concomitant up-regulation of CDK2 activity and down-regulation of p27.
    Collectively, we hypothesized peripheral nerve injury induced an
    up-regulation of Spy1 in lumbar spinal cord, which was associated with
    glial proliferation.
 C1 [Huang, Ye; Liu, Yonghua; Yu, Xiaowei; Shen, Aiguo; Yan, Meijuan] Nantong Univ, Jiangsu Key Lab Neuroregenerat, Nantong 226001, Peoples R China.
    [Huang, Ye; Liu, Yonghua; Yu, Xiaowei; Shen, Aiguo; Yan, Meijuan] Nanjing Med Univ, Orthopaed Affiliated Hosp 2, Nantong 226001, Peoples R China.
    [Liu, Yonghua; Yang, Junling; Lu, Mudan; Lu, Qiuyan; Ke, Qing] Nantong Univ, Coll Med, Dept Microbiol & Immunol, Nantong 226001, Peoples R China.
    [Chen, Ying] Nantong Univ, Coll Med, Dept Histol & Embryol, Nantong 226001, Peoples R China.
 RP Shen, AG, Nantong Univ, Jiangsu Key Lab Neuroregenerat, 19 Qi Xiu Rd,
    Nantong 226001, Peoples R China.
 EM lyh656338268_2006@126.com
    ymz_888@yahoo.com.cn
 FU National Natural Scientific Foundation of China [30300099, 30770488];
    Natural Scientific Foundation of Jiangsu Province [BK2003035,
    BK2006547]; College and University Natural Scientific Research
    Programme of Jiangsu Province [03KJB180109, 04KJB320114]; Technology
    Guidance Plan for Social Development of Jiangsu Province [BS2004526];
    Health Project of Jiangsu Province [H200632]; Jiangsu Province [CX08S_
    026Z]
 FX This study was supported by the National Natural Scientific Foundation
    of China Grant (No. 30300099 and No. 30770488), Natural Scientific
    Foundation of Jiangsu Province Grant (No. BK2003035 and No. BK2006547),
    College and University Natural Scientific Research Programme of Jiangsu
    Province (No. 03KJB180109 and No. 04KJB320114), Technology Guidance
    Plan for Social Development of Jiangsu Province Grant (BS2004526),
    Health Project of Jiangsu Province (H200632), and Liu- Da- Ren- Cai-
    Gao- Feng'' Financial Assistance of Jiangsu Province Grant (No. 2),
    Postgraduate Scientific Innovation Program of Jiangsu Province (No.
    CX08S_ 026Z).
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 NR 20
 TC 0
 PU SPRINGER/PLENUM PUBLISHERS
 PI NEW YORK
 PA 233 SPRING ST, NEW YORK, NY 10013 USA
 SN 0272-4340
 J9 CELL MOL NEUROBIOL
 JI Cell. Mol. Neurobiol.
 PD MAY
 PY 2009
 VL 29
 IS 3
 BP 403
 EP 411
 DI 10.1007/s10571-008-9332-8
 PG 9
 SC Cell Biology; Neurosciences
 GA 438SI
 UT ISI:000265575300012
 ER
 
 PT J
 AU Zhang, BH
    Li, M
    Chen, L
    Yang, K
    Shan, YF
    Zhu, LH
    Sun, SG
    Li, L
    Wang, C
 AF Zhang, Bianhong
    Li, Meng
    Chen, Liang
    Yang, Kai
    Shan, Yufei
    Zhu, Lianhui
    Sun, Shaogang
    Li, Lin
    Wang, Chen
 TI The TAK1-JNK cascade is required for IRF3 function in the innate immune
    response
 SO CELL RESEARCH
 LA English
 DT Article
 DE JNK; TAK1; IRF3; innate immunity
 ID INTERFERON REGULATORY FACTOR-3; NF-KAPPA-B; DOUBLE-STRANDED-RNA;
    TOLL-LIKE RECEPTORS; PROTEIN-KINASE-C; SIGNAL-TRANSDUCTION; ANTIVIRAL
    RESPONSE; TERMINAL KINASE; ADAPTER MOLECULE; CUTTING EDGE
 AB Interferon regulatory factor (IRF)3 is critical for the transcriptional
    induction of chemokines and cytokines during viral or bacterial
    invasion. The kinases Tank binding kinase (TBK)1 and Ikappa B kinase
    (IKK)epsilon can phosphorylate the C-terminal part of IRF3 and play
    important roles in IRF3 activation. In this study, we show that another
    kinase, c-Jun-NH2-terminal kinase (JNK), phosphorylates IRF3 on its
    N-terminal serine 173 residue, and TAK1 can stimulate IRF3
    phosphorylation via JNK. JNK specific inhibitor SP600125 inhibits the
    N-terminal phosphorylation without affecting the C-terminal
    phosphorylation. In addition, IRF3-mediated gene expressions on
    lipopolysaccharide (LPS) or polyinosinic-cytidylic acid (polyI:C)
    treatment are severely impaired by SP600125, as well as for reporter
    gene assay of IRF3 activation. Knockdown of TAK1 further confirmed
    these observations. Interestingly, constitutive active IRF3(5D) can be
    inhibited by SP600125; JNK1 can synergize the action of IRF3(5D), but
    not the S173A-IRF3( 5D) mutant. More importantly, polyI: C failed to
    induce the phosphorylation of mutant S173A and SP600125 dramatically
    abrogated IRF3 phosphorylation and dimerization that was stimulated by
    polyI: C. Thus, this study demonstrates that the TAK1-JNK cascade is
    required for IRF3 function, in addition to TBK1/IKK epsilon, uncovering
    a new mechanism for mitogen-activated protein (MAP) kinase to regulate
    the innate immunity.
 C1 [Zhang, Bianhong; Li, Meng; Chen, Liang; Yang, Kai; Shan, Yufei; Zhu, Lianhui; Sun, Shaogang; Li, Lin; Wang, Chen] Chinese Acad Sci, Shanghai Inst Biol Sci, Inst Biochem & Cell Biol, Mol Cell Biol Lab, Shanghai 200031, Peoples R China.
 RP Wang, C, Chinese Acad Sci, Shanghai Inst Biol Sci, Inst Biochem & Cell
    Biol, Mol Cell Biol Lab, 320 Yue Yang Rd, Shanghai 200031, Peoples R
    China.
 EM lli@sibs.ac.cn
    cwang01@sibs.ac.cn
 FU Chinese Academy Renovation Program [KSCX1-YW-R-06]; Ministry of Science
    and Technology of China [2002CB513000, 2006AA02Z121, 2007CB914504)];
    National Natural Science Foundation of China [30225013, 30623003,
    30521005]
 FX We thank Prof. John Hiscott (McGill University, Canada), Melanie Cobb
    (University of Texas Southwest Medical Center, USA), Stephan Ludwig
    (Heinrich-Heine-University, Duesseldorf, Germany) and Hong-Bing Shu
    (College of Life Sciences, Wuhan University, Wuhan, China) for
    providing plasmids for this study. We thank Prof. Zhengfan Jiang
    (Beijing University, China) for providing the 293-TLR3 cell line. This
    study is partly supported by grants from the Chinese Academy Renovation
    Program (KSCX1-YW-R-06), the Ministry of Science and Technology of
    China (2002CB513000, 2006AA02Z121 and 2007CB914504) and the National
    Natural Science Foundation of China (30225013, 30623003 and 30521005).
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 NR 56
 TC 11
 PU NATURE PUBLISHING GROUP
 PI NEW YORK
 PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
 SN 1001-0602
 J9 CELL RES
 JI Cell Res.
 PD APR
 PY 2009
 VL 19
 IS 4
 BP 412
 EP 428
 DI 10.1038/cr.2009.8
 PG 17
 SC Cell Biology
 GA 440KV
 UT ISI:000265700100004
 ER
 
 PT J
 AU Zuo, Y
    Xiang, BG
    Yang, J
    Sun, XX
    Wang, YM
    Cang, H
    Yi, J
 AF Zuo, Yong
    Xiang, Binggang
    Yang, Jie
    Sun, Xuxu
    Wang, Yumei
    Cang, Hui
    Yi, Jing
 TI Oxidative modification of caspase-9 facilitates its activation via
    disulfide-mediated interaction with Apaf-1
 SO CELL RESEARCH
 LA English
 DT Article
 DE oxidative modification; ROS; caspase-9; apoptosis; disulfide
 ID CYTOCHROME-C; INHIBITS APOPTOSIS; MAMMALIAN-CELLS; IN-VIVO;
    MITOCHONDRIA; PROTEINS; STRESS; DEATH; CYTOTOXICITY; THIOREDOXIN
 AB Intracellular reactive oxygen species (ROS) are known to regulate
    apoptosis. Activation of caspase-9, the initial caspase in the
    mitochondrial apoptotic cascade, is closely associated with ROS, but it
    is unclear whether ROS regulate caspase-9 via direct oxidative
    modification. The present study aims to elucidate the molecular
    mechanisms by which ROS mediate caspase-9 activation. Our results show
    that the cellular oxidative state facilitates caspase-9 activation.
    Hydrogen peroxide treatment causes the activation of caspase-9 and
    apoptosis, and promotes an interaction between caspase-9 and apoptotic
    protease-activating factor 1 (Apaf-1) via disulfide formation. In
    addition, in an in vitro mitochondria-free system, the thiol-oxidant
    diamide promotes auto-cleavage of caspase-9 and the caspase-9/Apaf-1
    interaction by facilitating the formation of disulfide-linked
    complexes. Finally, a point mutation at C403 of caspase-9 impairs both
    H2O2-promoted caspase-9 activation and interaction with Apaf-1 through
    the abolition of disulfide formation. The association between
    cytochrome c and the C403S mutant is significantly weaker than that
    between cytochrome c and wild-type caspase-9, indicating that oxidative
    modification of caspase-9 contributes to apoptosome formation under
    oxidative stress. Taken together, oxidative modification of caspase-9
    by ROS can mediate its interaction with Apaf-1, and can thus promote
    its auto-cleavage and activation. This mechanism may facilitate
    apoptosome formation and caspase-9 activation under oxidative stress.
 C1 [Zuo, Yong; Xiang, Binggang; Yang, Jie; Sun, Xuxu; Wang, Yumei; Cang, Hui; Yi, Jing] Shanghai Jiao Tong Univ, Sch Med, Inst Med Sci,Dept Cell Biol, Educ Minist Cell Differentiat & Apoptosis,Key Lab, Shanghai 200025, Peoples R China.
 RP Yi, J, Shanghai Jiao Tong Univ, Sch Med, Inst Med Sci,Dept Cell Biol,
    Educ Minist Cell Differentiat & Apoptosis,Key Lab, Shanghai 200025,
    Peoples R China.
 EM yangjieyj@126.com
    yijing@shsmu.edu.cn
 FU National Natural Science Foundation of China [30570965, 30600105];
    Ministry of Sciences and Technologies of China [2006CB910104]; Shanghai
    Education Committee [05BZ17]
 FX We thank Drs T Ozaki and T Yamamoto(Kochi University Medical School,
    Japan) for their gifts of the wild-type and antisense Mn-SOD OSC cell
    lines. We also thank Drs GS Salvesen and SJ Riedl (Burnham Institute
    for Medical Research, USA) for their gift of the caspase-9 construct.
    Dr Hua Jing (Scripps Research Institute, USA) is especially thanked for
    her aid with the cysteine-positioning predictions. This work was
    supported by grants from the National Natural Science Foundation of
    China (30570965, J Yi; 30600105, J Yang), the Ministry of Sciences and
    Technologies of China (2006CB910104, J Yi) and the Shanghai Education
    Committee (05BZ17, J Yang).
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 NR 35
 TC 6
 PU NATURE PUBLISHING GROUP
 PI NEW YORK
 PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
 SN 1001-0602
 J9 CELL RES
 JI Cell Res.
 PD APR
 PY 2009
 VL 19
 IS 4
 BP 449
 EP 457
 DI 10.1038/cr.2009.19
 PG 9
 SC Cell Biology
 GA 440KV
 UT ISI:000265700100007
 ER
 
 PT J
 AU Jiang, H
    Wu, JC
    He, C
    Yang, WD
    Li, HL
 AF Jiang, Hai
    Wu, Jianchun
    He, Chen
    Yang, Wending
    Li, Honglin
 TI Tumor suppressor protein C53 antagonizes checkpoint kinases to promote
    cyclin-dependent kinase 1 activation
 SO CELL RESEARCH
 LA English
 DT Article
 DE C53; Cdk1; checkpoint kinases
 ID DNA-DAMAGE CHECKPOINT; BINDING-PROTEIN; WIP1 PHOSPHATASE; AURORA-A;
    CHK1; CELL; PHOSPHORYLATION; ATR; CENTROSOMES; REPLICATION
 AB Cyclin-dependent kinase 1 (Cdk1)/cyclin B1 complex is the driving force
    for mitotic entry, and its activation is tightly regulated by the G2/M
    checkpoint. We originally reported that a novel protein C53 (also known
    as Cdk5rap3 and LZAP) potentiates DNA damage-induced cell death by
    modulating the G2/M checkpoint. More recently, Wang et al. (2007) found
    that C53/LZAP may function as a tumor suppressor by way of inhibiting
    NF-kappa B signaling. We report here the identification of C53 protein
    as a novel regulator of Cdk1 activation. We found that knockdown of C53
    protein causes delayed Cdk1 activation and mitotic entry. During DNA
    damage response, activation of checkpoint kinase 1 and 2 (Chk1 and
    Chk2) is partially inhibited by C53 overexpression. Intriguingly, we
    found that C53 interacts with Chk1 and antagonizes its function.
    Moreover, a portion of C53 protein is localized at the centrosome, and
    centrosome-targeting C53 potently promotes local Cdk1 activation. Taken
    together, our results strongly suggest that C53 is a novel negative
    regulator of checkpoint response. By counteracting Chk1, C53 promotes
    Cdk1 activation and mitotic entry in both unperturbed cell-cycle
    progression and DNA damage response.
 C1 [Jiang, Hai; Wu, Jianchun; He, Chen; Yang, Wending; Li, Honglin] Northwestern Univ, Feinberg Sch Med, Childrens Mem Res Ctr, Chicago, IL 60614 USA.
 RP Li, HL, Northwestern Univ, Feinberg Sch Med, Childrens Mem Res Ctr,
    Chicago, IL 60614 USA.
 EM h-li2@northwestern.edu
 FU NIH [R21 AG027840, R01 GM081776]; Children's Memorial Research Center ;
    Clarke family 
 FX We thank Dr J Bartek (Danish Cancer Society) for Chk1-GFP-PACT
    construct. We are grateful for the insightful advice from Drs Junying
    Yuan (Harvard Medical School), Qingshen Gao, Jacek Topczewski, Kathy
    Randell, Bernard Mirkin (Northwestern University) and Marcus Peter
    (University of Chicago), and the help from Drs Francis Szele and Ed
    Kang (Children's Memorial Research Center and Northwestern University)
    on time-lapse video-microscopy and William Goossens (Children's
    Memorial Research Center) on confocal microscopy. The project was
    supported by NIH grant R21 AG027840 and R01 GM081776 (to H Li),
    Children's Memorial Research Center and the Clarke family.
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 NR 37
 TC 6
 PU NATURE PUBLISHING GROUP
 PI NEW YORK
 PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
 SN 1001-0602
 J9 CELL RES
 JI Cell Res.
 PD APR
 PY 2009
 VL 19
 IS 4
 BP 458
 EP 468
 DI 10.1038/cr.2009.14
 PG 11
 SC Cell Biology
 GA 440KV
 UT ISI:000265700100008
 ER
 
 PT J
 AU Yang, XR
    Chan, C
 AF Yang, Xuerui
    Chan, Christina
 TI Repression of PKR mediates palmitate-induced apoptosis in HepG2 cells
    through regulation of Bcl-2
 SO CELL RESEARCH
 LA English
 DT Article
 DE palmitate; apoptosis; HepG2; PKR; phosphorylation of Bcl-2; NF-kappa B;
    JNK
 ID DOUBLE-STRANDED-RNA; DEPENDENT PROTEIN-KINASE; NF-KAPPA-B; FREE
    FATTY-ACIDS; ENDOPLASMIC-RETICULUM STRESS; TUMOR-SUPPRESSOR P53;
    HEPATOMA-CELLS; HEPATOCELLULAR-CARCINOMA; SIGNALING PATHWAYS;
    IMMUNOHISTOCHEMICAL DETECTION
 AB The present study shows that double-stranded RNA-dependent protein
    kinase (PKR) regulates the protein expression level and phosphorylation
    of Bcl-2 and plays an anti-apoptotic role in human hepatocellular
    carcinoma cells (HepG2). In various types of cells, saturated free
    fatty acids (FFAs), such as palmitate, have been shown to induce
    cellular apoptosis by several mechanisms. Palmitate down-regulates the
    activity of PKR and thereby decreases the level of Bcl-2 protein,
    mediated in part by reduced activation of the NF-kappa B transcription
    factor. In addition to the level of Bcl-2 protein, the phosphorylation
    of Bcl-2 at different amino acid residues, such as Ser70 and Ser87, is
    also important in regulating cellular apoptosis. The decrease in the
    phosphorylation of Bcl-2 at Ser70 upon exposure to palmitate is
    mediated by inhibition of PKR and possibly by c-Jun N-terminal kinase
    (JNK), whereas the phosphorylation of Bcl-2 at Ser87 is unaffected by
    palmitate or PKR. In summary, PKR mediates the regulation of the
    protein level and the phosphorylation status of Bcl-2, providing a
    novel mechanism of palmitate-induced apoptosis in HepG2 cells.
 C1 [Yang, Xuerui; Chan, Christina] Michigan State Univ, Dept Chem Engn & Mat Sci, E Lansing, MI 48824 USA.
    [Yang, Xuerui; Chan, Christina] Michigan State Univ, Dept Biochem & Mol Biol, E Lansing, MI 48824 USA.
 RP Chan, C, Michigan State Univ, Dept Chem Engn & Mat Sci, E Lansing, MI
    48824 USA.
 EM krischan@egr.msu.edu
 FU National Science Foundation [BES 0425821]; Environmental Protection
    Agency [RD83184701]; Whitaker Foundation ; National Institute of Health
    [R01GM079688-01, R21CA126136-01, R21RR024439]; MSU Foundation ; Center
    for Systems Biology 
 FX We thank Michael J Opperman for his help with some of the experiments.
    The work was supported in part by the National Science Foundation (BES
    0425821), the Environmental Protection Agency (RD83184701), the
    Whitaker Foundation, the National Institute of Health (R01GM079688-01,
    R21CA126136-01, and R21RR024439), and the MSU Foundation and the Center
    for Systems Biology.
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 NR 88
 TC 7
 PU NATURE PUBLISHING GROUP
 PI NEW YORK
 PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
 SN 1001-0602
 J9 CELL RES
 JI Cell Res.
 PD APR
 PY 2009
 VL 19
 IS 4
 BP 469
 EP 486
 DI 10.1038/cr.2009.25
 PG 18
 SC Cell Biology
 GA 440KV
 UT ISI:000265700100009
 ER
 
 PT J
 AU Du, J
    Yang, S
    An, D
    Hu, F
    Yuan, W
    Zhai, CL
    Zhu, TH
 AF Du, Jun
    Yang, Shuang
    An, Di
    Hu, Fen
    Yuan, Wei
    Zhai, Chunli
    Zhu, Tianhui
 TI BMP-6 inhibits microRNA-21 expression in breast cancer through
    repressing delta EF1 and AP-1
 SO CELL RESEARCH
 LA English
 DT Article
 DE BMP-6; microRNA-21; AP-1; delta EF1; breast cancer invasion
 ID BONE MORPHOGENETIC PROTEIN-6; TUMOR-SUPPRESSOR GENE; TGF-BETA; CADHERIN
    EXPRESSION; CELLS; METASTASIS; TARGETS; MIR-21; PROGRESSION; PATHWAYS
 AB MicroRNAs (miRNAs), which are small noncoding RNA molecules, play
    important roles in the post-transcriptional regulation process. The
    microRNA-21 gene (miR-21) has been reported to be highly expressed in
    various solid tumors, including breast cancer. Bone morphogenetic
    protein-6 (BMP-6) has been identified as an inhibitor of breast cancer
    epithelial-mesenchymal transition (EMT) through rescuing E-cadherin
    expression. We initiated experiments to identify the relationships
    between miR-21 and BMP-6 in breast cancer progression. Real-time PCR
    analysis showed that miR-21 expression was very high in MDA-MB-231
    cells that expressed little BMP-6. A reverse correlation between BMP-6
    and miR-21 was also determined in breast cancer tissue samples.
    Moreover, BMP-6 inhibited miR-21 transcription in MDA-MB-231 cells. In
    order to investigate how BMP-6 inhibited the miR-21 promoter
    (miPPR-21), we constructed a series of miPPR-21 reporters. Luciferase
    assay results indicated that BMP-6 inhibited miPPR-21 activity through
    the E2-box and AP-1-binding sites. We also demonstrated that both delta
    EF1 and TPA induced miR-21 expression. Using site-directed mutation and
    CHIP assay, we found that delta EF1 induced miPPR-21 activity by
    binding to the E2-box on miPPR-21. Moreover, TPA triggered miPPR-21
    activity through the AP-1 binding sites. BMP-6 treatment significantly
    reduced the binding of these factors to miPPR-21 by decreasing the
    expression of delta EF1 and c-Fos/c-Jun. We also demonstrated that
    BMP-6-induced downregulation of miR-21 modified the activity of PDCD4
    3'UTR and inhibited MDA-MB-231 cell invasion. delta EF1 overexpression
    and TPA induction blocked this inhibitory effect of BMP-6. In
    conclusion, BMP-6-induced inhibition of miR-21 suggests that BMP-6 may
    function as an anti-metastasis factor by a mechanism involving
    transcriptional repression of miR-21 in breast cancer.
 C1 [Du, Jun; Yang, Shuang; An, Di; Hu, Fen; Yuan, Wei; Zhai, Chunli; Zhu, Tianhui] Nankai Univ, Coll Med, Lab Med Mol Biol, Tianjin 300071, Peoples R China.
 RP Zhu, TH, Nankai Univ, Coll Med, Lab Med Mol Biol, 94 Weijin Rd, Tianjin
    300071, Peoples R China.
 EM zhuth@nankai.edu.cn
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 NR 25
 TC 14
 PU NATURE PUBLISHING GROUP
 PI NEW YORK
 PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
 SN 1001-0602
 J9 CELL RES
 JI Cell Res.
 PD APR
 PY 2009
 VL 19
 IS 4
 BP 487
 EP 496
 DI 10.1038/cr.2009.34
 PG 10
 SC Cell Biology
 GA 440KV
 UT ISI:000265700100010
 ER
 
 PT J
 AU Pan, K
    Yan, S
    Ge, S
    Li, S
    Zhao, Y
    Yang, P
 AF Pan, K.
    Yan, S.
    Ge, S.
    Li, S.
    Zhao, Y.
    Yang, P.
 TI Effects of core binding factor alpha 1 or bone morphogenic protein-2
    overexpression on osteoblast/cementoblast-related gene expressions in
    NIH3T3 mouse cells and dental follicle cells
 SO CELL PROLIFERATION
 LA English
 DT Article
 ID HUMAN OSTEOGENIC PROTEIN-1; GROWTH-FACTOR BETA-1; OSTEOBLAST
    DIFFERENTIATION; PERIODONTAL REGENERATION; CLEIDOCRANIAL DYSPLASIA;
    PRECURSOR CELLS; PAPIO-URSINUS; IN-VITRO; REPAIR; CBFA1
 AB Bone morphogenic protein-2 (BMP-2) has long been used to promote bone
    and periodontal regeneration, while core binding factor alpha 1 (CBFA1)
    plays important roles in both osteogenic differentiation and tooth
    morphogenesis. The aim of this study was to evaluate the effects of
    CBFA1 or BMP-2 overexpression on osteoblast/cementoblast-related gene
    expressions in NIH3T3 cells and dental follicle cells (DFCs).
    CBFA1 or BMP-2 overexpression in NIH3T3 and DFCs was achieved by
    infection with retroviral vectors containing CBFA1 or BMP-2 cDNA. Cells
    stably integrated with CBFA1 or BMP-2 cDNA were selected with G418 for
    14 days. Western blotting, real-time reverse transcriptase-polymerase
    chain reaction, and in vitro mineralization assay were performed to
    evaluate effects of CBFA1 or BMP-2 overexpression in cells undergoing
    osteoblast/cementoblast differentiation.
    Our results demonstrated that osteoblast/cementoblast-related gene
    expression levels in CBFA1-overexpressing NIH3T3 cells were higher than
    those in BMP-2-overexpressing cells. More mineral nodules were observed
    in CBFA1-overexpressing NIH3T3 cells than in BMP-2-overexpressing
    cells. CBFA1 overexpression in DFCs also increased
    osteoblast/cementoblast-related gene expression and promoted mineral
    nodule formation. However, no significant changes in gene expression
    levels nor mineral nodule formation were found in BMP-2-overexpressing
    DFCs when compared with empty vector transduced DFCs.
    CBFA1 overexpression up-regulated expression levels of
    osteoblast/cementoblast-related genes and enhanced in vitro osteogenic
    differentiation more efficiently than BMP-2 in both NIH3T3 cells and
    DFCs.
 C1 [Pan, K.; Yan, S.; Ge, S.; Li, S.; Yang, P.] Shandong Univ, Sch Dent, Dept Periodontol, Jinan 250012, Peoples R China.
    [Pan, K.; Yan, S.; Ge, S.; Li, S.; Yang, P.] Shandong Univ, Sch Dent, Inst Oral Biomed, Jinan 250012, Peoples R China.
    [Zhao, Y.] Tianjin Med Univ, Stomatol Hosp, Dept Orthodont, Tianjin, Peoples R China.
 RP Yang, P, Shandong Univ, Sch Dent, Dept Periodontol, 44-1 Wenhuaxi Rd,
    Jinan 250012, Peoples R China.
 EM yangps@sdu.edu.cn
 FU Doctoral Foundation of China [20050422044]
 FX This work was supported by Doctoral Foundation of China (20050422044).
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 NR 50
 TC 1
 PU WILEY-BLACKWELL PUBLISHING, INC
 PI MALDEN
 PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
 SN 0960-7722
 J9 CELL PROLIFERATION
 JI Cell Prolif.
 PD JUN
 PY 2009
 VL 42
 IS 3
 BP 364
 EP 372
 DI 10.1111/j.1365-2184.2009.00599.x
 PG 9
 SC Cell Biology
 GA 437IT
 UT ISI:000265481300010
 ER
 
 PT J
 AU Li, LD
    Borodyansky, L
    Yang, YX
 AF Li, Linda
    Borodyansky, Laura
    Yang, Youxin
 TI Genomic instability en route to and from cancer stem cells
 SO CELL CYCLE
 LA English
 DT Article
 DE cancer stem cells; genomic instability; CSC; GIN; hES; mES
 ID CHROMOSOMAL INSTABILITY; TRANSFORMATION; ABNORMALITIES; ENGINE
 AB Cancer is caused by successive gene mutations that amount to confer
    malignant phenotype. Genomic instability (GIN) is considered a key
    endogenous mechanism for accumulation of mutations, and therefore, has
    been proposed as an engine of tumorigenesis. Recently, cancer stem
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    human cancers. These cancer stem cells (CSCs) are believed to be
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    unstable? Could GIN in CSCs be the cause of the observed cancer cell
    heterogeneity? In this article, we will discuss some early clues
    indicating that these two driving forces of tumorigenesis appear to be
    intimately connected.
 C1 [Li, Linda; Borodyansky, Laura; Yang, Youxin] Harvard Univ, Sch Med, Beth Israel Deaconess Med Ctr, GI Canc Lab,Div Gastroenterol, Boston, MA 02215 USA.
 RP Yang, YX, Harvard Univ, Sch Med, Beth Israel Deaconess Med Ctr, GI Canc
    Lab,Div Gastroenterol, 330 Brookline Ave, Boston, MA 02215 USA.
 EM yyang@BIDMC.harvard.edu
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 NR 28
 TC 5
 PU LANDES BIOSCIENCE
 PI AUSTIN
 PA 1002 WEST AVENUE, 2ND FLOOR, AUSTIN, TX 78701 USA
 SN 1538-4101
 J9 CELL CYCLE
 JI Cell Cycle
 PD APR 1
 PY 2009
 VL 8
 IS 7
 BP 1000
 EP 1002
 PG 3
 SC Cell Biology
 GA 438YW
 UT ISI:000265593900012
 ER
 
 PT J
 AU Yang, Q
    Mao, ZX
 AF Yang, Qian
    Mao, Zixu
 TI Regulation of MEF2s by chaperone-mediated autophagy
 SO CELL CYCLE
 LA English
 DT Editorial Material
 ID SURVIVAL
 C1 [Mao, Zixu] Emory Univ, Sch Med, Dept Pharmacol, Atlanta, GA 30322 USA.
    Emory Univ, Sch Med, Dept Neurol, Atlanta, GA 30322 USA.
 RP Mao, ZX, Emory Univ, Sch Med, Dept Pharmacol, Atlanta, GA 30322 USA.
 EM zmao@pharm.emory.edu
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 NR 8
 TC 0
 PU LANDES BIOSCIENCE
 PI AUSTIN
 PA 1002 WEST AVENUE, 2ND FLOOR, AUSTIN, TX 78701 USA
 SN 1538-4101
 J9 CELL CYCLE
 JI Cell Cycle
 PD APR 15
 PY 2009
 VL 8
 IS 8
 BP 1105
 EP 1105
 PG 1
 SC Cell Biology
 GA 438YZ
 UT ISI:000265594200001
 ER
 
 PT J
 AU Tao, YG
    Leteur, C
    Yang, CY
    Zhang, P
    Castedo, M
    Pierre, A
    Golsteyn, RM
    Bourhis, J
    Kroemer, G
    Deutsch, E
 AF Tao, Yungan
    Leteur, Celine
    Yang, Ceyao
    Zhang, Ping
    Castedo, Maria
    Pierre, Alain
    Golsteyn, Roy M.
    Bourhis, Jean
    Kroemer, Guido
    Deutsch, Eric
 TI Radiosensitization by Chir-124, a selective CHK1 inhibitor Effects of
    p53 and cell cycle checkpoints
 SO CELL CYCLE
 LA English
 DT Article
 DE CHK1; radiation; G(2)-M checkpoint; p53
 ID P53-DEFICIENT CANCER-CELLS; DNA-DAMAGE CHECKPOINT; MITOTIC CATASTROPHE;
    SPINDLE CHECKPOINT; RADIATION RESPONSE; KINASE; INDUCTION; ARREST;
    CYTOTOXICITY; CHEMOTHERAPY
 AB Checkpoint kinase-1 (CHK1) is a key regulator of the DNA
    damage-elicited G(2)-M checkpoints. The aim of the present study was to
    investigate the effects of a selective CHK1 inhibitor, Chir124, on cell
    survival and cell cycle progression following ionizing radiation (IR).
    Treatment with Chir-124 resulted in reduced clonogenic survival and
    abrogated the IR-induced G(2)-M arrest in a panel of isogenic HCT116
    cell lines after IR. This radiosensitizing effect was relatively
    similar between p53(-/-) and p53-sufficient wild type (WT) HCT116
    cells. However, the number of mitotic cells (as measured by assessing
    the phosphorylation of mitotic proteins) increased dramatically in
    p53(-/-) HCT116 cells after concomitant Chir-124 exposure, compared to
    IR alone, while no such effect was observed in p53-sufficient WT HCT116
    cells. In p53(-/-) cells, Chir-124 treatment induced a marked
    accumulation of polyploid cells that were characterized by
    micronucleation or multinucleation. p21(-/-) HCT116 cells displayed a
    similar pattern of response as p53(-/-) cells. Chir-124 was able to
    radiosensitize HCT116 cells that lack checkpoint kinase-2 (CHK2) or
    that were deficient for the spindle checkpoint protein Mad2. Finally,
    Chir-124 could radiosensitize tetraploid cell lines, which were
    relatively resistant against DNA damaging agents. Altogether these
    results suggest that Chir-124-mediated radiosensitization is profoundly
    influenced by the p53 and cell cycle checkpoint system.
 C1 [Kroemer, Guido] Inst Gustave Roussy, INSERM, U848, F-94805 Villejuif, France.
    [Tao, Yungan; Yang, Ceyao; Bourhis, Jean; Deutsch, Eric] Univ Paris 11, Le Kremlin Bicetre, France.
    [Pierre, Alain] Servier Lab, Res Ctr, Croissy Sur Seine, France.
    [Golsteyn, Roy M.] Univ Lethbridge, Lethbridge, AB T1K 3M4, Canada.
 RP Kroemer, G, Inst Gustave Roussy, INSERM, U848, PR1,39 Rue Camille
    Desmoulins, F-94805 Villejuif, France.
 EM kroemer@igr.fr
    deutsch@igr.fr
 FU Association pour la Recherche sur le Cancer ; Ligue contre le Cancer ;
    Agence Nationale pour la Recherche ; Institut National du Cancer ;
    Canceropole Ile-de-France and European Union 
 FX We are grateful to Dr. Bert Vogelstein, Johns Hopkins University, for
    kindly providing the wild-type, p53<SUP>-/-</SUP>, p21<SUP>-/-</SUP>,
    CHK2<SUP>-/-</SUP> and 14-3-3 sigma<SUP>-/-</SUP> HCT116 cell lines. We
    also thank Dr. Robert Benezra, Memorial Sloan-Kettering Cancer Center
    for kindly providing Mad<SUP>+/-</SUP> HCT116 cells. We thank Servier
    for kindly providing Chir-124 for experimental studies. We thank
    Safietou Mansaly for her assistance in the experiments. This study was
    supported by a grant from Association pour la Recherche sur le Cancer
    (to E. D.), as well as by grants from Ligue contre le Cancer (equipe
    labellisee), Agence Nationale pour la Recherche, Institut National du
    Cancer, Canceropole Ile-de-France and European Union (Active p53,
    Apop-Train, Apo-Sys, RIGHT) to G. K.
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 NR 39
 TC 9
 PU LANDES BIOSCIENCE
 PI AUSTIN
 PA 1002 WEST AVENUE, 2ND FLOOR, AUSTIN, TX 78701 USA
 SN 1538-4101
 J9 CELL CYCLE
 JI Cell Cycle
 PD APR 15
 PY 2009
 VL 8
 IS 8
 BP 1196
 EP 1205
 PG 10
 SC Cell Biology
 GA 438YZ
 UT ISI:000265594200022
 ER
 
 PT J
 AU Dabaghmanesh, N
    Matsubara, A
    Miyake, A
    Nakano, K
    Ishida, T
    Katano, H
    Horie, R
    Umezawa, K
    Watanabe, T
 AF Dabaghmanesh, Nazanin
    Matsubara, Aiko
    Miyake, Ariko
    Nakano, Kazumi
    Ishida, Takaomi
    Katano, Harutaka
    Horie, Ryoichi
    Umezawa, Kazuo
    Watanabe, Toshiki
 TI Transient inhibition of NF-kappa B by DHMEQ induces cell death of
    primary effusion lymphoma without HHV-8 reactivation
 SO CANCER SCIENCE
 LA English
 DT Article
 ID VIVO ANTITUMOR-ACTIVITY; IN-VIVO; INDUCED APOPTOSIS; KAPOSIS-SARCOMA;
    HERPES-VIRUS; BIOLOGICAL-ACTIVITIES; KSHV VFLIP; LEUKEMIA; EXPRESSION;
    INDUCTION
 AB Primary effusion lymphoma (PEL) is a refractory malignancy caused by
    human herpes virus 8 (HHV-8) in immunocompromised individuals. The
    tumor cells of PEL are characterized by constitutive NF-kappa B
    activation. Dehydroxymethylepoxyquinomicin (DHMEQ) is a new NF-kappa B
    inhibitor and is effective on various tumor cells with constitutively
    activated NF-kappa B. Thus, in search for a new therapeutic modality of
    PEL, we examined the effect of DHMEQ on PEL cells. We confirmed
    constitutive activation of NF-kappa B with subcomponents of p50 and p65
    in PEL cell lines. DHMEQ quickly and transiently abrogated NF-kappa B
    activation and reduced the cell viability in dose- and time-dependent
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    and membrane pathways. Array analysis revealed that DHMEQ
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    interleukin-6 (IL6), Myc, chemokine (C-C motif) receptor 5 (CCR5) and
    NF-kappa B1, whereas it up-regulated expression levels of some genes
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    HHV-8 lytic genes, indicating that NF-kB inhibition by DHMEQ did not
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    suggest DHMEQ as a promising candidate for molecular target therapy of
    the PEL. (Cancer Sci 2009; 100: 737-746)
 C1 [Dabaghmanesh, Nazanin; Matsubara, Aiko; Miyake, Ariko; Nakano, Kazumi; Ishida, Takaomi; Watanabe, Toshiki] Univ Tokyo, Grad Sch Frontier Sci, Dept Med Genome Sci, Minato Ku, Tokyo 1088639, Japan.
    [Matsubara, Aiko] Univ Tokyo, Fac Med, Bunkyo Ku, Tokyo 1130033, Japan.
    [Katano, Harutaka] Natl Inst Infect Dis, Dept Pathol, Shinjyuku Ku, Tokyo 1628640, Japan.
    [Horie, Ryoichi] Kitasato Univ, Fac Med, Dept Hematol, Sagamihara, Kanagawa 2288555, Japan.
    [Umezawa, Kazuo] Keio Univ, Fac Sci & Technol, Dept Appl Chem, Kohoku Ku, Yokohama, Kanagawa 2238522, Japan.
 RP Watanabe, T, Univ Tokyo, Grad Sch Frontier Sci, Dept Med Genome Sci,
    Minato Ku, 4-6-1 Shirokanedai, Tokyo 1088639, Japan.
 EM tnabe@ims.u-tokyo.ac.jp
 FU Ministry of Education, Culture, Sports, Science and Technology ;
    Ministry of Health, Labour and Welfare, Japan 
 FX This work was supported in part by Grants-in-Aid for Scientific
    Research from the Ministry of Education, Culture, Sports, Science and
    Technology, and by a Research Grant from the Ministry of Health, Labour
    and Welfare, Japan.
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 JI Cancer Sci.
 PD APR
 PY 2009
 VL 100
 IS 4
 BP 737
 EP 746
 DI 10.1111/j.1349-7006.2009.01083.x
 PG 10
 SC Oncology
 GA 438TK
 UT ISI:000265578100025
 ER
 
 PT J
 AU Chen, JG
    Fiskus, W
    Eaton, K
    Fernandez, P
    Wang, YC
    Rao, R
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    Bhalla, KN
 AF Chen, Jianguang
    Fiskus, Warren
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    Balusu, Ramesh
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    Atadja, Peter
    Bhalla, Kapil N.
 TI Cotreatment with BCL-2 antagonist sensitizes cutaneous T-cell lymphoma
    to lethal action of HDAC7-Nur77-based mechanism
 SO BLOOD
 LA English
 DT Article
 ID HISTONE DEACETYLASE INHIBITORS; ORPHAN STEROID-RECEPTOR; ACUTE
    MYELOID-LEUKEMIA; CYTOCHROME-C RELEASE; NEGATIVE SELECTION; CANCER
    CELLS; APOPTOSIS; NUR77; VORINOSTAT; EXPRESSION
 AB Pan-histone deacetylase inhibitors, for example, vorinostat and
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    panobinostat rapidly inhibits the in vitro and intracellular activity,
    as well as the mRNA and protein levels of HDAC7, and induces expression
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    panobinostat improved survival of athymic nude mice implanted with
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 C1 [Chen, Jianguang; Fiskus, Warren; Eaton, Kelly; Fernandez, Pravina; Wang, Yongchao; Rao, Rekha; Lee, Pearl; Joshi, Rajeshree; Yang, Yonghua; Kolhe, Ravindra; Balusu, Ramesh; Chappa, Prasanthi; Natarajan, Kavita; Jillella, Anand; Bhalla, Kapil N.] Med Coll Georgia, Ctr Canc, Augusta, GA 30912 USA.
    [Atadja, Peter] Novartis Inst Biomed Res, Cambridge, MA USA.
 RP Bhalla, KN, Med Coll Georgia, Ctr Canc, 1120 15th St,CN 2101, Augusta,
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 EM kbhalla@mcg.edu
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 TC 12
 PU AMER SOC HEMATOLOGY
 PI WASHINGTON
 PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
 SN 0006-4971
 J9 BLOOD
 JI Blood
 PD APR 23
 PY 2009
 VL 113
 IS 17
 BP 4038
 EP 4048
 DI 10.1182/blood-2008-08-176024
 PG 11
 SC Hematology
 GA 436WO
 UT ISI:000265447000023
 ER
 
 PT J
 AU Yang, O
    Popova, OV
    Suthoff, U
    Luking, I
    Dietz, KJ
    Golldack, D
 AF Yang, Oksoon
    Popova, Olga V.
    Suethoff, Ulrike
    Lueking, Ines
    Dietz, Karl-Josef
    Golldack, Dortje
 TI The Arabidopsis basic leucine zipper transcription factor AtbZIP24
    regulates complex transcriptional networks involved in abiotic stress
    resistance
 SO GENE
 LA English
 DT Article
 DE AtbZIP24; Transcription factor; RNAi; Salt tolerance; Arabidopsis
 ID VACUOLAR H+-ATPASE; NA+/H+ ANTIPORTER GENE; ZINC-FINGER PROTEIN;
    ORYZA-SATIVA L.; SALT TOLERANCE; HIGH-SALINITY; ABSCISIC-ACID;
    PLANT-CELLS; FUNCTIONAL-ANALYSIS; FREEZING TOLERANCE
 AB Soil salinity severely affects plant growth and agricultural
    productivity. AtbZIP24 encodes a bZIP transcription factor that is
    induced by salt stress in Arabidopsis thaliana but suppressed in the
    salt-tolerant relative Lobularia maritima. Transcriptional repression
    of AtbZIP24 using RNA interference improved salt tolerance in A.
    thaliana. Under non-stress growth conditions, transgenic A. thaliana
    lines with decreased AtbZIP24 expression activated the expression of
    stress-inducible genes involved in cytoplasmic ion homeostasis and
    osmotic adjustment: the Na+ transporter AtHKT1, the Na+/H+ antiporter
    AtSOS1, the aquaporin AtPIP2.1, and a glutamine synthetase. In
    addition, candidate target genes of AtbZIP24 with functions in plant
    growth and development were identified such as an argonaute
    (AGO1)-related protein and cyclophilin AtCYP19. The salt tolerance in
    transgenic plants correlated with reduced Na+ accumulation in leaves.
    In vivo interaction of AtbZIP24 as a homodimer was shown using
    fluorescence energy transfer (FRET) with cyan fluorescent protein (CFP)
    and yellow fluorescent protein (YFP) as fused FRET pairs. Translational
    fusion of AtbZIP24 with GFP showed subcellular localization of the
    protein in nucleus and cytoplasm in plants grown under control
    conditions whereas in response to salt stress AtbZIP24 was
    preferentially targeted to the nucleus. It is concluded that AtbZIP24
    is an important regulator of salt stress response in plants. The
    modification of transcriptional control by regulatory transcription
    factors provides a useful strategy for improving salt tolerance in
    plants. (C) 2009 Elsevier B.V. All rights reserved.
 C1 [Yang, Oksoon; Popova, Olga V.; Suethoff, Ulrike; Lueking, Ines; Dietz, Karl-Josef; Golldack, Dortje] Univ Bielefeld, Fac Biol, Dept Biochem & Physiol Plants, D-33615 Bielefeld, Germany.
 RP Golldack, D, Univ Bielefeld, Fac Biol, Dept Biochem & Physiol Plants,
    D-33615 Bielefeld, Germany.
 EM dortje.golldack@uni-bielefeld.de
 FU Deutsche Forschungsgerneinschaft (Germany) 
 FX The work was supported by the Deutsche Forschungsgerneinschaft
    (Germany).
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 NR 56
 TC 4
 PU ELSEVIER SCIENCE BV
 PI AMSTERDAM
 PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
 SN 0378-1119
 J9 GENE
 JI Gene
 PD MAY 1
 PY 2009
 VL 436
 IS 1-2
 BP 45
 EP 55
 DI 10.1016/j.gene.2009.02.010
 PG 11
 SC Genetics & Heredity
 GA 435KO
 UT ISI:000265343000007
 ER
 
 PT J
 AU Kim, S
    Choi, JH
    Lim, HI
    Lee, SK
    Kim, WW
    Cho, SJ
    Kim, JS
    Kim, JH
    Choe, JH
    Nam, SJ
    Lee, JE
    Yang, JH
 AF Kim, Sangmin
    Choi, Jae Hyuck
    Lim, Hye In
    Lee, Se-Kyung
    Kim, Wan Wook
    Cho, Sungjin
    Kim, Jee Soo
    Kim, Jung-Han
    Choe, Jun-Ho
    Nam, Seok Jin
    Lee, Jeong Eon
    Yang, Jung-Hyun
 TI EGF-induced MMP-9 expression is mediated by the JAK3/ERK pathway, but
    not by the JAK3/STAT-3 pathway in a SKBR3 breast cancer cell line
 SO CELLULAR SIGNALLING
 LA English
 DT Article
 DE JAKs; STAT-3; ERK; MMP-9; SKBR3 cells
 ID EPIDERMAL-GROWTH-FACTOR; MATRIX METALLOPROTEINASES; CONSTITUTIVE
    ACTIVATION; STAT PATHWAY; RECEPTOR; KINASE; METASTASIS; INVASION;
    MATRIX-METALLOPROTEINASE-9; ANGIOGENESIS
 AB The number of epidermal growth factor receptors (FGFRs) and their
    ligands are highly expressed in malignant tumor cells. The EGF
    signaling pathway is also activated in up to one-third of patients with
    breast cancer. In this study, we investigated the novel function of the
    JAK3 inhibitor, WHI-P131, on EGF-induced MMP-9 expression and the
    regulatory mechanism of EGF-induced MMP-9 expression in SKBR3 cells. We
    observed that EGF increased MMP-9 mRNA and protein expression in a
    dose-dependent manner. EGF also induced the phosphorylation of ECFR,
    ERK, and STAT-3, and these effects were inhibited by the EGFR
    inhibitor, AG1478. To investigate the involvement of the STAT-3 pathway
    on EGF-induced MMP-9 expression, we pretreated SKBR3 cells with JAK1,
    JAK2, and JAK3 inhibitors prior to EGF treatment. The results showed
    that the JAK3 inhibitor, WHI-P131, as well as JAK3 siRNA transfection,
    but not the JAK1 and JAK2 inhibitors, significantly decreased
    EGF-induced MMP-9 expression. In addition, EGF-induced STAT-3
    phosphorylation was only inhibited by WHI-P131. We then transfected
    cells with adenoviral STAT-3 (Ad-STAT-3), followed by treatment with
    EGF. Interestingly, EGF-induced MMP-9 expression was decreased by
    Ad-STAT-3 overexpression in a dose-dependent manner, while it was
    significantly increased by STAT-3 siRNA transfection. Our results also
    showed that basal levels of MMP-9 expression were significantly
    increased by constitutive active-MEK (CA-MEK) overexpression.
    EGF-induced ERK phosphorylation was prevented by WHI-P131, but not by
    JAM and JAK2 inhibitors. On the other hand, EGF-induced MMP-9
    expression was decreased by the MEK1/2 inhibitor, UO126. Therefore, for
    the first time, we suggest that the JAK3 inhibitor, WHI-P131, inhibits
    EGF-induced STAT3 phosphorylation as well as ERK phosphorylation. The
    JAK3/ERK pathway may play an important role in EGF-induced MMP-9
    expression in SKBR3 cells. (C) 2009 Elsevier Inc. All rights reserved.
 C1 [Kim, Sangmin; Choi, Jae Hyuck; Lim, Hye In; Lee, Se-Kyung; Kim, Wan Wook; Cho, Sungjin; Kim, Jee Soo; Kim, Jung-Han; Choe, Jun-Ho; Nam, Seok Jin; Lee, Jeong Eon; Yang, Jung-Hyun] Sungkyunkwan Univ, Sch Med, Samsung Med Ctr, Dept Surg, Seoul 135710, South Korea.
 RP Lee, JE, Sungkyunkwan Univ, Sch Med, Samsung Med Ctr, Dept Surg, Ilwon
    Dong 50, Seoul 135710, South Korea.
 EM paojlus@hanmail.net
    drjh.yang@samsung.com
 FU In-SUNG Foundation [C-A8-826-1]; Samsung Biomedical Research Institute
    [C-A9-313-1]
 FX This work was supported in part by Grant C-A8-826-1 from In-SUNG
    Foundation for Medical Research and by the Samsung Biomedical Research
    Institute grant, #SBRI C-A9-313-1.
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 NR 38
 TC 10
 PU ELSEVIER SCIENCE INC
 PI NEW YORK
 PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
 SN 0898-6568
 J9 CELL SIGNAL
 JI Cell. Signal.
 PD JUN
 PY 2009
 VL 21
 IS 6
 BP 892
 EP 898
 DI 10.1016/j.cellsig.2009.01.034
 PG 7
 SC Cell Biology
 GA 437FK
 UT ISI:000265471900008
 ER
 
 PT J
 AU Huang, YL
    Shi, GY
    Lee, H
    Jiang, MJ
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    Wu, HL
    Yang, HY
 AF Huang, Yuan-Li
    Shi, Guey-Yueh
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    Wu, Hua-Lin
    Yang, Hsi-Yuan
 TI Thrombin induces nestin expression via the transactivation of EGFR
    signalings in rat vascular smooth muscle cells
 SO CELLULAR SIGNALLING
 LA English
 DT Article
 DE Nestin; Proliferation; Thrombin; EGFR transactivation; Vascular smooth
    muscle cells
 ID INTERMEDIATE FILAMENT PROTEIN; GROWTH-FACTOR RECEPTOR; ACTIVATED
    RECEPTORS; COUPLED RECEPTORS; ENDOTHELIAL-CELLS; SKELETAL-MUSCLE;
    DNA-SYNTHESIS; PHOSPHORYLATION; THROMBOMODULIN; VIMENTIN
 AB Regulation of nestin gene expression is largely unknown despite that it
    is widely used as a progenitor cell marker. In this study, we showed
    that nestin expression is regulated by the thrombin-mediated EGFR
    transactivation in serum-deprived primary cultures of rat vascular
    smooth muscle cells (VSMCs). This resulted from the direct binding of
    thrombin to PAR-1 rather than indirectly affecting through the binding
    to thrombomodulin, as demonstrated by thrombomodulin RNAi. In this
    process, the PAR-1-induced c-Src plays a critical role through two
    routes; one was the direct intracellular phosphorylation of EGFR and
    the other was the extracellular activation of the MMP-2-mediated
    shedding of HB-EGF. The transactivated EGFR then led to the downstream
    Ras-Raf-ERK signaling axis, but not the p38 or JNK pathways. In
    addition, the EMSA experiment showed that the transcriptional factor
    Sp1 is critical for the thrombin-induced nestin expression in rat
    VSMCs. Furthermore, RNAi of nestin attenuated the thrombin-induced cell
    proliferation, indicating that thrombin-induced nestin expression and
    cell proliferation share the same EGFR transactivation mechanism. This
    study also suggested that nestin may play an important role in cell
    proliferation induced by the thrombin-mediated EGFR transactivation.
    Crown Copyright (C) 2009 Published by Elsevier Inc. All rights reserved.
 C1 [Yang, Hsi-Yuan] Natl Taiwan Univ, Inst Mol & Cellular Biol, Taipei 106, Taiwan.
    [Shi, Guey-Yueh; Wu, Hua-Lin] Natl Cheng Kung Univ, Dept Biochem & Mol Biol, Tainan 701, Taiwan.
    [Shi, Guey-Yueh; Wu, Hua-Lin] Natl Cheng Kung Univ, Cardiovasc Res Ctr, Tainan 701, Taiwan.
    [Lee, Hsinyu] Natl Taiwan Univ, Inst Zool, Taipei 106, Taiwan.
    [Jiang, Meei-Jyh] Natl Cheng Kung Univ, Coll Med, Dept Cell Biol & Anat, Tainan 701, Taiwan.
 RP Wu, HL, Natl Taiwan Univ, Inst Mol & Cellular Biol, 1,Sec 4,Roosevelt
    Rd, Taipei 106, Taiwan.
 EM hyhy@ntu.edu.tw
 FU National Science Council, Executive Yuan, Taiwan
    [NSC96-2752-B-006-003-PAE, NSC96-2752-B-006-004-PAE,
    NSC96-2752-B-006-005-PAE]
 FX We would like to thank Georgiana Cho-Chen Wu for editing assistance.
    This work was supported by the National Science Council, Executive
    Yuan, Taiwan through grant NSC96-2752-B-006-003-PAE,
    NSC96-2752-B-006-004-PAE, and NSC96-2752-B-006-005-PAE.
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 NR 40
 TC 4
 PU ELSEVIER SCIENCE INC
 PI NEW YORK
 PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
 SN 0898-6568
 J9 CELL SIGNAL
 JI Cell. Signal.
 PD JUN
 PY 2009
 VL 21
 IS 6
 BP 954
 EP 968
 DI 10.1016/j.cellsig.2009.02.005
 PG 15
 SC Cell Biology
 GA 437FK
 UT ISI:000265471900015
 ER
 
 PT J
 AU Gwak, SJ
    Bhang, SH
    Yang, HS
    Kim, SS
    Lee, DH
    Lee, SH
    Kim, BS
 AF Gwak, So-Jung
    Bhang, Suk H.
    Yang, Hee S.
    Kim, Sang-Soo
    Lee, Dae-Hee
    Lee, Soo-Hong
    Kim, Byung-Soo
 TI In vitro cardiomyogenic differentiation of adipose-derived stromal
    cells using transforming growth factor-beta 1
 SO CELL BIOCHEMISTRY AND FUNCTION
 LA English
 DT Article
 DE adult stem cell; adipose-derived stromal cells; cardiomyogenic
    differentiation; transforming growth factor-beta 1; osteogenic
    differentiation
 ID MESENCHYMAL STEM-CELLS; HUMAN BONE-MARROW; MYOCARDIAL-INFARCTION;
    TGF-BETA; TISSUE; TRANSPLANTATION; CARDIOMYOCYTES; EXPRESSION;
    IMPLANTATION; GROWTH
 AB Transplanting stem cells differentiated towards a cardiac lineage can
    regenerate cardiac muscle tissues to treat myocardial infarction. In
    this study, we tested the hypothesis that transforming growth
    factor-beta 1 (TGF-beta 1) induces cardiomyogenic differentiation of
    adipose-derived stromal cells (ADSCs) in vitro. Rat ADSCs were cultured
    with TGF-beta 1 (10 ng ml(-1)) for 2 weeks in vitro. ADSCs cultured
    without TGF-beta 1 served as a control. The mRNA expression of
    cardiac-specific gene was induced by TGF-beta 1, while the control
    culture did not show cardiac-specific gene expression.
    Immunocytochemical analyses showed that a small fraction of ADSCs
    cultured with TGF-beta 1 for 2 weeks stained positively for cardiac
    myosin heavy chain (MHC) and alpha-sarcomeric actin. Flow cytometric
    analyses showed that the proportion of cells expressing cardiac MHC
    increased with TGF-beta 1. However, no mesenchymal differentiation
    (e.g., osteogenic and adipogenic differentiation) was detected other
    than cardiomyogenic differentiation. These results showed that TGF-beta
    1 induce ADSC cardiomyogenic differentiation in vitro, which could be
    useful for myocardial infarction stem cell therapy. Copyright (c) 2009
    John Wiley & Sons, Ltd.
 C1 [Bhang, Suk H.; Yang, Hee S.; Kim, Sang-Soo; Kim, Byung-Soo] Hanyang Univ, Dept Bioengn, Seoul 133791, South Korea.
    [Gwak, So-Jung] Hanyang Univ, Dept Chem Engn, Seoul 133791, South Korea.
    [Lee, Dae-Hee; Lee, Soo-Hong] Pochon CHA Univ, Cell & Gene Therapy Res Inst, Seoul, South Korea.
 RP Kim, BS, Hanyang Univ, Dept Bioengn, Seoul 133791, South Korea.
 EM bskim@hanyang.ac.kr
 FU Korea Health 21 R&D project, Ministry of Health & Welfare, Republic of
    Korea [A050082]
 FX This work was supported by the Korea Health 21 R&D project, Ministry of
    Health & Welfare (A050082), Republic of Korea.
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 NR 40
 TC 9
 PU JOHN WILEY & SONS LTD
 PI CHICHESTER
 PA THE ATRIUM, SOUTHERN GATE, CHICHESTER PO19 8SQ, W SUSSEX, ENGLAND
 SN 0263-6484
 J9 CELL BIOCHEM FUNCT
 JI Cell Biochem. Funct.
 PD APR
 PY 2009
 VL 27
 IS 3
 BP 148
 EP 154
 DI 10.1002/cbf.1547
 PG 7
 SC Biochemistry & Molecular Biology; Cell Biology
 GA 434ZI
 UT ISI:000265312500005
 ER
 
 PT J
 AU Sun, XF
    Xiao, B
    Zhang, GC
    Yang, XE
 AF Sun, Xiao-Feng
    Xiao, Bin
    Zhang, Guang Cheng
    Yang, Xiao-E
 TI INFRARED AND C-13 MAS NUCLEAR MAGNETIC RESONANCE SPECTROSCOPIC STUDY OF
    PERIPLOCA SEPIUM ACETYLATION
 SO CELLULOSE CHEMISTRY AND TECHNOLOGY
 LA English
 DT Article
 DE fiber; acetylation; N-bromosccinamide; infrared spectroscopy; nuclear
    magnetic resonance
 ID WOOD; HEMICELLULOSES; CELLULOSE; WHEAT
 AB Periploca sepium represents in important part of the local vegetation
    in the sandy land of China. This paper describes a novel method for
    modifying the Periploca sepium fiber under mild conditions. Both raw
    and modified Fibers were chemically studied by non-destructive methods,
    infrared spectroscopy (IR) and cross-polarisation nuclear magnetic
    resonance (CP-MAS C-13 NMR). The results showed that, during the
    reaction with acetic anhydride, the use of N-bromosuccinamide (NBS)
    catalyst resulted in a high mass percent gain (WPG - 20%). IR and
    CP-MAS C-13 NMR analysis elucidated in detail the chemical features of
    the natural and acetylated fiber, providing clear evidence of the
    successful acetylation.
 C1 [Sun, Xiao-Feng; Zhang, Guang Cheng] NW Polytech Univ, Coll Sci, Dept Appl Chem, Xian 710072, Peoples R China.
    [Xiao, Bin] NW A&F Univ, Coll Hort, Yangling 712100, Peoples R China.
    [Yang, Xiao-E] Zhejiang Univ, Inst Agrichem, MOE Key Lab Environm Remediat & Ecosyst Hlth, Hangzhou 310029, Zhejiang, Peoples R China.
 RP Sun, XF, NW Polytech Univ, Coll Sci, Dept Appl Chem, Xian 710072,
    Peoples R China.
 FU National Natural Science Foundation of China [20707016]; Northwestern
    Polytechnical University 
 FX The authors are grateful for the financial support provided by the
    National Natural Science Foundation of China (No. 20707016) and by the
    Northwestern Polytechnical University.
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 NR 21
 TC 0
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 PI BUCURESTI
 PA CALEA 13 SEPTEMBRIE NR 13, SECTOR 5, BUCURESTI 050711, ROMANIA
 SN 0576-9787
 J9 CELL CHEM TECHNOL
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 PD JAN-MAR
 PY 2008
 VL 42
 IS 1-3
 BP 17
 EP 22
 PG 6
 SC Materials Science, Paper & Wood
 GA 434IE
 UT ISI:000265267600003
 ER
 
 PT J
 AU Yang, P
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    Shi, ZB
    Huang, X
    Dang, XQ
    Xu, SL
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 AF Yang, Pei
    Wang, Chunsheng
    Shi, Zhibin
    Huang, Xin
    Dang, Xiaoqian
    Xu, Shanglong
    Wang, Kunzheng
 TI Prefabrication of Vascularized Porous Three-Dimensional Scaffold
    Induced from rhVEGF(165): A Preliminary Study in Rats
 SO CELLS TISSUES ORGANS
 LA English
 DT Article
 DE Tissue engineering; Angiogenesis; Scaffolds, prefabrication; Vascular
    endothelial growth factor
 ID ENDOTHELIAL GROWTH-FACTOR; CALCIUM-PHOSPHATE CEMENT; SEGMENTAL BONE
    DEFECTS; CHEMOTACTIC MIGRATION; ANGIOGENESIS; VEGF; TISSUE;
    REGENERATION; MATRICES; RELEASE
 AB Background/Aims: Several shortcomings have limited the routine use of
    autogenous vascularized bone graft. The present study investigates the
    prefabrication of vascularized scaffold with the desired shape and
    microarchitecture combined with recombinant human vascular endothelial
    growth factor 165 (rhVEGF(165)) to mimic autogenous vascularized bone
    graft. Methods: Eighty-five porous calcium phosphate cement scaffolds
    constructed by rapid prototyping technology were divided into four
    groups: group A [rhVEGF(165)-fibrin sealant (FS) scaffold], group B
    (hVEGF(165) scaffold), group C (FS scaffold), and group D (scaffold
    alone). The release of rhVEGF(165) from the scaffolds was examined in
    vitro. The vessel density, relative functionalized vessels, vessel
    diameter and relative vessel area were also measured. Results: The
    sustained release of hVEGF(165) lasted 14 days in the absence of
    plasmin and 12 days in the presence of plasmin in group A and 10 days
    in group B. There was no statistical difference between groups A and B
    at 2 or 4 weeks in terms of vessel density, relative functionalized
    vessels, vessel diameter, and relative vessel area, as between groups C
    and D. However, the above parameters were greater in groups A and B
    than groups C and D. Conclusion: The scaffolds with the desired shape
    and microarchitecture combined with rhVEGF(165) could shorten the time
    needed for the construction of prefabricated vascularized grafts and
    accelerate the maturation of the vessels. Copyright (C) 2008 S. Karger
    AG, Basel
 C1 [Yang, Pei; Wang, Chunsheng; Shi, Zhibin; Dang, Xiaoqian; Wang, Kunzheng] Xi An Jiao Tong Univ, Coll Med, Affiliated Hosp 2, Dept Orthoped, Xian 710004, Shaanxi, Peoples R China.
    [Huang, Xin] Xi An Jiao Tong Univ, Coll Med, Affiliated Hosp 1,Dept Cardiol,Educ Minist, Ion Channel Dis Lab,Key Lab Environm & Genes Rela, Xian 710004, Shaanxi, Peoples R China.
    [Xu, Shanglong] Xi An Jiao Tong Univ, State Key Lab Mfg Syst Engn, Xian 710004, Shaanxi, Peoples R China.
 RP Wang, KZ, Xi An Jiao Tong Univ, Coll Med, Affiliated Hosp 2, Dept
    Orthoped, 157 Xiwu Rd, Xian 710004, Shaanxi, Peoples R China.
 EM kunzhengwang@126.com
 FU National Science Foundation of China [30371443]
 FX This study was supported by the National Science Foundation of China
    (30371443). We thank Prof. Zengtie Zhang for his help with histology.
    We also thank Dr. Xudong Li of the Department of Orthopaedic Surgery,
    University of Virginia for the preparation of the manuscript.
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 PU KARGER
 PI BASEL
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 SN 1422-6405
 J9 CELLS TISSUES ORGANS
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 PY 2009
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 BP 327
 EP 337
 DI 10.1159/000142162
 PG 11
 SC Anatomy & Morphology; Cell Biology; Developmental Biology
 GA 433BM
 UT ISI:000265178600003
 ER
 
 PT J
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    Bergsmedh, A
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 AF Ehnfors, J.
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 TI Horizontal transfer of tumor DNA to endothelial cells in vivo
 SO CELL DEATH AND DIFFERENTIATION
 LA English
 DT Article
 DE cell fusion; apoptosis; gene transfer; phagocytosis; neovascularization
 ID FIBROBLAST-GROWTH-FACTOR; GENETIC ALTERATIONS; APOPTOTIC BODIES;
    MICRODISSECTED STROMA; BREAST-CANCER; FUSION; TUMORIGENESIS;
    ANGIOGENESIS; CARCINOMA
 AB Tumor endothelial cells have long been regarded as genomically stable
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    cells maintained the ability to form functional vessels in an in vivo
    assay and concurrently express tumor-encoded and endothelial-specific
    genes.
 C1 [Ehnfors, J.; Persson, N. Luna; Bergsmedh, A.; Castro, J.; Levchenko-Tegnebratt, T.; Yang, L.; Panaretakis, T.; Holmgren, L.] CCK, Karolinska Inst, Dept Pathol & Oncol, S-17176 Stockholm, Sweden.
    [Kost-Alimova, M.] Karolinska Inst, Dept Microbiol Tumor & Cell Biol, S-17177 Stockholm, Sweden.
 RP Holmgren, L, CCK, Karolinska Inst, Dept Pathol & Oncol, S-17176
    Stockholm, Sweden.
 EM lars.holmgren@ki.se
 FU Swedish Research Council ; Swedish Cancer Society ; Karolinska
    Institutet, Cancerforeningen, Stockholm, Sweden ; EUCAAD [FP7]
 FX We dedicate this paper to the memory of Judah Folkman. This study was
    supported by grants from the Swedish Research Council, Swedish Cancer
    Society, Karolinska Institutet, Cancerforeningen, Stockholm, Sweden,
    and EUCAAD FP7. We thank Dr. Raja Choudhury for proofreading the paper.
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 UT ISI:000265245400010
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 PT J
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 SO CANCER SCIENCE
 LA English
 DT Article
 ID ENDOTHELIAL GROWTH-FACTOR; BREAST-CANCER METASTASIS; RENAL-CELL
    CARCINOMA; STEM-CELLS; ANGIOGENESIS; LYMPHANGIOGENESIS;
    THROMBOSPONDIN-1; BEVACIZUMAB; MECHANISMS; RESISTANCE
 AB Antiangiogenic therapy is a potent cancer treatment, however, the
    possibility of recurrence and resistance to this approach remains. Here
    we show that hypoxia and low-nutrition double-deprivation stress
    induces reversible tumor aggressiveness. In a stress-cycle-dependent
    manner, murine melanoma cells showed morphological changes,
    up-regulated phospho-Akt, and abnormal regulation of multiple genes
    including fibroblast growth factor-21, a metabolic regulator, resulting
    in increased cell proliferation in vitro, and increased tumorigenesis
    and invasive potential in vivo. In this system, altered cellular
    metabolism participates in the adaptation of tumor to the
    double-deprivation stress. Our results suggest the targeting of a minor
    population of cancer cells resistant to both hypoxia and low nutrition
    to be an effective new antitumor strategy in combination with
    antiangiogenic therapy. (Cancer Sci 2009; 100: 844-851).
 C1 [Osawa, Tsuyoshi; Muramatsu, Masashi; Shibuya, Masabumi] Tokyo Med & Dent Univ, Grad Sch Med & Dent, Dept Mol Oncol, Tokyo, Japan.
    [Watanabe, Makoto] Univ Tokyo, Inst Med Sci, Div Syst Biomed Technol, Tokyo, Japan.
 RP Shibuya, M, Tokyo Med & Dent Univ, Grad Sch Med & Dent, Dept Mol Oncol,
    Tokyo, Japan.
 EM shibuya@ims.u-tokyo.ac.jp
 FU Ministry of Education, Culture, Sports, Science and Technology of Japan
    [17014020]; Japan Society for Promotion of Science ; Organization for
    Pharmaceutical Safety and Research 
 FX This work was supported by a Grant-in-Aid for Special Project Research
    on Cancer-Bioscience (No. 17014020) from the Ministry of Education,
    Culture, Sports, Science and Technology of Japan; a grant from the
    program 'Research for the Future' from the Japan Society for Promotion
    of Science; and a grant from the program 'Promotion of Fundamental
    Research in Health Science' from the Organization for Pharmaceutical
    Safety and Research. We thank Dr Y. Yuasa and Dr T. Koda (Tokyo Dental
    and Medical University, Tokyo, Japan), and Dr M. Murakami, Dr S.
    Yamamoto, and Ms. S Yamaguchi (Institute of Medical Science, University
    of Tokyo, Tokyo, Japan) for helpful discussions.
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 NR 41
 TC 3
 PU WILEY-BLACKWELL PUBLISHING, INC
 PI MALDEN
 PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
 SN 1347-9032
 J9 CANCER SCI
 JI Cancer Sci.
 PD MAY
 PY 2009
 VL 100
 IS 5
 BP 844
 EP 851
 DI 10.1111/j.1349-7006.2009.01105.x
 PG 8
 SC Oncology
 GA 434CA
 UT ISI:000265251600009
 ER
 
 PT J
 AU Shibata, H
    Yamakoshi, H
    Sato, A
    Ohori, H
    Kakudo, Y
    Kudo, C
    Takahashi, Y
    Watanabe, M
    Takano, H
    Ishioka, C
    Noda, T
    Iwabuchi, Y
 AF Shibata, Hiroyuki
    Yamakoshi, Hiroyuki
    Sato, Atsuko
    Ohori, Hisatsugu
    Kakudo, Yuichi
    Kudo, Chieko
    Takahashi, Yayoi
    Watanabe, Mika
    Takano, Hiroshi
    Ishioka, Chikashi
    Noda, Tetsuo
    Iwabuchi, Yoshiharu
 TI Newly synthesized curcumin analog has improved potential to prevent
    colorectal carcinogenesis in vivo
 SO CANCER SCIENCE
 LA English
 DT Article
 ID FAMILIAL ADENOMATOUS POLYPOSIS; BETA-CATENIN; COLON-CANCER; APC;
    TRANSCRIPTION; ACTIVATION; MODEL
 AB Curcumin (diferuloylmethane) has chemopreventive and chemotherapeutic
    potentials against various types of cancers. We have developed a series
    of curcumin analogs to improve its low bioavailability by enhancing its
    potentials. The newly synthesized analog GO-Y030 [(1E,
    4E)-1,5-bis-(3,5(-bismethoxymethoxyphenyl) penta-1,4-dien-3-one] showed
    a 30-fold greater growth suppression in vitro via similar molecular
    mechanisms to curcumin. The availability of this analog was examined by
    using a mouse model harboring the germ-line mutation of Apc,
    Apc(580D/+), in vivo. Apc(580D/+) mice had a very limited survival time
    with an intestinal obstruction due to polyposis. The average tumor
    number in mice fed GO-Y030 was reduced to 61.2% of those that were fed
    the basal diet (P < 0.05). Compared with Apc(580D/+) mice fed the basal
    diet (median survival time = 166.5 days), a significantly prolonged
    lifespan (213 days) was observed in Apc(580D/+) mice fed GO-Y030. The
    chemopreventive effect with GO-Y030 was improved, compared with
    curcumin (191 days). The survival benefit corresponded to the
    diminished intestinal tumor incidence in Apc(580D/+) mice fed GO-Y030.
    No adverse reactions were observed, judging from body weight or
    biochemical data concerning liver and renal damage. Degradation of
    accumulated beta-catenin with curcumin is one of the major mechanisms
    of chemoprevention in colorectal carcinogenesis. It was demonstrated
    that the number of beta-catenin-positive adenoma cells in Apc(580D/+)
    mice fed GO-Y030 was reduced. (Cancer Sci 2009; 100: 956-960).
 C1 [Shibata, Hiroyuki; Sato, Atsuko; Ohori, Hisatsugu; Kakudo, Yuichi; Kudo, Chieko; Ishioka, Chikashi] Tohoku Univ, Inst Dev Aging & Canc, Dept Clin Oncol, Sendai, Miyagi 980, Japan.
    [Shibata, Hiroyuki; Ohori, Hisatsugu; Kakudo, Yuichi; Kudo, Chieko; Ishioka, Chikashi] Tohoku Univ, Univ Hosp, Dept Clin Oncol, Sendai, Miyagi 980, Japan.
    [Yamakoshi, Hiroyuki; Iwabuchi, Yoshiharu] Tohoku Univ, Grad Sch Pharmaceut, Dept Organ Chem, Sendai, Miyagi 980, Japan.
    [Takahashi, Yayoi; Watanabe, Mika] Tohoku Univ Hosp, Dept Pathol, Sendai, Miyagi, Japan.
    [Takano, Hiroshi; Noda, Tetsuo] Japanese Fdn Canc Res, Inst Canc, Dept Cell Biol, Tokyo 170, Japan.
 RP Shibata, H, Tohoku Univ, Inst Dev Aging & Canc, Dept Clin Oncol,
    Sendai, Miyagi 980, Japan.
 EM hiroyuki@idac.tohoku.ac.jp
 FU Ministry of Education, Culture, Sports, Science and Technology, Japan
    [17015002]
 FX Grants-in-aid were received from the HIROMI Medical Reserarch
    Foundation, Sendai, Japan (H. Shibata) and Miyagi Health Service
    Association (C. Ishioka). Grants-in-Aid for Scientific Research on
    Priority Areas (Cancer, No. 17015002) were received from the Ministry
    of Education, Culture, Sports, Science and Technology, Japan (H.
    Shibata and C. Ishioka). The immunohistchemical analysis of
    beta-catenin was conducted at Kotobiken Medical Laboratories, Tokyo,
    Japan.
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 NR 18
 TC 6
 PU WILEY-BLACKWELL PUBLISHING, INC
 PI MALDEN
 PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
 SN 1347-9032
 J9 CANCER SCI
 JI Cancer Sci.
 PD MAY
 PY 2009
 VL 100
 IS 5
 BP 956
 EP 960
 DI 10.1111/j.1349-7006.2009.01127.x
 PG 5
 SC Oncology
 GA 434CA
 UT ISI:000265251600024
 ER
 
 PT J
 AU Xu, XL
    Yang, YJ
    Zhu, NS
 AF Xu, Xiulin
    Yang, Yujing
    Zhu, Naishuo
 TI Characteristics and Molecular Mechanism of Adhesion Proteins on Reused
    Hemodialysis Membranes
 SO BLOOD PURIFICATION
 LA English
 DT Article
 DE Reusable dialysis; Adhesion protein; Two-dimensional electrophoresis;
    Mass spectrum; Adhesion mechanism
 ID DIALYZER REUSE; PERACETIC-ACID; POLYSULFONE; ACTIVATION; ADSORPTION;
    SOLUTE; COMPLEMENT; TRANSPORT; FICOLINS; REMOVAL
 AB In order to study the mechanism of protein adhesion on the Fresenius F6
    polysulfone membrane dialyzer, two-dimensional gel electrophoresis,
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    protein which adhered to the dialyzer membrane. Six of the adhered
    proteins account for more than 50% of the total 179 proteins, i.e.
    ficolin precursor, complement C3 precursor, 3 variants of MASP1 and
    albumin. The results also showed that easily adhered proteins have a
    greater percentage of acidic amino acids (p < 0.01). The isoelectric
    point of the 20 proteins with the most deposits is 6.2 +/- 1.08, which
    is obviously lower than of those with the least deposits (7.56 +/-
    1.36, p < 0.01). The dipole moment of a polysulfone membrane molecule
    has a tendency to absorb molecules with a negative charge. These
    results are of significance in understanding and improving membrane
    protein interactions. Copyright (C) 2009 S. Karger AG, Basel
 C1 [Zhu, Naishuo] Fudan Univ, Sch Life Sci, State Key Lab Genet Engn, Lab Mol Immunol, Shanghai 200433, Peoples R China.
    [Xu, Xiulin; Yang, Yujing] Shanghai Univ Sci & Technol, Inst Med Device & Food Sci, Shanghai 201800, Peoples R China.
 RP Zhu, NS, Fudan Univ, Sch Life Sci, State Key Lab Genet Engn, Lab Mol
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 EM nzhu@fudan.edu.cn
 FU science foundation of the Shanghai education committee [04EB18]
 FX This work was supported by the science foundation of the Shanghai
    education committee (No. 04EB18).
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 NR 35
 TC 2
 PU KARGER
 PI BASEL
 PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND
 SN 0253-5068
 J9 BLOOD PURIFICAT
 JI Blood Purif.
 PY 2009
 VL 27
 IS 4
 BP 321
 EP 329
 DI 10.1159/000207199
 PG 9
 SC Hematology; Urology & Nephrology
 GA 432HE
 UT ISI:000265123300002
 ER
 
 PT J
 AU Qi, XH
    Yang, JH
    Yu, JQ
    Zhang, MF
 AF Qi, Xiao-Hua
    Yang, Jing-Hua
    Yu, Jing-Quan
    Zhang, Ming-Fang
 TI Genetic and heterosis analysis for important agronomic traits of
    Chinese vegetable mustard (Brassica juncea) in different environments
 SO GENETICA
 LA English
 DT Article
 DE Agronomic traits; Brassica juncea; Genetic analysis; Genotype
    environment interaction; Heterosis
 ID QUALITY TRAITS; RICE; IDENTIFICATION; CROSSES; MODEL
 AB Genetic effects and genotype by environment (GE) interaction effects
    for some important agronomic traits of Chinese vegetable mustard were
    analyzed by using a genetic model including additive, dominance,
    additive x additive effects and their interaction effects with the
    environment. Four variations of Chinese vegetable mustard as parental
    lines and their F-1s, F-2s were evaluated in two locations. It was
    revealed that the agronomic traits of Chinese vegetable mustard were
    mainly controlled by genetic effects except plant weight (PW) and leaf
    weight (LW) were observed to be more affected by GE interaction
    effects. Among the genetic effects, additive effects took the main
    proportion for tiller number (TN), leaf number (LN), leaf breadth (LB)
    and LW; dominance effects were the main components of PW, leaf length
    (LL), root weight (RW) and plant height (PH); additive x additive
    effects were the main components of plant breadth (PB). Among the GE
    interaction effects, additive x environment interaction effects mainly
    affected LB, LW and RW, while PW, LL, PH and PB were mainly controlled
    by dominance x environment interaction effects. Besides, additive x
    additive x environment interaction was the main factor, which
    controlled TN and LN of Chinese vegetable mustard. For heterosis
    analyses, TN, LN, LB and LW of Chinese vegetable mustard showed
    positive H-PM and negative H-PB. The other traits showed positive H-PM
    and H-PB. Heterosis arising from GE interaction was found to varying
    degree for different environments. It was shown that genetic heterosis
    and GE interaction effects were important factors for agronomic traits
    in Chinese vegetable mustard.
 C1 [Qi, Xiao-Hua; Yang, Jing-Hua; Yu, Jing-Quan; Zhang, Ming-Fang] Zhejiang Univ, Dept Hort Sci, Lab Genet Resources & Funct Improvement Hort Plan, Hangzhou 310029, Zhejiang, Peoples R China.
    [Qi, Xiao-Hua; Yang, Jing-Hua; Yu, Jing-Quan; Zhang, Ming-Fang] Minist Agr, Lab Hort Plant Growth Dev & Biotechnol, Hangzhou 310029, Zhejiang, Peoples R China.
 RP Zhang, MF, Zhejiang Univ, Dept Hort Sci, Lab Genet Resources & Funct
    Improvement Hort Plan, Hangzhou 310029, Zhejiang, Peoples R China.
 EM xiaohuasea@126.com
    mfzhang@zju.edu.cn
 FU National Natural Science Foundation of China (NSFC) [30571270]
 FX Our work was supported by a grant from the National Natural Science
    Foundation of China (NSFC, 30571270). We are grateful Shaoxing Academy
    of Agricultural Science of Zhejiang province for providing us
    experiment locations. We appreciate Dr. Hai-Ming Xu and Dr. Mikio
    Nakazono, for their generous advice and support in the study. The
    authors are very grateful to two anonymous referees for their helpful
    and valuable suggestions.
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 NR 20
 TC 0
 PU SPRINGER
 PI DORDRECHT
 PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
 SN 0016-6707
 J9 GENETICA
 JI Genetica
 PD MAY
 PY 2009
 VL 136
 IS 1
 BP 89
 EP 95
 DI 10.1007/s10709-008-9316-0
 PG 7
 SC Genetics & Heredity
 GA 428GJ
 UT ISI:000264835700010
 ER
 
 PT J
 AU Yang, F
    Green, JJ
    Dinio, T
    Keung, L
    Cho, SW
    Park, H
    Langer, R
    Anderson, DG
 AF Yang, F.
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    Cho, S-W
    Park, H.
    Langer, R.
    Anderson, D. G.
 TI Gene delivery to human adult and embryonic cell-derived stem cells
    using biodegradable nanoparticulate polymeric vectors
 SO GENE THERAPY
 LA English
 DT Article
 DE stem cells; gene delivery; biodegradable; polymeric vectors
 ID POLY(BETA-AMINO ESTER)S; CATIONIC POLYMERS; PLASMID DNA; THERAPY;
    TRANSFECTION; LIBRARY; TISSUE; EFFICIENT; NEURONS; MODEL
 AB Gene delivery to stem cells holds great potential for tissue
    regeneration and delivery of therapeutic proteins. The major barrier is
    the lack of safe and efficient delivery methods. Here, we report
    enhanced gene delivery systems for human stem cells using biodegradable
    polymeric vectors. A library of poly (beta- amino esters) end-modified
    derivatives was developed and optimized for high transfection
    efficiency and low cytotoxicity for three human stem cell lines
    including human mesenchymal stem cells (hMSCs), human adipose-derived
    stem cells (hADSCs) and human embryonic stem cell-derived cells
    (hESCds). In the presence of 10% serum, leading end-modified C32
    polymeric vectors exhibited significantly high transfection efficiency
    in hMSCs (27 +/- 2%), hADSCs (24 +/- 3%) and hESCds (56 +/- 11%), with
    high cell viability (87 - 97%) achieved in all cell types. Our results
    show that poly(beta-amino esters) as a class, and end-modified versions
    of C32 in particular, are efficient polymeric vectors for gene delivery
    to both adult and embryonic-derived stem cells.
 C1 [Yang, F.; Green, J. J.; Keung, L.; Cho, S-W; Langer, R.] MIT, Dept Chem Engn, Cambridge, MA 02139 USA.
    [Dinio, T.] Univ Calif Berkeley, Dept Chem Engn, Berkeley, CA 94720 USA.
    [Park, H.] Harvard Univ, Sch Med, Dept Surg, Massachusetts Gen Hosp, Boston, MA 02115 USA.
    [Langer, R.] MIT, Harvard Mit Div Hlth Sci & Technol, Cambridge, MA 02139 USA.
    [Langer, R.; Anderson, D. G.] MIT, David H Koch Inst Integrat Canc Res, Cambridge, MA 02139 USA.
 RP Anderson, DG, MIT, Koch Inst Integrat Canc Res, 77 Massachusetts
    Ave,E25-342, Cambridge, MA 02139 USA.
 EM dgander@mit.edu
 FU NIH [R01-EB000244-27, R01-DE01651603]; National Institutes of Health
    for National Research Service [1F32 AR056567-01]
 FX We thank the NIH (R01-EB000244-27 and R01-DE01651603) for funding. FY
    gratefully acknowledge the National Institutes of Health for National
    Research Service Award postdoctoral fellowship (1F32 AR056567-01). We
    also thank the laboratory of Professor Johnny Huard at the University
    of Pittsburgh for kindly providing us the DNA plasmid-encoding human
    vascular endothelial growth factor 165 used in this study.
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 NR 41
 TC 13
 PU NATURE PUBLISHING GROUP
 PI LONDON
 PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
 SN 0969-7128
 J9 GENE THERAPY
 JI Gene Ther.
 PD APR
 PY 2009
 VL 16
 IS 4
 BP 533
 EP 546
 DI 10.1038/gt.2008.182
 PG 14
 SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology;
    Genetics & Heredity; Medicine, Research & Experimental
 GA 430WL
 UT ISI:000265021400011
 ER
 
 PT J
 AU Huang, HG
    Zhao, WM
    Tang, ZL
    Yang, SL
    Wu, ZF
    Zhao, SH
    Cui, WT
    Mu, YL
    Chu, MX
    Li, K
 AF Huang, Honggang
    Zhao, Weimin
    Tang, Zhonglin
    Yang, Shulin
    Wu, Zhengfang
    Zhao, Shuhong
    Cui, Wentao
    Mu, Yulian
    Chu, Mingxing
    Li, Kui
 TI Characterization of porcine MMP-2 and its association with immune traits
 SO GENE
 LA English
 DT Article
 DE Pig; MMP-2; Genomic structure; Promotor; Mapping; Association analysis;
    Immune traits
 ID NF-KAPPA-B; MATRIX-METALLOPROTEINASE; GELATINASE-A; CYTOKINE
    REGULATION; GENE-EXPRESSION; INFLAMMATION; ANGIOGENESIS; INVASION;
    CELLS; MICE
 AB Matrix metalloproteinase-2 (MMP-2) plays important roles in
    inflammation and immunity besides its basic role in degrading and
    remodelling extracellular matrix (ECM). The expression of MMP-2 is
    up-regulated in many human as well as animal models of inflammatory and
    immune diseases. In this study, we cloned the 5'-upstream sequence,
    3'-downstream sequence as well as other missed genomic sequences of
    porcine MMP-2, the genomic Structure and the promotor sequence were
    analyzed and found to share high similarity with those of human MMP-2.
    Porcine MMP-2 was assigned to SSC6p14-p15, and closely linked to
    microsatellite SW1108 (53cR, LOD score 7.59) by IMpRH panel. Real-time
    PCR analysis revealed that the expression of porcine MMP-2 was
    remarkably different in diverse tissues, a high level expression was
    observed in the testis and uterus, relatively low expression in other
    tissues. Allele frequencies determination in different pig breeds and
    association study were performed on the selected SNP and indel. The
    results showed that the SNP Acyl in exon 12 was significantly
    associated with white blood cell count (WBC) of neonate piglets at 0
    day (P=0.0079), and classical swine fever virus antibody level
    (CSFV-AB) of pigs at 17 days (P=0.0461), the indel MspI in intron 4 had
    remarkable correlation with mean corpuscular hemoglobin (MCH) of pigs
    at 17 days (P<0.0001). (C) 2009 Elsevier B.V. All rights reserved.
 C1 [Huang, Honggang; Zhao, Weimin; Tang, Zhonglin; Yang, Shulin; Cui, Wentao; Mu, Yulian; Chu, Mingxing; Li, Kui] Chinese Acad Agr Sci, Inst Anim Sci, Minist Agr China, Key Lab Farm Anim Genet Resources & Utilizat, Beijing 100193, Peoples R China.
    [Zhao, Weimin; Zhao, Shuhong] Huazhong Agr Univ, Coll Anim Sci & Technol, Minist Educ China, Key Lab Agr Anim Genet Breeding & Repprod, Wuhan 430070, Hubei, Peoples R China.
    [Wu, Zhengfang] Huanan Agr Univ, Coll Anim Sci, Guangzhou 510642, Guangdong, Peoples R China.
 RP Li, K, Chinese Acad Agr Sci, Inst Anim Sci, Minist Agr China, Key Lab
    Farm Anim Genet Resources & Utilizat, Beijing 100193, Peoples R China.
 EM kuili@iascaas.net.cn
 FU National Natural Science Foundation of China ; National High Science
    and Technology Foundation of China ; Key Project of National Basic
    Research and Development Plan of China ; State Platform of Technology
    Infrastructure [2005DK21101]; National Support Plan and Innovation
    Group Foundation of IAS, CAAS 
 FX The authors thank Dr Martine Yerle of INRA, France for Providing the RH
    panel. We thank Xiangdong Liu, Prof Qin Zhang and Yong Li for advice
    and help. This work was supported by National Natural Science
    Foundation of China, National High Science and Technology Foundation of
    China, Key Project of National Basic Research and Development Plan of
    China and State Platform of Technology Infrastructure (2005DK21101),
    National Support Plan and Innovation Group Foundation of IAS, CAAS.
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 NR 48
 TC 4
 PU ELSEVIER SCIENCE BV
 PI AMSTERDAM
 PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
 SN 0378-1119
 J9 GENE
 JI Gene
 PD APR 15
 PY 2009
 VL 435
 IS 1-2
 BP 63
 EP 71
 DI 10.1016/j.gene.2009.01.002
 PG 9
 SC Genetics & Heredity
 GA 430UL
 UT ISI:000265014600009
 ER
 
 PT J
 AU Wang, F
    Feng, MH
    Xu, P
    Xiao, H
    Niu, P
    Yang, XB
    Bai, Y
    Peng, Y
    Yao, PF
    Tan, H
    Tanguay, RM
    Wu, TC
 AF Wang, Feng
    Feng, Maohui
    Xu, Ping
    Xiao, Han
    Niu, Piye
    Yang, Xiaobo
    Bai, Yun
    Peng, Ying
    Yao, Pinfang
    Tan, Hao
    Tanguay, Robert M.
    Wu, Tangchun
 TI The level of Hsp27 in lymphocytes is negatively associated with a
    higher risk of lung cancer
 SO CELL STRESS & CHAPERONES
 LA English
 DT Article
 DE Biomarker; Hsp27; Hsp70; Hsps; Lung cancer; Lymphocyte; Risk
 ID HEAT-SHOCK PROTEINS; MOLECULAR CHAPERONES; OXIDATIVE STRESS;
    GENE-EXPRESSION; HEAT-SHOCK-PROTEIN-70 LEVELS; ESTROGEN-RECEPTOR;
    TRANSGENIC MICE; ISCHEMIC-INJURY; HUMAN MONOCYTES; TOBACCO-SMOKE
 AB Heat shock proteins (Hsps) can protect cells, organs, and whole
    organisms against damage caused by abnormal environmental hazards. Some
    studies have reported that lymphocyte Hsps may serve as biomarkers for
    evaluating disease status and exposure to environmental stresses;
    however, few epidemiologic studies have examined the associations
    between lymphocyte Hsps levels and lung cancer risk. We examined
    lymphocyte levels of Hsp27 and Hsp70 in 263 lung cancer cases and age-
    and gender-matched cancer-free controls by flow cytometry. Multivariate
    logistic regression models were used to estimate the association
    between lymphocyte Hsps levels and lung cancer risk. Our results showed
    that Hsp27 levels were significantly lower in lung cancer cases than in
    controls (16.5 vs 17.8 mean fluorescence intensity, P < 0.001). This
    was not observed for Hsp70 levels. Further stratification analysis
    revealed that lymphocyte Hsp27 levels were negatively associated with
    lung cancer risk especially in males and heavy smokers. There was a
    statistical trend of low odd ratios (95% confidence intervals) and
    upper tertile levels of Hsp27 [1.000, 0.904 (0.566-1.444) and 0.382
    (0.221-0.658, P (trend) = 0.001) in males and 1.000, 0.9207
    (0.465-1.822) and 0.419 (0.195-0.897, P (trend) = 0.036) in heavy
    smokers] after adjustment for confounding factors. These results
    suggest that lower lymphocyte Hsp27 levels might be associated with an
    increased risk of lung cancer. Our findings need to be validated in a
    large prospective study.
 C1 [Wang, Feng; Feng, Maohui; Xiao, Han; Niu, Piye; Yang, Xiaobo; Bai, Yun; Tan, Hao; Wu, Tangchun] Huazhong Univ Sci & Technol, Tongji Med Coll, Sch Publ Hlth, Dept Occupat & Environm Hlth, Wuhan 430030, Hubei, Peoples R China.
    [Wang, Feng; Feng, Maohui; Xiao, Han; Niu, Piye; Yang, Xiaobo; Bai, Yun; Tan, Hao; Wu, Tangchun] Huazhong Univ Sci & Technol, Tongji Med Coll, Sch Publ Hlth, Minist Educ,Key Lab Environm & Hlth, Wuhan 430030, Hubei, Peoples R China.
    [Feng, Maohui] Wuhan Univ, Zhongnan Hosp, Dept Oncol, Wuhan 430071, Peoples R China.
    [Xu, Ping; Peng, Ying] Wugang Staff Worker Hosp, Dept Oncol, Wuhan 430085, Peoples R China.
    [Yao, Pinfang] Hubei Canc Hosp, Inst Canc, Wuhan 430030, Peoples R China.
    [Tanguay, Robert M.] Univ Laval, Dept Med, Fac Med, Lab Cellular & Dev Genet, Quebec City, PQ G1V 0A6, Canada.
    [Tanguay, Robert M.] Univ Laval, PROTEO, Quebec City, PQ G1V 0A6, Canada.
 RP Wu, TC, Huazhong Univ Sci & Technol, Tongji Med Coll, Sch Publ Hlth,
    Dept Occupat & Environm Hlth, 2nd Bldg,13 Hangkong Rd, Wuhan 430030,
    Hubei, Peoples R China.
 EM wut@mails.tjmu.edu.cn
 FU National Natural Science Foundation of China [30525031, 30600491];
    National Key Basic Research and Development Program [2002CB512905];
    NNSFC-CIHR 
 FX We thank all individuals who volunteered to participate in this study
    and the members of health examination center of Wugang Worker-Staff
    Hospital and Qingyi Wei of The University of M. D. Anderson Cancer
    Center for his critical review and scientific editing. This work was
    supported by research funds from the National Natural Science
    Foundation of China (NNSFC 30525031 and 30600491) and the National Key
    Basic Research and Development Program (2002CB512905), and a NNSFC-CIHR
    (Canadian Institutes of Health Research) joint research program to
    Tangchun Wu and Robert M Tanguay.
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 NR 52
 TC 1
 PU SPRINGER
 PI DORDRECHT
 PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
 SN 1355-8145
 J9 CELL STRESS CHAPERONES
 JI Cell Stress Chaperones
 PD MAY
 PY 2009
 VL 14
 IS 3
 BP 245
 EP 251
 DI 10.1007/s12192-008-0078-5
 PG 7
 SC Cell Biology
 GA 428FI
 UT ISI:000264833000002
 ER
 
 PT J
 AU Liu, XH
    Ren, Z
    Zhan, R
    Wang, XX
    Wang, XM
    Zhang, ZQ
    Leng, X
    Yang, ZH
    Qian, LJ
 AF Liu, XiaoHua
    Ren, Zhe
    Zhan, Rui
    Wang, XinXing
    Wang, XiaoMing
    Zhang, ZhiQing
    Leng, Xue
    Yang, ZhiHua
    Qian, LingJia
 TI Prohibitin protects against oxidative stress-induced cell injury in
    cultured neonatal cardiomyocyte
 SO CELL STRESS & CHAPERONES
 LA English
 DT Article
 DE Apoptosis; Cardiomyocyte; Mitochondria; Oxidative stress; Prohibitin
 ID MITOCHONDRIAL PROTEINS; SACCHAROMYCES-CEREVISIAE; CANCER CELLS;
    APOPTOSIS; RAT; FAMILY; PROLIFERATION; STABILIZATION; INHERITANCE;
    MAINTAINS
 AB Oxidative stress is one of the main causes of myocardial injury, which
    is associated with cardiomyocyte death. Mitochondria play a key role in
    triggering the necrosis and apoptosis pathway of cardiomyocytes under
    oxidative stress. Although prohibitin (PHB) has been acknowledged as a
    mitochondrial chaperone, its functions in cardiomyocytes are poorly
    characterized. The present research was designed to investigate the
    cardioprotective role of PHB in mitochondria. Oxidative stress can
    increase the PHB content in mitochondria in a time-dependent manner.
    Overexpression of PHB in cultured cardiomyocytes by transfection of
    recombinant adenovirus vector containing PHB sense cDNA resulted in an
    increase of PHB in mitochondria. Compared with the non-transfection
    cardiomyocytes, PHB overexpression could protect the mitochondria from
    oxidative stress-induced injury. The mitochondria-mediated apoptosis
    pathway was consistently suppressed in PHB-overexpressed cardiomyocytes
    after hydrogen peroxide (H2O2) treatment, including a reduced change in
    mitochondrial membrane permeability transition and an inhibited release
    of cytochrome c from mitochondria to cytoplasma. As a result, the
    oxidative stress-induced cardiomyocyte apoptosis was suppressed. These
    data indicated that PHB protected the cardiomyocytes from oxidative
    stress-induced damage, and that increasing PHB content in mitochondria
    constituted a new therapeutic target for myocardium injury.
 C1 [Liu, XiaoHua; Ren, Zhe; Zhan, Rui; Wang, XinXing; Wang, XiaoMing; Zhang, ZhiQing; Leng, Xue; Yang, ZhiHua; Qian, LingJia] Inst Hlth Environm Med, Dept Stress Med, Tianjin 300050, Peoples R China.
 RP Qian, LJ, Inst Hlth Environm Med, Dept Stress Med, DaLi Rd 1, Tianjin
    300050, Peoples R China.
 EM newjia@vip.sina.com
 FU Chinese National Natural Science Foundation [30570753]; Major Research
    Plan of the Chinese National Natural Science Foundation [30430590,
    30393134]
 FX This research was supported by the General Program of the Chinese
    National Natural Science Foundation (grant no. 30570753) and the Major
    Research Plan of the Chinese National Natural Science Foundation (grant
    nos. 30430590 and 30393134).
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 TC 7
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 PI DORDRECHT
 PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
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 J9 CELL STRESS CHAPERONES
 JI Cell Stress Chaperones
 PD MAY
 PY 2009
 VL 14
 IS 3
 BP 311
 EP 319
 DI 10.1007/s12192-008-0086-5
 PG 9
 SC Cell Biology
 GA 428FI
 UT ISI:000264833000009
 ER
 
 PT J
 AU Shih, TTF
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    Liu, CY
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    Tang, JL
    Chen, HY
    Wei, SY
    Yao, M
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 AF Shih, Tiffany Ting-Fang
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 TI Bone marrow angiogenesis magnetic resonance imaging in patients with
    acute myeloid leukemia: peak enhancement ratio is an independent
    predictor for overall survival
 SO BLOOD
 LA English
 DT Article
 ID ENDOTHELIAL GROWTH-FACTOR; MICROVESSEL DENSITY; MULTIPLE-MYELOMA;
    MYELODYSPLASTIC SYNDROMES; VASCULOGENIC MIMICRY; TUMOR ANGIOGENESIS;
    IN-VIVO; CERVICAL-CARCINOMA; LUMBAR SPINE; DYNAMIC MRI
 AB Emerging evidence suggests that progression of hematologic malignancies
    is associated with angiogenesis. Dynamic contrast-enhanced magnetic
    resonance imaging (DCE-MRI) can provide global and functional imaging
    of tumor angiogenesis. In this study, we performed bone marrow DCE-MRI
    prospectively at diagnosis and after induction chemotherapy in 78 de
    novo acute myeloid leukemia (AML) patients and correlated it with
    treatment outcome. An algorithm to assess bone marrow angiogenesis by
    measuring the DCE-MRI time-intensity curve pixel by pixel was developed
    using 3 distinct parameters: peak enhancement ratio (Peak) to indicate
    tissue blood perfusion; amplitude (Amp) to reflect vascularity; and
    volume transfer constant (K trans) to indicate vascular permeability.
    The Peak and Amp decreased significantly at remission status after
    induction chemotherapy. Patients with higher Peak or Amp at diagnosis
    had shorter overall survival and disease-free survival than others. Cox
    multivariate analysis identified higher Peak value (hazard ratio,
    9.181; 95% confidence interval, 1.740-48.437; P = .009) as an
    independent predictor for overall survival in addition to unfavorable
    karyotype and old age. Our findings provide evidence that increased
    bone marrow angiogenesis measured by DCE-MRI can predict adverse
    clinical outcome in AML patients. DCE-MRI may help to select high-risk
    phenotype AML patients for tailored antiangiogenic therapy and to
    monitor treatment response. (Blood. 2009; 113:3161-3167)
 C1 [Hou, Hsin-An; Tang, Jih-Luh; Yao, Ming; Huang, Shang-Yi; Tsay, Woei; Tien, Hwei-Fang; Yang, Pan-Chyr] Natl Taiwan Univ Hosp & Coll Med, Dept Internal Med, Taipei, Taiwan.
    [Shih, Tiffany Ting-Fang; Chen, Bang-Bin; Wei, Shwu-Yuan; Yu, Chih-Wei; Hsu, Chao-Yu] Natl Taiwan Univ Hosp & Coll Med, Dept Med Imaging & Radiol, Taipei, Taiwan.
    [Hou, Hsin-An] Natl Taiwan Univ Hosp, Dept Internal Med, Yun Lin Branch, Taipei, Yun Lin County, Taiwan.
    [Liu, Chieh-Yu] Natl Taipei Coll Nursing, Biostat Consulting Lab, Dept Nursing, Taipei, Taiwan.
    [Chen, Hsuan-Yu] Acad Sinica, Inst Stat Sci, Taipei 11529, Taiwan.
    [Chou, Wen-Chien; Hsu, Szu-Chun] Natl Taiwan Univ Hosp & Coll Med, Dept Lab Med, Taipei, Taiwan.
 RP Tien, HF, Natl Taiwan Univ Hosp & Coll Med, Dept Internal Med, 7 Chung
    Shan S Rd, Taipei, Taiwan.
 EM hftien@ntu.edu.tw
    pcyang@ntu.edu.tw
 FU National Science Council [NSC 94-2314-B-002-182, NSC
    95-2314-B-002-061]; National Taiwan University Hospital [NTUH. 94A19-1]
 FX This work was supported by a grant from the National Science Council
    (NSC 94-2314-B-002-182; NSC 95-2314-B-002-061) and the National Taiwan
    University Hospital (NTUH. 94A19-1).
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 TC 10
 PU AMER SOC HEMATOLOGY
 PI WASHINGTON
 PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
 SN 0006-4971
 J9 BLOOD
 JI Blood
 PD APR 2
 PY 2009
 VL 113
 IS 14
 BP 3161
 EP 3167
 DI 10.1182/blood-2008-08-173104
 PG 7
 SC Hematology
 GA 428LH
 UT ISI:000264848900008
 ER
 
 PT J
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    Shaknovich, R
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    Polo, JM
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 AF Cerchietti, Leandro C.
    Yang, Shao Ning
    Shaknovich, Rita
    Hatzi, Katerina
    Polo, Jose M.
    Chadburn, Amy
    Dowdy, Steven F.
    Melnick, Ari
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    vitro and in vivo
 SO BLOOD
 LA English
 DT Article
 ID GERMINAL-CENTER FORMATION; B-CELL LYMPHOMAS; BTB DOMAIN; EXPRESSION;
    PEPTIDE; DIFFERENTIATION; GENE; TRANSCRIPTION; INFLAMMATION; COREPRESSOR
 AB The BCL6 transcriptional repressor is the most commonly involved
    oncogene in diffuse large B-cell lymphomas (DLBCLs). BCL6 lymphomagenic
    activity is dependent on its ability to recruit corepressor proteins to
    a unique binding site on its N-terminal BTB domain. A recombinant
    peptide fragment of the SMRT (silencing mediator for retinoid and
    thyroid hormone receptor) corepressor that blocks this site can inhibit
    BCL6 biologic functions. Shortening and conversion of this peptide to
    D-amino acid and retro configuration as well as the addition of a
    fusogenic motif yielded a far more potent and stable BCL6 inhibitor
    that still retained the specificity of the original SMRT fragment. Like
    the L-peptide, retroinverso BCL6 peptide inhibitor (RI-BPI) selectively
    killed BCR rather than OxPhos-type DLBCL cells. The RI-BPI could
    recapitulate the failure to form germinal centers seen in BCL6 null
    mice yet was nontoxic and nonimmunogenic even when administered for up
    to 52 weeks. RI-BPI showed superior duration of tissue penetration and
    could accordingly powerfully suppress the growth of human DLBCLs
    xenografts in a dose-dependent manner. Finally, RI-BPI could kill
    primary human DLBCL cells but had no effect on normal lymphoid tissue
    or other tumors. (Blood. 2009; 113: 3397-3405)
 C1 [Cerchietti, Leandro C.; Yang, Shao Ning; Hatzi, Katerina; Melnick, Ari] Weill Cornell Coll Med, Dept Med, Div Hematol & Med Oncol, New York, NY USA.
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 RP Melnick, A, Cornell Univ, Div Hematol & Med Oncol, Dept Med, Weill
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 EM amm2014@med.cornell.edu
 FU National Cancer Institute [R01 CA104348]; Chemotherapy Foundation ; Sam
    Waxman Cancer Research Foundation ; GP Foundation ; Leukemia & Lymphoma
    Society 
 FX A. M. was supported by the National Cancer Institute (Bethesda, MD; R01
    CA104348), The Chemotherapy Foundation (New York, NY), The Sam Waxman
    Cancer Research Foundation (New York, NY), and the G&P Foundation (New
    York, NY) and is a Leukemia & Lymphoma Society (White Plains, NY)
    Scholar.
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 JI Blood
 PD APR 9
 PY 2009
 VL 113
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 BP 3397
 EP 3405
 DI 10.1182/blood-2008-07-168773
 PG 9
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 GA 431HN
 UT ISI:000265052300004
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    Wang, MG
    Wang, SM
    Sykes, M
    Yang, YG
 AF Wang, Hui
    Asavaroengchai, Wannee
    Yeap, Beow Yong
    Wang, Min-Guang
    Wang, Shumei
    Sykes, Megan
    Yang, Yong-Guang
 TI Paradoxical effects of IFN-gamma in graft-versus-host disease reflect
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    inhibition of epithelial tissue injury
 SO BLOOD
 LA English
 DT Article
 ID BONE-MARROW-TRANSPLANTATION; CD8 T-CELLS; REFRACTORY HEMATOLOGIC
    MALIGNANCIES; IDIOPATHIC PNEUMONIA SYNDROME; CYTOKINE GENE-EXPRESSION;
    ANTIGEN-PRESENTING CELLS; MURINE RENAL-CANCER; INTERFERON-GAMMA; ALPHA;
    MICE
 AB Interferon-gamma (IFN-gamma) inhibits graft-versus-host disease (GVHD)
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    transplantation (allo-HCT) but promotes lethality in unirradiated and
    sublethally irradiated recipients. We investigated the role of
    IFN-gamma in GVHD in sublethally irradiated B6D2F1 recipients of B6
    allo-HCT. B6D2F1 mice receiving wild-type B6 splenocytes alone died
    rapidly, whereas those receiving wild-type B6 splenocytes plus marrow
    survived long-term. Mice in both groups showed rapid elimination of
    host hematopoietic cells but minimal parenchymal tissue injury.
    However, mice receiving allo-HCT from IFN-gamma-deficient donors died
    rapidly regardless of whether donor marrow was given, and they
    exhibited severe parenchymal injury but prolonged survival of host
    hematopoietic cells. IFN-gamma plays a similar role in another model
    involving delayed B6 donor leukocyte infusion (DLI) to established
    mixed allogeneic (B6 -> BALB/c) chimeras. IFN-gamma promotes
    DLI-mediated conversion from mixed to full donor chimerism while
    attenuating GVHD. Importantly, IFN-gamma enhances graft-versus-leukemia
    (GVL) effects in both models. Our data indicate that previously
    reported IFN-gamma-induced early mortality in allo-HCT recipients is
    due to augmentation of lymphohematopoietic graft-versus-host reaction
    (LGVHR) and can be avoided by providing an adequate source of donor
    hematopoietic stem/progenitor cells. Furthermore, the magnitude of GVL
    is correlated with the strength of LGVHR, and IFN-gamma reduces the
    potential of this allo-reactivity to cause epithelial tissue GVHD.
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 C1 [Wang, Hui; Asavaroengchai, Wannee; Wang, Shumei; Sykes, Megan; Yang, Yong-Guang] Harvard Univ, Transplantat Biol Res Ctr, Massachusetts Gen Hosp, Sch Med,Bone Marrow Transplantat Sect, Boston, MA 02129 USA.
    [Yeap, Beow Yong] Harvard Univ, Dept Med, Massachusetts Gen Hosp, Sch Med, Boston, MA 02129 USA.
    [Wang, Min-Guang] Lower Columbia Pathologists, Longview, WA USA.
 RP Yang, YG, Harvard Univ, Transplantat Biol Res Ctr, Massachusetts Gen
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 EM yongguang.yang@tbrc.mgh.harvard.edu
 FU National Institutes of Health (Bethesda, MD) [5P01CA111519-020002];
    American Cancer Society (Atlanta, GA) [RSG-03-227-01-LIB]
 FX The authors thank Drs Christene Huang and Giovanna Andreola for
    critical review of this manuscript, Mr Orlando Moreno for outstanding
    animal husbandry, and Ms Kelly Walsh for expert assistance with the
    manuscript.
    This work was supported by grants from National Institutes of Health
    (Bethesda, MD; 5P01CA111519-020002) and American Cancer Society
    (Atlanta, GA; RSG-03-227-01-LIB).
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 PG 8
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 GA 431HN
 UT ISI:000265052300030
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 PT J
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    Mortin, MA
    Shahabuddin, M
 AF Yan, Jizhou
    Yang, Xiang
    Mortin, Mark A.
    Shahabuddin, Mohammed
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    Drosophila
 SO GENESIS
 LA English
 DT Article
 DE Drosophila melanogaster; immunity; malaria; microarray; mosquito;
    Plasmodium falciparum
 ID PARASITE PLASMODIUM-FALCIPARUM; CIRCUMSPOROZOITE PROTEIN;
    IMMUNE-RESPONSE; SURFACE PROTEIN-2; ANOPHELES-GAMBIAE; BLOOD STAGES;
    INVASION; SEQUENCE; GENE; THROMBOSPONDIN
 AB Malaria kills a million people annually. Understanding the relationship
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    adhesive protein (TRAP) and circumsporozoite protein (CSP), found on
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    insect's response, we induced these proteins separately and together,
    performing whole genome microarray analysis measuring gene expression
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    TRAP and CSP strongly and differentially influence Drosophila genes
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    the most striking effects are on the immune system. While
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    to sepsis, there is a marked repression of the Toll pathway. This
    suggests: (1) how Plasmodium infection of the mosquito might use TRAP
    and CSP to modulate the host insect's physiology to promote sporozoite
    survival and transmission to man and (2) that approaches to elevate
    expression of the mosquito's Toll pathway might lead to novel methods
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    Inc.
 C1 [Mortin, Mark A.] Eunice Kennedy Shriver NICHHD, Mol Genet Lab, NIH, Bethesda, MD 20892 USA.
    [Yan, Jizhou; Shahabuddin, Mohammed] NIAID, Lab Malaria & Vector Res, Bethesda, MD 20892 USA.
    [Yan, Jizhou] Univ Penn, Abramson Family Canc Res Inst, Philadelphia, PA 19104 USA.
    [Yang, Xiang; Mortin, Mark A.] NCI, Biochem Lab, Bethesda, MD 20892 USA.
 RP Mortin, MA, Eunice Kennedy Shriver NICHHD, Mol Genet Lab, NIH, 6 Ctr
    Dr,Bldg 6B,Room 3B331, Bethesda, MD 20892 USA.
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 NR 23
 TC 1
 PU WILEY-LISS
 PI HOBOKEN
 PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA
 SN 1526-954X
 J9 GENESIS
 JI Genesis
 PD MAR
 PY 2009
 VL 47
 IS 3
 BP 196
 EP 203
 DI 10.1002/dvg.20483
 PG 8
 SC Developmental Biology; Genetics & Heredity
 GA 425RT
 UT ISI:000264655500008
 ER
 
 PT J
 AU Zuber, J
    Radtke, I
    Pardee, TS
    Zhao, Z
    Rappaport, AR
    Luo, WJ
    McCurrach, ME
    Yang, MM
    Dolan, ME
    Kogan, SC
    Downing, JR
    Lowe, SW
 AF Zuber, Johannes
    Radtke, Ina
    Pardee, Timothy S.
    Zhao, Zhen
    Rappaport, Amy R.
    Luo, Weijun
    McCurrach, Mila E.
    Yang, Miao-Miao
    Dolan, M. Eileen
    Kogan, Scott C.
    Downing, James R.
    Lowe, Scott W.
 TI Mouse models of human AML accurately predict chemotherapy response
 SO GENES & DEVELOPMENT
 LA English
 DT Article
 DE AML; AML1/ETO; MLL; chemotherapy; mouse models
 ID ACUTE MYELOID-LEUKEMIA; MLL FUSION PROTEINS; DNA-DAMAGE; STEM-CELLS;
    P53; MUTATIONS; CANCER; RESISTANCE; CHEMORESISTANCE; LEUKEMOGENESIS
 AB The genetic heterogeneity of cancer influences the trajectory of tumor
    progression and may underlie clinical variation in therapy response. To
    model such heterogeneity, we produced genetically and pathologically
    accurate mouse models of common forms of human acute myeloid leukemia
    (AML) and developed methods to mimic standard induction chemotherapy
    and efficiently monitor therapy response. We see that murine AMLs
    harboring two common human AML genotypes show remarkably diverse
    responses to conventional therapy that mirror clinical experience.
    Specifically, murine leukemias expressing the AML1/ETO fusion
    oncoprotein, associated with a favorable prognosis in patients, show a
    dramatic response to induction chemotherapy owing to robust activation
    of the p53 tumor suppressor network. Conversely, murine leukemias
    expressing MLL fusion proteins, associated with a dismal prognosis in
    patients, are drug-resistant due to an attenuated p53 response. Our
    studies highlight the importance of genetic information in guiding the
    treatment of human AML, functionally establish the p53 network as a
    central determinant of chemotherapy response in AML, and demonstrate
    that genetically engineered mouse models of human cancer can accurately
    predict therapy response in patients.
 C1 [Zuber, Johannes; Pardee, Timothy S.; Zhao, Zhen; Rappaport, Amy R.; Luo, Weijun; McCurrach, Mila E.; Yang, Miao-Miao; Lowe, Scott W.] Cold Spring Harbor Lab, Cold Spring Harbor, NY 11724 USA.
    [Radtke, Ina; Downing, James R.] St Jude Childrens Hosp, Dept Pathol, Memphis, TN 38105 USA.
    [Zhao, Zhen] SUNY Stony Brook, Genet Program, Stony Brook, NY 11794 USA.
    [Rappaport, Amy R.; Lowe, Scott W.] Watson Sch Biol Sci, Cold Spring Harbor, NY 11724 USA.
    [Dolan, M. Eileen] Univ Chicago, Dept Med, Hematol Oncol Sect, Chicago, IL 60637 USA.
    [Kogan, Scott C.] Univ Calif San Francisco, Dept Lab Med, San Francisco, CA 94143 USA.
    [Lowe, Scott W.] Cold Spring Harbor Lab, Howard Hughes Med Inst, Cold Spring Harbor, NY 11724 USA.
 RP Lowe, SW, Cold Spring Harbor Lab, POB 100, Cold Spring Harbor, NY 11724
    USA.
 EM lowe@cshl.edu
 FU Specialized Center of Research grant from the Leukemia and Lymphoma
    Society ; Ambassador Felix Schnyder Memorial Grant ; Lauri Strauss
    Leukemia Foundation ; German Research Foundation ( DFG) ; Andrew
    Seligson Memorial Fellow at CSHL ; NIH traineeship and the Barbara
    McClintock fellowship ; Leslie Rutherford Leukemia and Lymphoma Society
    Scholar ; Howard Hughes Medical Institute 
 FX We thank Christian Buske and Irving Weissman for providing cDNA
    constructs. We gratefully acknowledge Meredith Taylor, Mei Lin
    Maunakea, Shannon Delaney, Eileen Earl, Lisa Bianco, and her team for
    excellent technical assistance; Zhenyu Xuan and Sohail Khan for
    microarray analysis, and Jeffrey Rubnitz, Raul Ribeiro, Stanley Pounds,
    and Xueyuan Cao for sharing clinical data and providing statistical
    analysis. We also thank Enrique Cepero, Lars Zender, Cornelius
    Miething, Mona Spector, Katherine McJunkin, Christof Fellmann, and
    other members of the Lowe lab as well as Michelle LeBeau, Kevin
    Shannon, and David Largaespada for constructive criticism and advice.
    This work was supported by a Specialized Center of Research grant from
    the Leukemia and Lymphoma Society, generous gifts from the Don Monti
    Memorial Research Foundation, and the Ambassador Felix Schnyder
    Memorial Grant of the Lauri Strauss Leukemia Foundation. J. Z. was
    supported by a research fellowship from the German Research Foundation
    ( DFG) and is the Andrew Seligson Memorial Fellow at CSHL. A. R. R. was
    supported by an NIH traineeship and the Barbara McClintock fellowship.
    S. C. K. is the Leslie Rutherford Leukemia and Lymphoma Society
    Scholar; S. W. L. is a Howard Hughes Medical Institute investigator.
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 NR 45
 TC 16
 PU COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT
 PI WOODBURY
 PA 500 SUNNYSIDE BLVD, WOODBURY, NY 11797-2924 USA
 SN 0890-9369
 J9 GENE DEVELOP
 JI Genes Dev.
 PD APR 1
 PY 2009
 VL 23
 IS 7
 BP 877
 EP 889
 DI 10.1101/gad.1771409
 PG 13
 SC Cell Biology; Developmental Biology; Genetics & Heredity
 GA 427MP
 UT ISI:000264783700011
 ER
 
 PT J
 AU McCrann, DJ
    Yang, D
    Chen, HJ
    Carroll, S
    Ravid, K
 AF McCrann, Donald J.
    Yang, Dan
    Chen, Hongjie
    Carroll, Shannon
    Ravid, Katya
 TI Upregulation of Nox4 in the aging vasculature and its association with
    smooth muscle cell polyploidy
 SO CELL CYCLE
 LA English
 DT Article
 DE NADPH oxidase 4 (Nox4); vascular smooth muscle; polyploidy; aging;
    hypertrophy
 ID ANGIOTENSIN-II; OXIDATIVE STRESS; NAD(P)H OXIDASE; NADPH OXIDASE;
    CANCER-CELLS; GENETIC-HYPERTENSION; RESISTANCE ARTERIES; INDUCED
    APOPTOSIS; DOWN-REGULATION; P38 MAPK
 AB Our recent reports indicated that polyploidization of aortic vascular
    smooth muscle cells (VSMC) serves as a biomarker for aging, and that
    the polyploid state is linked to a higher incidence of senescence in
    vivo. Here, we found that NADPH oxidase 4 (Nox4) expression is
    augmented in VSMC from aortas of old rats and that Nox4 levels are
    increased in polyploid VSMC in comparison to diploid cells in vivo.
    Seeking to determine if Nox4 upregulation plays a causal role in the
    accumulation of polyploid cells, we performed ploidy analysis on
    primary VSMC transduced with Nox4 adenovirus. We observed a consistent
    accumulation of polyploid cells and a concomitant decrease in the
    percentage of diploid cells in Nox4 overexpressing cells in comparison
    to controls or to cells overexpressing dominant negative Nox4. Further
    exploration of this phenomenon in VSMC cultures identified a
    Nox4-induced decrease in the chromosome passenger protein, survivin,
    whose absence and mislocalization during polyploidization was
    previously shown to induce VSMC polyploidy. Taken together, our study
    is the first to show increased Nox4 levels in VSMC during aging, and to
    demonstrate its role in induction of polyploidy in this lineage.
 C1 [Ravid, Katya] Boston Univ, Sch Med, Dept Biochem, Boston, MA 02118 USA.
    Boston Univ, Sch Med, Whitaker Cardiovasc Inst, Boston, MA 02118 USA.
 RP Ravid, K, Boston Univ, Sch Med, Dept Biochem, K225, Boston, MA 02118
    USA.
 EM ravid@biochem.bumc.bu.edu
 FU NHLBI [HL80442]
 FX We thank Hao G. Nguyen and Maria Makitalo for their technical
    assistance. This work was supported by NHLBI grant HL80442 to K. R. K.
    R. is an Established Investigator with the American Heart Association.
    The authors declare no competing financial interests.
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 NR 61
 TC 11
 PU LANDES BIOSCIENCE
 PI AUSTIN
 PA 1002 WEST AVENUE, 2ND FLOOR, AUSTIN, TX 78701 USA
 SN 1538-4101
 J9 CELL CYCLE
 JI Cell Cycle
 PD MAR 15
 PY 2009
 VL 8
 IS 6
 BP 902
 EP 908
 PG 7
 SC Cell Biology
 GA 426KG
 UT ISI:000264706600020
 ER
 
 PT J
 AU Yang, ZJ
    Rao, ZR
    Jiang, XD
    Yuan, H
    Duan, L
    Chen, LW
    Wang, Y
    Xu, RX
    Zeng, YJ
 AF Yang, Zhijun
    Rao, Zhiren
    Jiang, Xiaodan
    Yuan, Hua
    Duan, Li
    Chen, Liangwei
    Wang, Ying
    Xu, Ruxiang
    Zeng, Yanjun
 TI Reciprocal pathway between medullary visceral zone and hypothalamic
    supraoptic nucleus or paraventricular nucleus involved in hyperosmotic
    regulation
 SO CELL BIOLOGY INTERNATIONAL
 LA English
 DT Article
 DE Neuron; Astrocyte; Osmotic pressure; Medullary visceral zone; Glial
    fibrillary acidic protein; Rat
 ID GLIAL-NEURONAL INTERACTIONS; SYNAPTIC-TRANSMISSION;
    NOXIOUS-STIMULATION; MATURE ASTROCYTES; RAT; BRAIN; CELLS;
    REGENERATION; SYNAPSES; EXPRESSION
 AB In this study we try to simultaneously investigate the response of
    neurons and astrocytes of rats following hyperosmotic stimulation and
    test the possibility that the reciprocal pathways between medullary
    visceral zone (MVZ) and hypothalamic paraventricular nucleus (PVN) or
    supraoptic nucleus (SON). Hyperosmotic pressure animal model was
    established by administering 3% sodium chloride as drinking water to
    rats. The distribution and expression of the HRP retrogradely labeled
    neurons, Fos, tyrosine hydroxylase (TH) or vasopressin (VP) positive
    neuron and glial fibrillary acidic protein (GFAP) positive astrocytes
    in the MVZ, SON and PVN were observed by quadruplicate-labeling methods
    of WGA-HRP retrograde tracing combined with anti-Fos, TH (or VP) and
    GFAP immunohistochemical technique. Fos positive neurons within the
    MVZ, PVN and SON increased markedly. There were also a large number of
    GFAP positive structures in the brain and their distribution pattern
    was fundamentally similar or analogous to Fos positive neurons in the
    above-mentioned areas. The augmented GFAP reactivities took on
    hypertrophic cell bodies, thicker and longer processes. Quadruplicate
    immunohistochemical staining showed that a neuron could be closely
    surrounded by many astrocytes and they formed neuron-astrocytic complex
    (N-ASC). Fos+/TH+/HRP+/GFAP+ and Fos+/VP+/HRP+/GFAP+ quadruplicate
    labeled N-ASC could be found in the MVZ, PVN and SON, respectively. The
    present results indicated that the neurons and astrocytes might be very
    active following hyperosmotic pressure and N-ASC as a functional unit
    might serve to modulate osmotic pressure. There were reciprocal
    osmoregulation pathways between the MVZ and SON or PVN in the brain.
    (C) 2008 Published by Elsevier Ltd on behalf of International
    Federation for Cell Biology.
 C1 [Yang, Zhijun; Jiang, Xiaodan; Xu, Ruxiang] So Med Univ, Zhujiang Hosp, Neuromed Inst, Guangzhou 510282, Guangdong, Peoples R China.
    [Yang, Zhijun; Rao, Zhiren; Yuan, Hua; Duan, Li; Chen, Liangwei; Wang, Ying] Fourth Mil Med Univ, Inst Neurosci, Xian 710032, Peoples R China.
    [Zeng, Yanjun] Beijing Univ Technol, Biomech & Med Informat Inst, Beijing 100022, Peoples R China.
 RP Xu, RX, So Med Univ, Zhujiang Hosp, Neuromed Inst, 253 Gongye Rd,
    Guangzhou 510282, Guangdong, Peoples R China.
 EM zjxuruxiang@163.com
    yjzeng@bjpu.edu.cn
 FU Natural Science Found of China [30270491, 30400464]; Funds for Key
    Sci-tech Research Projects of Guangdong Province ; PLA of PR China
    [01Z054]
 FX This research was supported by Natural Science Found of China
    (30270491, 30400464) and also by the Funds for Key Sci-tech Research
    Projects of Guangdong Province [YUEKEJIBAN (2000) 25, (2004) 08, (2007)
    05/06:7005206], [YUE CAIQI (2001) 367, (2003) 209, YUE KEJIZI (2004)
    112] and PLA [01Z054] of PR China.
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 NR 35
 TC 0
 PU ACADEMIC PRESS LTD ELSEVIER SCIENCE LTD
 PI LONDON
 PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
 SN 1065-6995
 J9 CELL BIOL INT
 JI Cell Biol. Int.
 PD APR
 PY 2009
 VL 33
 IS 4
 BP 475
 EP 482
 DI 10.1016/j.cellbi.2008.07.024
 PG 8
 SC Cell Biology
 GA 427XX
 UT ISI:000264813500003
 ER
 
 PT J
 AU Yang, XF
    Figueiredo, LM
    Espinal, A
    Okubo, E
    Li, B
 AF Yang, Xiaofeng
    Figueiredo, Luisa M.
    Espinal, Amin
    Okubo, Eiji
    Li, Bibo
 TI RAP1 Is Essential for Silencing Telomeric Variant Surface Glycoprotein
    Genes in Trypanosoma brucei
 SO CELL
 LA English
 DT Article
 ID DNA-BINDING DOMAIN; CELL-CYCLE ARREST; ANTIGENIC VARIATION; AFRICAN
    TRYPANOSOMES; SACCHAROMYCES-CEREVISIAE; EXPRESSION SITES; FISSION
    YEAST; HISTONE H3; PROTEIN; KU
 AB Trypanosoma brucei expresses variant surface glycoprotein (VSG) genes
    in a strictly monoallelic fashion in its mammalian hosts, but it is
    unclear how this important virulence mechanism is enforced. Telomere
    position effect, an epigenetic phenomenon, has been proposed to play a
    critical role in VSG regulation, yet no telomeric protein has been
    identified whose disruption led to VSG derepression. We now identify
    tbRAP1 as an intrinsic component of the T. brucei telomere complex and
    a major regulator for silencing VSG expression sites (ESs). Knockdown
    of tbRAP1 led to derepression of all VSGs in silent ESs, but not VSGs
    located elsewhere, and resulted in stronger derepression of genes
    located within 10 kb from telomeres than genes located further
    upstream. This graduated silencing pattern suggests that telomere
    integrity plays a key role in tbRAP1-dependent silencing and VSG
    regulation.
 C1 [Yang, Xiaofeng; Li, Bibo] Cleveland State Univ, Dept Biol Geol & Environm Sci, Ctr Gene Regulat Hlth Dis, Cleveland, OH 44115 USA.
    [Yang, Xiaofeng] Xi An Jiao Tong Univ, Coll Med, Affiliated Hosp 1, Dept Obstet & Gynecol, Xian 710061, Shaanxi Prov, Peoples R China.
    [Figueiredo, Luisa M.; Espinal, Amin; Okubo, Eiji; Li, Bibo] Rockefeller Univ, Mol Parasitol Lab, New York, NY 10065 USA.
 RP Li, B, Cleveland State Univ, Dept Biol Geol & Environm Sci, Ctr Gene
    Regulat Hlth Dis, Cleveland, OH 44115 USA.
 EM b.li37@csuohio.edu
 FU National Institute of Health [AI050614, AI21729, AI066095]
 FX We are grateful to Piet Borst for the VSG9 antibody and Keith Gull for
    the RNA Pol I and tubulin antibodies. We greatly appreciate Titia de
    Lange and George A.M. Cross for insightful discussions, and we thank
    Margaret J. Irwin, Audrey Lynn, and members of the Li and Cross labs
    for comments on the manuscript, critical discussions, and technical
    support. DeltaVision Microscopy was carried out at the RU Bio-Imaging
    Resource Center with guidance from Alison North and in BGES Department
    at CSU. FACS analysis was done at the Flow Cytometry Resource Center at
    RU and the Flow Cytometry Core at CCF. This work was supported by
    National Institute of Health grants to G.A.M. Cross (AI050614 and
    AI21729) and to B.L. (AI066095).
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 NR 68
 TC 20
 PU CELL PRESS
 PI CAMBRIDGE
 PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
 SN 0092-8674
 J9 CELL
 JI Cell
 PD APR 2
 PY 2009
 VL 137
 IS 1
 BP 99
 EP 109
 DI 10.1016/j.cell.2009.01.037
 PG 11
 SC Biochemistry & Molecular Biology; Cell Biology
 GA 427XV
 UT ISI:000264813300017
 ER
 
 PT J
 AU Piao, LZ
    Li, YW
    Kim, SJ
    Sohn, KC
    Yang, KJ
    Park, YA
    Byun, HS
    Won, MH
    Hong, JH
    Hur, GM
    Seok, JH
    Shong, MH
    Sack, R
    Brazil, DP
    Hemmings, BA
    Park, J
 AF Piao, Longzhen
    Li, Yuwen
    Kim, Soung Jung
    Sohn, Kyung-Cheol
    Yang, Keum-Jin
    Park, Yeong Ah
    Byun, Hee Sun
    Won, Minho
    Hong, Janghee
    Hur, Gang Min
    Seok, Jeong Ho
    Shong, Minho
    Sack, Ragna
    Brazil, Derek P.
    Hemmings, Brian A.
    Park, Jongsun
 TI Regulation of OPA1-mediated mitochondrial fusion by leucine
    zipper/EF-hand-containing transmembrane protein-1 plays a role in
    apoptosis
 SO CELLULAR SIGNALLING
 LA English
 DT Article
 DE CTMP; Mitochondria; Apoptosis; Wolf-Hirschhorn syndrome; LETM11
 ID WOLF-HIRSCHHORN-SYNDROME; DOMINANT OPTIC ATROPHY; CYTOCHROME-C RELEASE;
    MAMMALIAN-CELLS; LIVING CELLS; OPA1; GENE; MORPHOLOGY; MEMBRANE; FISSION
 AB Carboxyl-terminal modulator protein (CTMP) is a tumor suppressor-like
    binding partner of Protein kinase B (PKB/Akt) that negative regulates
    this kinase. In the course of our recent work, we identified that CTMP
    is consistently associated with leucine zipper/EF-hand-containing
    transmembrane-1 (LETM1). Here, we report that adenovirus-LETM1
    increased the sensitivity of HeLa cells to apoptosis, induced by either
    staurosporine or actinomycin D. As shown previously, LETM1 localized to
    the inner mitochondrial membrane. Electron-microscopy analysis of
    adenovirus-LETM1 transduced cells revealed that mitochondrial cristae
    were swollen in these cells, a phenotype similar to that observed in
    optic atrophy type-1 (OPA1)-ablated cells. OPA1 cleavage was increased
    in LETM1-overexpressing cells, and this phenotype was reversed by
    overexpression of OPA1 variant-7, a cleavage resistant form of OPA1.
    Taken together, these data suggest that LETM1 is a novel binding
    partner for CTMP that may play an important role in mitochondrial
    fragmentation via OPA1-cleavage. (C) 2009 Elsevier Inc. All rights
    reserved
 C1 [Piao, Longzhen; Li, Yuwen; Yang, Keum-Jin; Park, Yeong Ah; Byun, Hee Sun; Won, Minho; Hong, Janghee; Hur, Gang Min; Seok, Jeong Ho; Park, Jongsun] Chungnam Natl Univ, Coll Med, Dept Pharmacol,Daejeon Reg Canc Ctr, Canc Res Inst,Res Inst Med Sci, Taejon 301131, South Korea.
    [Kim, Soung Jung; Shong, Minho] Chungnam Natl Univ, Dept Internal Med, Coll Med, Taejon 301131, South Korea.
    [Sohn, Kyung-Cheol] Chungnam Natl Univ, Coll Med, Dept Dermatol, Taejon 301131, South Korea.
    [Sack, Ragna; Hemmings, Brian A.] Friedrich Miescher Inst Biomed Res, CH-4058 Basel, Switzerland.
    [Brazil, Derek P.] Univ Coll Dublin, UCD Conway Inst, UCD Diabet Res Ctr, Dublin 4, Ireland.
 RP Park, J, Chungnam Natl Univ, Coll Med, Dept Pharmacol,Daejeon Reg Canc
    Ctr, Canc Res Inst,Res Inst Med Sci, 6 Munhwa Dong, Taejon 301131,
    South Korea.
 EM insulin@cnu.ac.kr
 FU Korea Science & Engineering Foundation (KOSEF) grant funded by the
    Korea government (MOST) [R11-2002-100-02006-0]; Cancer Control Ministry
    of Health & Welfare, Republic of Korea [0720560]; KOSEF/MOST
    [M10753020001-07N5302-00110]; Science Foundation Ireland ; Irish Health
    Research Board ; Novartis Research Foundation. 
 FX We would like to thank Dr. JW Lee (Korea Basic Science Institute,
    Korea) for TEM analysis. We also thank Drs. SY Jung and KS Yoon (Aju
    University, Korea) for critical comments on the manuscript. This work
    was supported by the Science Research Center (SRC)/Engineering Research
    Center (ERC) Program (R11-2002-100-02006-0) of the Korea Science &
    Engineering Foundation (KOSEF) grant funded by the Korea government
    (MOST) and by a grant from the National R&D Program for Cancer Control
    Ministry of Health & Welfare, Republic of Korea. (No: 0720560). SJ. Kim
    and M. Shong were supported by KOSEF/MOST (M10753020001-07N5302-00110).
    Work in the laboratory of D. Brazil is supported by Science Foundation
    Ireland and the Irish Health Research Board. The Friedrich Miescher
    Institute is part of the Novartis Research Foundation.
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 NR 40
 TC 3
 PU ELSEVIER SCIENCE INC
 PI NEW YORK
 PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
 SN 0898-6568
 J9 CELL SIGNAL
 JI Cell. Signal.
 PD MAY
 PY 2009
 VL 21
 IS 5
 BP 767
 EP 777
 DI 10.1016/j.cellsig.2009.01.020
 PG 11
 SC Cell Biology
 GA 423UN
 UT ISI:000264521300015
 ER
 
 PT J
 AU Biesinger, MC
    Payne, BP
    Lau, LWM
    Gerson, A
    Smart, RSC
 AF Biesinger, Mark C.
    Payne, Brad P.
    Lau, Leo W. M.
    Gerson, Andrea
    Smart, Roger St. C.
 TI X-ray photoelectron spectroscopic chemical state quantification of
    mixed nickel metal, oxide and hydroxide systems
 SO SURFACE AND INTERFACE ANALYSIS
 LA English
 DT Article
 DE X-ray photoelectron spectroscopy (XPS); nickel; oxides; film thickness;
    chemical state quantification
 ID XPS SPECTRA; SURFACES; OXYGEN; NIO; MECHANISM; CHROMIUM; NI(110);
    ALLOY; IRON
 AB Quantitative chemical state X-ray photoelectron spectroscopic analysis
    of mixed nickel metal, oxide, hydroxide and oxyhydroxide systems is
    challenging due to the complexity of the Ni 2p peak shapes resulting
    from multiplet splitting, shake-up and plasmon loss structures.
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    the 0 1s spectra. Quantification of a commercial nickel powder and a
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    min is demonstrated. The effect of uncertain relative sensitivity
    factors (e.g. Ni 2.67 +/- 0.54) is discussed, as is the depth of
    measurement for thin film analysis based on calculated inelastic mean
    free paths. Copyright (C) 2009 John Wiley & Sons, Ltd.
 C1 [Biesinger, Mark C.; Lau, Leo W. M.] Univ Western Ontario, Western Sci Ctr, London, ON N6A 5B7, Canada.
    [Biesinger, Mark C.; Gerson, Andrea; Smart, Roger St. C.] ACeSSS, Mawson Lakes, SA 5095, Australia.
    [Payne, Brad P.; Lau, Leo W. M.] Univ Western Ontario, Dept Chem, London, ON N6A 5B7, Canada.
 RP Biesinger, MC, Univ Western Ontario, Western Sci Ctr, Room G1, London,
    ON N6A 5B7, Canada.
 EM biesingr@uwo.co
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 NR 34
 TC 14
 PU JOHN WILEY & SONS LTD
 PI CHICHESTER
 PA THE ATRIUM, SOUTHERN GATE, CHICHESTER PO19 8SQ, W SUSSEX, ENGLAND
 SN 0142-2421
 J9 SURF INTERFACE ANAL
 JI Surf. Interface Anal.
 PD APR
 PY 2009
 VL 41
 IS 4
 BP 324
 EP 332
 DI 10.1002/sia.3026
 PG 9
 SC Chemistry, Physical
 GA 422MB
 UT ISI:000264431100007
 ER
 
 PT J
 AU Yang, ZH
    MacQuarrie, KL
    Analau, E
    Tyler, AE
    Dilworth, FJ
    Cao, Y
    Diede, SJ
    Tapscott, SJ
 AF Yang, Zhihong
    MacQuarrie, Kyle L.
    Analau, Erwin
    Tyler, Ashlee E.
    Dilworth, F. Jeffery
    Cao, Yi
    Diede, Scott J.
    Tapscott, Stephen J.
 TI MyoD and E-protein heterodimers switch rhabdomyosarcoma cells from an
    arrested myoblast phase to a differentiated state
 SO GENES & DEVELOPMENT
 LA English
 DT Article
 DE E2A; Musculin; MyoD; myogenesis; rhabdomyosarcoma
 ID LOOP-HELIX PROTEINS; E-BOX ELEMENTS; TRANSCRIPTION FACTOR; TERMINAL
    DIFFERENTIATION; HOMEODOMAIN PROTEIN; MUSCLE DEVELOPMENT;
    GENE-EXPRESSION; MYOGENESIS; E2A; ACTIVATION
 AB Rhabdomyosarcomas are characterized by expression of myogenic
    specification genes, such as MyoD and/or Myf5, and some muscle
    structural genes in a population of cells that continues to replicate.
    Because MyoD is sufficient to induce terminal differentiation in a
    variety of cell types, we have sought to determine the molecular
    mechanisms that prevent MyoD activity in human embryonal
    rhabdomyosarcoma cells. In this study, we show that a combination of
    inhibitory Musculin: E-protein complexes and a novel splice form of E2A
    compete with MyoD for the generation of active full-length E-protein:
    MyoD heterodimers. A forced heterodimer between MyoD and the
    full-length E12 robustly restores differentiation in rhabdomyosarcoma
    cells and broadly suppresses multiple inhibitory pathways. Our studies
    indicate that rhabdomyosarcomas represent an arrested progress through
    a normal transitional state that is regulated by the relative abundance
    of heterodimers between MyoD and the full-length E2A proteins. The
    demonstration that multiple inhibitory mechanisms can be suppressed and
    myogenic differentiation can be induced in the RD rhabdomyosarcomas by
    increasing the abundance of MyoD: E-protein heterodimers suggests a
    central integrating function that can be targeted to force
    differentiation in muscle cancer cells.
 C1 [Yang, Zhihong; MacQuarrie, Kyle L.; Analau, Erwin; Tyler, Ashlee E.; Cao, Yi; Diede, Scott J.; Tapscott, Stephen J.] Fred Hutchinson Canc Res Ctr, Div Human Biol, Seattle, WA 98109 USA.
    [MacQuarrie, Kyle L.] Univ Washington, Med Scientist Training Program, Seattle, WA 98105 USA.
    [Dilworth, F. Jeffery] Ottawa Hlth Res Inst, Sprott Ctr Stem Cell Res, Ottawa, ON K1Y 4E9, Canada.
    [Tapscott, Stephen J.] Univ Washington, Dept Neurol, Seattle, WA 98105 USA.
 RP Tapscott, SJ, Fred Hutchinson Canc Res Ctr, Div Human Biol, Seattle, WA
    98109 USA.
 EM stapscot@fhcrc.org
 FU NIH [AR045113]
 FX This work was supported by NIH-AR045113 ( to S. J. T.) and F32CA117622
    ( to Z. Y.), and FHCRC/ Amgen Interdisciplinary Training Grant ( to Z.
    Y.). We thank Z. Yao, A. E. Tyler, L. D. Snider, S. Collins, I.
    Bernstein, L. Rott, and P. Gafken for experimental support and review
    of the text.
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 NR 59
 TC 8
 PU COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT
 PI WOODBURY
 PA 500 SUNNYSIDE BLVD, WOODBURY, NY 11797-2924 USA
 SN 0890-9369
 J9 GENE DEVELOP
 JI Genes Dev.
 PD MAR 15
 PY 2009
 VL 23
 IS 6
 BP 694
 EP 707
 DI 10.1101/gad.1765109
 PG 14
 SC Cell Biology; Developmental Biology; Genetics & Heredity
 GA 421LM
 UT ISI:000264360400005
 ER
 
 PT J
 AU Huynh, KM
    Kim, G
    Kim, DJ
    Yang, SJ
    Park, SM
    Yeom, YI
    Fisher, PB
    Kang, D
 AF Huynh, Kim Mai
    Kim, Gyoungmi
    Kim, Dong-Joon
    Yang, Suk-Jin
    Park, Seong-Min
    Yeom, Young-Il
    Fisher, Paul B.
    Kang, Dongchul
 TI Gene expression analysis of terminal differentiation of human melanoma
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 SO GENE
 LA English
 DT Article
 DE Microarray; Mezerein; Interferon-beta; PKC; Mitosis; Calpain 3
 ID PROTEIN-KINASE-C; LEUKEMIA-CELLS; GROWTH ARREST; I INTERFERONS;
    MEZEREIN; INDUCTION; CANCER; FOXM1; RETRODIFFERENTIATION; MICROARRAYS
 AB Defects in differentiation are frequently observed in cancer cells. By
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    or 24 h post-treatment (166 up and 44 down). Major biological processes
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    B.V. All rights reserved.
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 RP Kang, D, Hallym Univ, Ilsong Inst Life Sci, 1605-4 Gwanyang Dong,
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 EM dckang@hallym.ac.kr
 FU Korea Research Foundation [C00421]
 FX The present studies were supported by Korea Research Foundation Grant
    C00421 to DK. PBF holds the Thelma Newmeyer Corman Chair in Cancer
    Research in the Massey Cancer Center of VCU, School of Medicine and is
    a Samuel Waxman Cancer Research Foundation (SWCRF) Investigator.
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 NR 38
 TC 4
 PU ELSEVIER SCIENCE BV
 PI AMSTERDAM
 PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
 SN 0378-1119
 J9 GENE
 JI Gene
 PD MAR 15
 PY 2009
 VL 433
 IS 1-2
 BP 32
 EP 39
 DI 10.1016/j.gene.2008.11.013
 PG 8
 SC Genetics & Heredity
 GA 421AX
 UT ISI:000264331400005
 ER
 
 PT J
 AU Li, HY
    Wang, YC
    Jiang, J
    Liu, GF
    Gao, CQ
    Yang, CP
 AF Li, Huiyu
    Wang, Yucheng
    Jiang, Jing
    Liu, Guifeng
    Gao, Caiqiu
    Yang, Chuanping
 TI Identification of genes responsive to salt stress on Tamarix hispida
    roots
 SO GENE
 LA English
 DT Article
 DE Roots; Salinity stress; Expressed sequence tags; Gene expression
    profiling; Real-time RT-PCR
 ID EXPRESSED SEQUENCE TAGS; TRANSLATION INITIATION-FACTOR; TOLERANCE;
    LEAVES; PLANTS; TRANSCRIPTOME; RICE; ESTS; NACL; PCR
 AB Plant roots are the primary site of perception and injury for salinity
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    from the three libraries, and were assembled into 1142 contigs and 3026
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    the three cDNA libraries. Ninety redundant unique transcripts
    responsive to NaCl treatment were identified. Of them, 21 genes were
    novel or of unknown function while others were involved in the
    functional activities, such as ROS scavenging, lipid metabolism,
    osmolyte biosynthesis, signal transduction, transport, lignin synthesis
    and homeostasis. The genes, including those for metallothionein-like
    protein, polyubiquitin, hypothetical protein, and glycine-rich cell
    wall structural protein, were abundant in the libraries and showed
    obvious up-regulation after NaCl treatments, suggesting important roles
    in NaCl tolerance. The results of this study may contribute to our
    understanding of the molecular mechanism of salt tolerance in the roots
    of plants. (C) 2008 Elsevier B.V. All rights reserved.
 C1 [Li, Huiyu; Wang, Yucheng; Jiang, Jing; Liu, Guifeng; Gao, Caiqiu; Yang, Chuanping] NE Forestry Univ, Minist Educ, Key Lab Forest Tree Genet Improvement & Biotechno, Harbin 150040, Peoples R China.
 RP Yang, CP, NE Forestry Univ, Minist Educ, Key Lab Forest Tree Genet
    Improvement & Biotechno, Hexing Rd 26, Harbin 150040, Peoples R China.
 EM yangchuanpingnefu@yahoo.com
 FU National Natural Science Foundation of China [30571509]; Chinese
    Ministry of Education [107037]; Key Research Projects of Heilongjiang
    Province [GB06B303-1]
 FX This work has been supported by the National Natural Science Foundation
    of China (No. 30571509), Key Project of Science-Technology Research
    granted by the Chinese Ministry of Education (No. 107037) and the Key
    Research Projects of Heilongjiang Province (GB06B303-1).
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 NR 29
 TC 7
 PU ELSEVIER SCIENCE BV
 PI AMSTERDAM
 PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
 SN 0378-1119
 J9 GENE
 JI Gene
 PD MAR 15
 PY 2009
 VL 433
 IS 1-2
 BP 65
 EP 71
 DI 10.1016/j.gene.2008.12.007
 PG 7
 SC Genetics & Heredity
 GA 421AX
 UT ISI:000264331400009
 ER
 
 PT J
 AU Hooper, AT
    Butler, JM
    Nolan, DJ
    Kranz, A
    Iida, K
    Kobayashi, M
    Kopp, HG
    Shido, K
    Petit, I
    Yanger, K
    James, D
    Witte, L
    Zhu, ZP
    Wu, Y
    Pytowski, B
    Rosenwaks, Z
    Mittal, V
    Sato, TN
    Rafii, S
 AF Hooper, Andrea T.
    Butler, Jason M.
    Nolan, Daniel J.
    Kranz, Andrea
    Iida, Kaoruko
    Kobayashi, Mariko
    Kopp, Hans-Georg
    Shido, Koji
    Petit, Isabelle
    Yanger, Kilangsungla
    James, Daylon
    Witte, Larry
    Zhu, Zhenping
    Wu, Yan
    Pytowski, Bronislaw
    Rosenwaks, Zev
    Mittal, Vivek
    Sato, Thomas N.
    Rafii, Shahin
 TI Engraftment and Reconstitution of Hematopoiesis Is Dependent on
    VEGFR2-Mediated Regeneration of Sinusoidal Endothelial Cells
 SO CELL STEM CELL
 LA English
 DT Article
 ID MARROW VASCULAR NICHE; STEM-CELLS; PROGENITOR CELLS; GROWTH-FACTOR;
    DIFFERENTIATION; IDENTIFICATION; ANGIOGENESIS; MOBILIZATION;
    QUIESCENCE; SURVIVAL
 AB Myelosuppression damages the bone marrow (BM) vascular niche, but it is
    unclear how regeneration of bone marrow vessels contributes to
    engraftment of transplanted hematopoietic stem and progenitor cells
    (HSPCs) and restoration of hematopoiesis. We found that chemotherapy
    and sublethal irradiation induced minor regression of BM sinusoidal
    endothelial cells (SECs), while lethal irradiation induced severe
    regression of SECs and required BM transplantation (BMT) for
    regeneration. Within the BM, VEGFR2 expression specifically demarcated
    a continuous network of arterioles and SECs, with arterioles uniquely
    expressing Sca1 and SECs uniquely expressing VEGFR3. Conditional
    deletion of VEGFR2 in adult mice blocked regeneration of SECs in
    sublethally irradiated animals and prevented hematopoietic
    reconstitution. Similarly, inhibition of VEGFR2 signaling in lethally
    irradiated wild-type mice rescued with BMT severely impaired SEC
    reconstruction and prevented engraftment and reconstitution of HSPCs.
    Therefore, regeneration of SECs via VEGFR2 signaling is essential for
    engraftment of HSPCs and restoration of hematopoiesis.
 C1 [Hooper, Andrea T.; Butler, Jason M.; Nolan, Daniel J.; Kobayashi, Mariko; Kopp, Hans-Georg; Shido, Koji; Petit, Isabelle; Yanger, Kilangsungla; James, Daylon; Rosenwaks, Zev; Rafii, Shahin] Weill Cornell Med Coll, Howard Hughes Med Inst, New York, NY 10065 USA.
    [Hooper, Andrea T.; Butler, Jason M.; Nolan, Daniel J.; Kobayashi, Mariko; Kopp, Hans-Georg; Shido, Koji; Petit, Isabelle; Yanger, Kilangsungla; James, Daylon; Rosenwaks, Zev; Rafii, Shahin] Weill Cornell Med Coll, Ansary Stem Cell Inst, New York, NY 10065 USA.
    [Hooper, Andrea T.; Butler, Jason M.; Nolan, Daniel J.; Kobayashi, Mariko; Kopp, Hans-Georg; Shido, Koji; Petit, Isabelle; Yanger, Kilangsungla; James, Daylon; Rosenwaks, Zev; Rafii, Shahin] Weill Cornell Med Coll, Dept Med Genet, New York, NY 10065 USA.
    [Kranz, Andrea; Iida, Kaoruko; Sato, Thomas N.] Weill Cornell Med Coll, Dept Cell & Dev Biol, New York, NY 10065 USA.
    [Witte, Larry; Zhu, Zhenping; Wu, Yan; Pytowski, Bronislaw] ImClone Syst Inc, New York, NY 10014 USA.
    [Mittal, Vivek] Weill Cornell Med Coll, Dept Surg, New York, NY 10065 USA.
    [Rosenwaks, Zev] Ronald O Perelman & Claudia Cohen Ctr Reprod Med, New York, NY 10065 USA.
 RP Rafii, S, Weill Cornell Med Coll, Howard Hughes Med Inst, New York, NY
    10065 USA.
 EM srafii@med.cornell.edu
 FU Howard Hughes Medical Institute ; Ansary Stem Cell Institute ; Deutsche
    Forschungsgerneinschaft [2154/2-1]
 FX S.R. and T.N.S. are funded by NIH. S,R. is supported by Howard Hughes
    Medical Institute and Ansary Stem Cell Institute. A.K. was supported in
    part by Deutsche Forschungsgerneinschaft (KR 2154/2-1). We thank Mollie
    Goetz, Keith Kobylarz, and Allison Spencer for their excellent
    technical assistance.
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 TC 36
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 PI CAMBRIDGE
 PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
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 J9 CELL STEM CELL
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 BP 263
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 UT ISI:000264369300016
 ER
 
 PT J
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    cells
 SO CELL BIOLOGY INTERNATIONAL
 LA English
 DT Article
 DE Chitosan; Chitooligosaccharide; Nerve cell affinity; Neuronal
    differentiation; PC-12 cells
 ID NERVE REGENERATION; IN-VITRO; NEUROFILAMENTS; EXPRESSION; VIVO
 AB Chitosan is now being widely used biomaterial in the tissue engineering
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    in vivo into chitooligosaccharide. We have investigated the in vitro
    effects of chitooligosaccharide on neuronal differentiation of PC-12
    cells to see what effects chitooligosaccharide have on certain
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    PC-12 cells were enhanced by treatment of chitooligosaccharide. The
    real-time quantitative RT-PCR and Western blot analysis revealed showed
    that chitooligosaccharide could upregulate the expression of
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    2 week culture. All the data suggest that chitooligosaccharide
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    and promoting neuronal differentiation and neurite outgrowth. (C) 2009
    International Federation for Cell Biology. Published by Elsevier Ltd.
    All rights reserved.
 C1 [Yang, Yumin; Liu, Mei; Gu, Yun; Lin, Sheyu; Ding, Fei; Gu, Xiaosong] Nantong Univ, Jiangsu Key Lab Neuroregenerat, Nantong 226001, Jiangsu, Peoples R China.
 RP Gu, XS, Nantong Univ, Jiangsu Key Lab Neuroregenerat, 19 Qixiu Rd,
    Nantong 226001, Jiangsu, Peoples R China.
 EM neurongu@public.nt.js.cn
 FU Hi-Tech Research and Development Program of China [2006AA02A128];
    Nature Science Foundation of china [30770585]; Basic Research Program
    of Jiangsu Education Department [07KJA31025]; Program for New Century
    Excellent Talents in University 
 FX The financial supports of the Hi-Tech Research and Development Program
    of China ( 863 Program, Grant no. 2006AA02A128), the Nature Science
    Foundation of china ( Grant no. 30770585), Basic Research Program of
    Jiangsu Education Department ( Grant no. 07KJA31025) and Program for
    New Century Excellent Talents in University are gratefully acknowledged.
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 TC 6
 PU ACADEMIC PRESS LTD ELSEVIER SCIENCE LTD
 PI LONDON
 PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
 SN 1065-6995
 J9 CELL BIOL INT
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 PD MAR
 PY 2009
 VL 33
 IS 3
 BP 352
 EP 356
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 PG 5
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 GA 414UH
 UT ISI:000263890200012
 ER
 
 PT J
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 AF Mancino, Mario
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    Nagaoka, Tadahiro
    Gonzales, Monica
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    Normanno, Nicola
    Salomon, David S.
    Strizzi, Luigi
 TI Neuronal Guidance Protein Netrin-1 Induces Differentiation in Human
    Embryonal Carcinoma Cells
 SO CANCER RESEARCH
 LA English
 DT Article
 ID MAMMARY-GLAND; SELF-RENEWAL; STEM-CELLS; TERATOCARCINOMA; EXPRESSION;
    CRIPTO-1; FAMILY; MORPHOGENESIS; GROWTH; TUMORS
 AB Pluripotent cells within embryonal carcinoma (EC) can differentiate in
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    glial filament acidic protein, Nestin, and gamma-ammobutyric acid and
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    Netrin-l to the Neogemn receptor and activation of SHP-2, resulting in
    increased levels of inactive phosphorylated c-sre((Y527)). These
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    differentiation of human EC cells by affecting c-src signaling via
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 C1 [Mancino, Mario; Watanabe, Kazuhide; Nagaoka, Tadahiro; Gonzales, Monica; Bianco, Caterina; Salomon, David S.; Strizzi, Luigi] NCI, Mammary Biol & Tumorigenesis Lab, Bethesda, MD 20892 USA.
    [Esposito, Claudia; Normanno, Nicola] CROM Ist Nazl Tumori Pascale Napoli, Mercogliano, AV, Italy.
    [Normanno, Nicola] Ist Nazl Tumori Fdn Pascale, Cell Biol & Proclin Models Unit, Naples, Italy.
 RP Mancino, M, NCI, Mammary Biol & Tumorigenesis Lab, 37 Convent Dr,Room
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 EM mario.mancino@cro-m.eu
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 NR 20
 TC 2
 PU AMER ASSOC CANCER RESEARCH
 PI PHILADELPHIA
 PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
 SN 0008-5472
 J9 CANCER RES
 JI Cancer Res.
 PD MAR 1
 PY 2009
 VL 69
 IS 5
 BP 1717
 EP 1721
 DI 10.1158/0008-5472.CAN-08-2985
 PG 5
 SC Oncology
 GA 415ML
 UT ISI:000263937800005
 ER
 
 PT J
 AU Hung, CY
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    Yang, CS
    Peng, SJ
 AF Hung, Chung-Ying
    Chen, Yung-Liang
    Chen, Chiou-Shya
    Yang, Chwei-Shiun
    Peng, Sheng-Jeng
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    Cross-Sectional Study
 SO BLOOD PURIFICATION
 LA English
 DT Article
 DE Cramps; Hemodialysis; Leptin; Neuronal activity
 ID CENTRAL-NERVOUS-SYSTEM; STAGE RENAL-DISEASE; PLASMA LEPTIN; SERUM
    LEPTIN; FOOD-INTAKE; OB RNA; EXPRESSION; OBESE; GENE; HEMODIAFILTRATION
 AB Background/Aims: The mechanism of muscle cramp in hemodialysis patients
    is not well understood. Leptin, a middle molecule uremic toxin, is able
    to affect neuronal activity. This study aimed to determine the
    association between leptin and hemodialysis-related muscle cramps.
    Methods: A total of 79 hemodialysis patients were enrolled. The
    episodes of hemodialysis-related muscle cramps were recorded over a
    28-day period. Serum levels of leptin were measured on the 15th day, a
    mid-week dialysis session. Results: Frequent hemodialysis-related
    cramps were associated with old age and elevated serum leptin levels.
    The risk of frequent hemodialysis-related cramps increased with
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    significant after adjustment for age, mean ultrafiltration ratio,
    gender, body mass index, insulin, resistin, c-reactive protein,
    albumin, peripheral arterial disease, electrolytes, and
    beta(2)-microglobulin. Conclusion: Leptin levels are associated with
    frequent hemodialysis-related cramps. Further studies are necessary to
    elucidate the underlying mechanisms. Copyright (C) 2009 S. Karger AG,
    Basel
 C1 [Yang, Chwei-Shiun; Peng, Sheng-Jeng] Cathay Gen Hosp, Dept Internal Med, Div Nephrol, Taipei 106, Taiwan.
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    [Chen, Chiou-Shya] Cathay Gen Hosp, Hsinchu Branch, Dept Lab Med, Hsinchu, Taiwan.
    [Chen, Chiou-Shya] Yuanpei Univ Sci & Technol, Dept Med Technol, Hsinchu, Taiwan.
    [Hung, Chung-Ying] Fu Jen Catholic Univ, Coll Med, Sch Med, Taipei, Taiwan.
 RP Peng, SJ, Cathay Gen Hosp, Dept Internal Med, Div Nephrol, 280,Sect
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 EM kennethpeng@cgh.org.tw
 FU Cathay General Hospital [CMRI9506]
 FX This study was supported by Cathay General Hospital grant CMRI9506. We
    would like to acknowledge the assistance of Hisahide Hiura of Japan
    Clinical Laboratories, Inc., who kindly supplied the anti-leptin
    antibodies 14C9 and 3D10. We also thank Chyi-Huey Bai, PhD, of the
    Central Laboratory, Shin Kong WHS Memorial Hospital, Taipei, Taiwan,
    for statistical advice. Furthermore, we express our appreciation to Dr.
    Simon J. T. Mao of National Chiao Tung University, Hsinchu, Taiwan, for
    important suggestions in preparing the manuscript.
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 PT J
 AU Quigley, M
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 AF Quigley, Michael
    Martinez, Jennifer
    Huang, Xiaopei
    Yang, Yiping
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 SO BLOOD
 LA English
 DT Article
 ID FORKHEAD TRANSCRIPTION FACTOR; TOLL-LIKE RECEPTORS; KAPPA-B ACTIVATION;
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 AB Recent advances have suggested a crucial role of the innate immunity in
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 C1 [Quigley, Michael; Martinez, Jennifer; Huang, Xiaopei; Yang, Yiping] Duke Univ, Med Ctr, Dept Med, Durham, NC 27710 USA.
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 RP Yang, YP, Duke Univ, Med Ctr, Dept Med, Box 103005, Durham, NC 27710
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 EM yang0029@mc.duke.edu
 FU National Institutes of Health [CA111807, CA047741]; Alliance for Cancer
    Gene Therapy 
 FX We thank S. Akira for providing MyD88<SUP>-/-</SUP> and
    TLR2<SUP>-/-</SUP> mice and Z. Songyang for providing the pMSCV and
    pMSCV-dnAkt constructs.
    This work was supported by the National Institutes of Health (grants
    CA111807 and CA047741) and a grant from the Alliance for Cancer Gene
    Therapy (Y.Y.).
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    Rimsza, Lisa M.
    Holte, Harald
    Cazier, Jean-Baptiste
    Johnson, Nathalie A.
    Campo, Elias
    Chan, Wing C.
    Gascoyne, Randy D.
    Young, Bryan D.
    Staudt, Louis M.
    Lister, T. Andrew
    Fitzgibbon, Jude
 TI Regions of acquired uniparental disomy at diagnosis of follicular
    lymphoma are associated with both overall survival and risk of
    transformation
 SO BLOOD
 LA English
 DT Article
 ID GENE-EXPRESSION; COPY NUMBER; REVEALS; EVOLUTION; CELLS; ARRAY
 AB Acquired homozygosity in the form of segmental acquired uniparental
    disomy (aUPD) has been described in follicular lymphoma (FL) and is
    usually due to mitotic recombination. SNP array analysis was performed
    with the use of the Affymetrix 10K 2.0 Gene-chip array on DNA from 185
    diagnostic FL patients to assess the prognostic relevance of aUPD.
    Genetic abnormalities were detected in 118 (65%) of 182 patients.
    Number of abnormalities was predictive of outcome; more than 3
    abnormalities was associated with inferior overall survival (OS; P <
    .03). Sites of recurrent aUPD were detected on 6p (n = 25), 16p (n =
    22), 12q (n = 17), 1p36 (n = 14), 10q (n = 8), and 6q (n = 8). On
    multivariate analysis aUPD on 1p36 correlated with shorter OS (P =
    .05). aUPD on 16p was predictive of transformation (P = .03) and
    correlated with poorer progression-free survival (P = .02). aUPD is
    frequent at diagnosis of FL and affects probability of disease
    transformation and clinical outcome. (Blood. 2009; 113: 2298-2301)
 C1 [O'Shea, Derville; O'Riain, Ciaran; Gupta, Manu; Yang, Youwen; Wrench, David; Gribben, John; Cazier, Jean-Baptiste; Gascoyne, Randy D.; Young, Bryan D.; Lister, T. Andrew; Fitzgibbon, Jude] Barts & London Queen Marys Sch Med & Dent, Ctr Med Oncol, London EC1M 6BQ, England.
    [Waters, Rachel] Univ Oxford, Ctr Stat Med, Oxford, England.
    [Rosenwald, Andreas; Ott, German] Univ Wurzburg, Inst Pathol, D-8700 Wurzburg, Germany.
    [Ott, German] Robert Bosch Krankenhaus, Dept Clin Pathol, Stuttgart, Germany.
    [Rimsza, Lisa M.] Univ Arizona, Dept Pathol, Tucson, AZ USA.
    [Rimsza, Lisa M.] Univ Arizona, Arizona Canc Ctr, Tucson, AZ USA.
    [Holte, Harald] Univ Oslo, Rikshosp, Norwegian Radium Hosp, Canc Clin,Dept Oncol, N-0027 Oslo, Norway.
    [Cazier, Jean-Baptiste] Canc Res UK, Bioinformat & Biostat, London, England.
    [Johnson, Nathalie A.] British Columbia Canc Agcy, Dept Pathol, Vancouver, BC V5Z 4E6, Canada.
    [Johnson, Nathalie A.] British Columbia Canc Agcy, Div Med Oncol, Vancouver, BC V5Z 4E6, Canada.
    [Campo, Elias] Univ Barcelona, IDIBAPS, Dept Pathol, Barcelona, Spain.
    [Campo, Elias] Univ Barcelona, IDIBAPS, Hosp Clin, Barcelona, Spain.
    [Chan, Wing C.] Univ Nebraska Med Ctr, Dept Pathol & Microbiol, Omaha, NE USA.
    [Staudt, Louis M.] NCI, NIH, Metab Branch, Ctr Canc Res, Bethesda, MD 20892 USA.
 RP O'Shea, D, Barts & London Queen Marys Sch Med & Dent, Ctr Med Oncol,
    London EC1M 6BQ, England.
 EM derville.oshea@cancer.org.uk
 FU Cancer Research UK ; Medical Research Council ; National Institutes of
    Health [5UO1CA114778]
 FX This work was supported by grants from Cancer Research UK, the Medical
    Research Council, and the National Institutes of Health (SPEC grant
    5UO1CA114778). D.O. is supported by a Medical Research Council Clinical
    Research Fellow grant. C.O. is a Cancer Research UK Barts-Cambridge
    Molecular Pathology Clinical Research Fellow.
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 NR 24
 TC 20
 PU AMER SOC HEMATOLOGY
 PI WASHINGTON
 PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
 SN 0006-4971
 J9 BLOOD
 JI Blood
 PD MAR 5
 PY 2009
 VL 113
 IS 10
 BP 2298
 EP 2301
 DI 10.1182/blood-2008-08-174953
 PG 4
 SC Hematology
 GA 415EZ
 UT ISI:000263918400023
 ER
 
 PT J
 AU Li, Y
    Chen, S
    Yuan, J
    Yang, YZ
    Li, JL
    Ma, J
    Wu, XH
    Freund, M
    Pollok, K
    Hanenberg, H
    Goebel, WS
    Yang, FC
 AF Li, Yan
    Chen, Shi
    Yuan, Jin
    Yang, Yanzhu
    Li, Jingling
    Ma, Jin
    Wu, Xiaohua
    Freund, Marcel
    Pollok, Karen
    Hanenberg, Helmut
    Goebel, W. Scott
    Yang, Feng-Chun
 TI Mesenchymal stem/progenitor cells promote the reconstitution of
    exogenous hematopoietic stem cells in Fancg(-/-) mice in vivo
 SO BLOOD
 LA English
 DT Article
 ID INDUCED APOPTOTIC RESPONSES; ACUTE MYELOID-LEUKEMIA; WILD-TYPE CELLS;
    FANCONI-ANEMIA; BONE-MARROW; PROGENITOR CELLS; STROMAL CELLS;
    OSTEOGENESIS IMPERFECTA; REPOPULATING ABILITY; ENHANCES ENGRAFTMENT
 AB Fanconi anemia (FA) is a heterogeneous genetic disorder characterized
    by bone marrow failure and complex congenital anomalies. Although
    mutations in FA genes result in a characteristic phenotype in the
    hematopoietic stem/progenitor cells (HSPCs), little is known about the
    consequences of a nonfunctional FA pathway in other stem/progenitor
    cell compartments. Given the intense functional interactions between
    HSPCs and the mesenchymal microenvironment, we investigated the FA
    pathway on the cellular functions of murine mesenchymal stem/progenitor
    cells (MSPCs) and their interactions with HSPCs in vitro and in vivo.
    Here, we show that loss of the murine homologue of FANCG (Fancg)
    results in a defect in MSPC proliferation and in their ability to
    support the adhesion and engraftment of murine syngeneic HSPCs in vitro
    or in vivo. Transplantation of wild-type (WT) but not Fancg(-/-) MSPCs
    into the tibiae of Fancg(-/-) recipient mice enhances the HSPC
    engraftment kinetics, the BM cellularity, and the number of progenitors
    per tibia of WT HSPCs injected into lethally irradiated Fancg(-/-)
    recipients. Collectively, these data show that FA proteins are required
    in the BM microenvironment to maintain normal hematopoiesis and provide
    genetic and quantitative evidence that adoptive transfer of WT MSPCs
    enhances hematopoietic stem cell engraftment. (Blood. 2009; 113:
    2342-2351)
 C1 [Yang, Feng-Chun] Indiana Univ, Sch Med, Canc Res Inst, Dept Pediat, Indianapolis, IN 46202 USA.
    [Li, Yan; Chen, Shi; Yuan, Jin; Yang, Yanzhu; Li, Jingling; Wu, Xiaohua; Pollok, Karen; Hanenberg, Helmut; Goebel, W. Scott; Yang, Feng-Chun] Indiana Univ, Sch Med, Herman B Wells Ctr Pediat Res, Indianapolis, IN 46202 USA.
    [Ma, Jin; Freund, Marcel; Hanenberg, Helmut] Univ Dusseldorf, Childrens Hosp, Dept Pediat Oncol Hematol & Clin Immunol, D-4000 Dusseldorf, Germany.
    [Yang, Feng-Chun] Indiana Univ, Sch Med, Dept Anat & Cell Biol, Indianapolis, IN 46202 USA.
 RP Yang, FC, Indiana Univ, Sch Med, Canc Res Inst, Dept Pediat, 1044 W
    Walnut St,R4-427, Indianapolis, IN 46202 USA.
 EM fyang@iupui.edu
 FU Simmons Clinical Studies Fund (Indiana University, Indianapolis, IN) ;
    Department of Defense [NF073112]; March of Dimes [6-FY08-246]; National
    Institutes of Health, (Bethesda, MD) ; Showalter Trust Award (Indiana
    University, Indianapolis, IN) ; Deutsche Forschungsgemeinschaft (Bonn,
    Germany) [K08 HL075253, DFG SPP1230 HA2322/2-1, PPG-P01-HL533586]
 FX This work was supported by the Simmons Clinical Studies Fund (Indiana
    University, Indianapolis, IN; F.-C.Y.), the Department of Defense
    (NF073112; F.-C.Y.), the March of Dimes (6-FY08-246; F.-C.Y.), National
    Institutes of Health, (Bethesda, MD), the Showalter Trust Award
    (Indiana University, Indianapolis, IN; W. S. G.), and Deutsche
    Forschungsgemeinschaft (Bonn, Germany; K08 HL075253; W. S. G.; DFG
    SPP1230 HA2322/2-1; H. H.; and PPG-P01-HL533586; H. H. and K. P.).
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 NR 73
 TC 13
 PU AMER SOC HEMATOLOGY
 PI WASHINGTON
 PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
 SN 0006-4971
 J9 BLOOD
 JI Blood
 PD MAR 5
 PY 2009
 VL 113
 IS 10
 BP 2342
 EP 2351
 DI 10.1182/blood-2008-07-168138
 PG 10
 SC Hematology
 GA 415EZ
 UT ISI:000263918400028
 ER
 
 PT J
 AU Chi, XF
    Lou, XY
    Yang, M
    Shu, QY
 AF Chi, Xiao-Fei
    Lou, Xiang-Yang
    Yang, Mark C. K.
    Shu, Qing-Yao
 TI An optimal DNA pooling strategy for progressive fine mapping
 SO GENETICA
 LA English
 DT Article
 DE Fine mapping; DNA pooling; Experimental cost; Genotyping efficiency;
    Experimental populations
 ID QUANTITATIVE TRAIT LOCUS; RECOMBINATION HOT-SPOTS; LARGE-SCALE
    ASSOCIATION; ORYZA-SATIVA L.; COMPLEX TRAITS; MEIOTIC RECOMBINATION;
    GENETIC DISSECTION; POSITIONAL CLONING; LINKAGE DISEQUILIBRIUM;
    ARABIDOPSIS-THALIANA
 AB We present a cost-effective DNA pooling strategy for fine mapping of a
    single Mendelian gene in controlled crosses. The theoretical argument
    suggests that it is potentially possible for a single-stage pooling
    approach to reduce the overall experimental expense considerably by
    balancing costs for genotyping and sample collection. Further, the
    genotyping burden can be reduced through multi-stage pooling. Numerical
    results are provided for practical guidelines. For example, the
    genotyping effort can be reduced to only a small fraction of that
    needed for individual genotyping at a small loss of estimation accuracy
    or at a cost of increasing sample sizes slightly when recombination
    rates are 0.5% or less. An optimal two-stage pooling scheme can reduce
    the amount of genotyping to 19.5%, 14.5% and 6.4% of individual
    genotyping efforts for identifying a gene within 1, 0.5, and 0.1 cM,
    respectively. Finally, we use a genetic data set for mapping the rice
    xl(t) gene to demonstrate the feasibility and efficiency of the DNA
    pooling strategy. Taken together, the results demonstrate that this DNA
    pooling strategy can greatly reduce the genotyping burden and the
    overall cost in fine mapping experiments.
 C1 [Lou, Xiang-Yang] Univ Virginia, Dept Psychiat & Neurobehav Sci, Charlottesville, VA 22911 USA.
    [Chi, Xiao-Fei; Shu, Qing-Yao] Zhejiang Univ, Zhejiang Univ Collaborating Ctr, IAEA, Hangzhou 310029, Zhejiang, Peoples R China.
    [Chi, Xiao-Fei; Shu, Qing-Yao] Zhejiang Univ, Inst Nucl Agr Sci, Natl Key Lab Rice Biol, Hangzhou 310029, Zhejiang, Peoples R China.
    [Yang, Mark C. K.] Univ Florida, Dept Stat, Gainesville, FL 32611 USA.
    [Shu, Qing-Yao] IAEA, Joint FAO IAEA Div Nucl Techn Food & Agr, A-1400 Vienna, Austria.
 RP Lou, XY, Univ Virginia, Dept Psychiat & Neurobehav Sci, 1670 Discovery
    Dr,Suite 110, Charlottesville, VA 22911 USA.
 EM XL5N@virginia.edu
    qyshu@zju.edu.cn
 FU National Science Foundation of China [30571131, 30000097]
 FX We greatly thank Dr. J. S. Wu for his assistance in checking the
    mathematical equations in this article for correctness. This project
    was funded in part by the National Science Foundation of China 30571131
    to QYS and 30000097 to XYL.
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 NR 58
 TC 3
 PU SPRINGER
 PI DORDRECHT
 PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
 SN 0016-6707
 J9 GENETICA
 JI Genetica
 PD APR
 PY 2009
 VL 135
 IS 3
 BP 267
 EP 281
 DI 10.1007/s10709-008-9275-5
 PG 15
 SC Genetics & Heredity
 GA 413ZO
 UT ISI:000263833900002
 ER
 
 PT J
 AU Fang, M
    Jiang, D
    Gao, HJ
    Sun, DX
    Yang, RQ
    Zhang, Q
 AF Fang, Ming
    Jiang, Dan
    Gao, Huijiang
    Sun, Dongxiao
    Yang, Runqing
    Zhang, Qin
 TI A new Bayesian automatic model selection approach for mapping
    quantitative trait loci under variance component model
 SO GENETICA
 LA English
 DT Article
 DE Bayesian; Mapping QTL; MCMC; Model selection
 ID CHAIN MONTE-CARLO; LINKAGE; PEDIGREES; IDENTITY; DESCENT; MARKERS;
    GENOME
 AB Bayesian variable selection implemented via reversible jump Markov
    chain Monte Carlo (RJMCMC) is an effective method for mapping multiple
    QTL. Recently, it has been used for QTL mapping both in inbred line
    crosses and in outbred populations. However, by RJMCMC, since the
    model-dimension is variable, the parameters are usually subject to poor
    mixing and difficult to converge. In inbred lines, the fixed effect
    model is used for mapping QTL, various approaches which keep the
    model-dimension unchanged have been proposed, and it is proved that the
    mixing properties of Markov chains is substantially improved compared
    with RJMCMC. In outbred populations, the random effect model is used
    and the implementation via RJMCMC for variable selection still is the
    mainstream to map multiple QTL. Due to the poor performance RJMCMC has,
    it is meaningful to develop a model-dimension fixed approach for
    mapping QTL under random effect model. In this article, we proposed a
    new model-dimension fixed approach called Bayesian automatic model
    selection method for mapping multiple QTL under random effect model. By
    the new approach, all variances of QTL are subject to estimate, in
    which the variance of zero-effect QTL will exactly converge to zero,
    and those of non-zero effect QTL will be estimated precisely.
    Therefore, no special model selection is required. A series of
    simulation experiments have been conducted to investigate the
    performance of the method, the result showed that the new approach is
    very efficient for mapping multiple QTL. A computer program written in
    FORTRAN is available to interested users on request.
 C1 [Fang, Ming] Heilongjiang August First Land Reclamat Univ, Life Sci Coll, Daqing 163319, Peoples R China.
    [Fang, Ming; Gao, Huijiang; Sun, Dongxiao; Zhang, Qin] China Agr Univ, Coll Anim Sci & Technol, Beijing 100094, Peoples R China.
    [Jiang, Dan] China Agr Univ, Coll Agron & Biotechnol, Beijing 100094, Peoples R China.
    [Gao, Huijiang] NE Agr Univ, Coll Anim Sci & Technol, Harbin 150030, Peoples R China.
    [Yang, Runqing] Shanghai Jiao Tong Univ, Sch Agr & Biol, Shanghai 201101, Peoples R China.
 RP Fang, M, Heilongjiang August First Land Reclamat Univ, Life Sci Coll,
    Daqing 163319, Peoples R China.
 EM fangming618@126.com
 FU Heilongjiang August First Land Reclamation University ; 863 Project
    [2007AA10Z157]
 FX The research was supported by Heilongjiang August First Land
    Reclamation University and the "863" Project Grant 2007AA10Z157 to DS.
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 NR 31
 TC 3
 PU SPRINGER
 PI DORDRECHT
 PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
 SN 0016-6707
 J9 GENETICA
 JI Genetica
 PD APR
 PY 2009
 VL 135
 IS 3
 BP 429
 EP 437
 DI 10.1007/s10709-008-9291-5
 PG 9
 SC Genetics & Heredity
 GA 413ZO
 UT ISI:000263833900018
 ER
 
 PT J
 AU Ma, FX
    Zhang, DM
    Yang, HS
    Sun, HQ
    Wu, W
    Gan, Y
    Balducci, J
    Wei, YQ
    Zhao, X
    Huang, Y
 AF Ma, Fanxin
    Zhang, Dongmei
    Yang, Hansuo
    Sun, Huaqin
    Wu, Wen
    Gan, Yan
    Balducci, James
    Wei, Yu-quan
    Zhao, Xia
    Huang, Yao
 TI Endothelial cell-specific molecule 2 (ECSM2) modulates actin remodeling
    and epidermal growth factor receptor signaling
 SO GENES TO CELLS
 LA English
 DT Article
 ID ACTIVATED PROTEIN-KINASE; FOCAL ADHESION PROTEIN; BREAST-CANCER CELLS;
    EGF RECEPTOR; CYTOSKELETAL DYNAMICS; VASCULAR DEVELOPMENT; INCREASED
    MOTILITY; TYROSINE KINASES; STRESS FIBERS; F-ACTIN
 AB Endothelial cell-specific molecules (ECSMs) play a pivotal role in the
    pathogenesis of many angiogenesis-related diseases. Since its initial
    discovery, the exact function of human ECSM2 has not been defined. In
    this study, by database mining, we identified a number of hypothetical
    proteins across species exhibiting substantial sequence homology to the
    human ECSM2. We showed that ECSM2 is preferentially expressed in
    endothelial cells and blood vessels. Their characteristic structures
    and unique expression patterns suggest that ECSM2 is an evolutionarily
    conserved gene and may have important functions. We further explored
    the potential roles of human ECSM2 at the molecular and cellular level.
    Using a reconstitution mammalian cell system, we demonstrated that
    ECSM2 mainly resides at the cell membrane, is critically involved in
    cell-shape changes and actin cytoskeletal rearrangement, and suppresses
    tyrosine phosphorylation signaling. More importantly, we uncovered that
    ECSM2 can cross-talk with epidermal growth factor receptor (EGFR) to
    attenuate the EGF-induced cell migration, possibly via inhibiting the
    Shc-Ras-ERK (MAP kinase) pathway. Given the importance of growth factor
    and receptor tyrosine kinase-mediated signaling and cell migration in
    angiogenesis-related diseases, our findings regarding the inhibitory
    effects of ECSM2 on EGF-mediated signaling and cell motility may have
    important therapeutic implications.
 C1 [Ma, Fanxin; Zhang, Dongmei; Yang, Hansuo; Sun, Huaqin; Wei, Yu-quan; Zhao, Xia] Sichuan Univ, Coll Life Sci, W China Hosp, State Key Lab Biotherapy, Chengdu 610064, Sichuan, Peoples R China.
    [Ma, Fanxin; Wu, Wen; Gan, Yan; Balducci, James; Huang, Yao] St Josephs Hosp, Dept Obstet & Gynecol, Lab Signal Transduct, Phoenix, AZ USA.
 RP Zhao, X, Sichuan Univ, Coll Life Sci, W China Hosp, State Key Lab
    Biotherapy, Chengdu 610064, Sichuan, Peoples R China.
 EM xiao-zhao@126.com
    yhuang@chw.edu
 FU St. Joseph's Foundation Startup Fund ; National Basic Research Program
    of China [2004CB518800, 2005CB522506]; National Natural Science
    foundation of China [30300408]; China Scholarship Council (CSC) 
 FX This work was supported by a St. Joseph's Foundation Startup Fund (to
    Y.H.) and grants from the National Basic Research Program of China
    (2004CB518800 and 2005CB522506) and the National Natural Science
    foundation of China (30300408) (to Y.Q.W.). F. Ma is the recipient of a
    China Scholarship Council (CSC) scholarship. The authors appreciate
    helpful discussion with Drs. Y. Chang, X. Mo, and G. Samuelson, and
    generous provision of reagents by those named in the text.
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 NR 60
 TC 6
 PU WILEY-BLACKWELL PUBLISHING, INC
 PI MALDEN
 PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
 SN 1356-9597
 J9 GENES CELLS
 JI Genes Cells
 PD MAR
 PY 2009
 VL 14
 IS 3
 BP 281
 EP 293
 DI 10.1111/j.1365-2443.2008.01267.x
 PG 13
 SC Cell Biology; Genetics & Heredity
 GA 411YY
 UT ISI:000263691600001
 ER
 
 PT J
 AU Yan, Y
    Li, YP
    Hu, CY
    Gu, XC
    Liu, JH
    Hu, YA
    Yang, Y
    Wei, YQ
    Zhao, CJ
 AF Yan, Yan
    Li, Yiping
    Hu, Chuanyin
    Gu, Xiaochun
    Liu, Junhua
    Hu, Yu-An
    Yang, Yang
    Wei, Yiquan
    Zhao, Chunjie
 TI Expression of Frizzled10 in mouse central nervous system
 SO GENE EXPRESSION PATTERNS
 LA English
 DT Article
 DE Wnt; Frizzled10; Telencephalon; Cortex; Hippocampus; Cortical hem;
    Diencephalon; Midbrain; Cerebellum; Spinal cord; Expression pattern;
    Mouse
 ID WNT; GENES; RECEPTORS; HEM
 AB Frizzled transmembrane proteins (Fzd) are receptors of Wnts, and they
    play key roles during central nervous system (CNS) development in
    vertebrates. Here we report the expression pattern of Frizzled 10 in
    mouse CNS from embryonic stages to adulthood. Frizzled10 is expressed
    strongly at embryonic days E8.5 and E9.5 in the neural tube and tail
    bud. At E10.5, Frizzled10 is expressed in the forebrain vesicle, the
    fourth ventricle and the dorsal spinal cord. From E12.5 to E16.5,
    Frizzled10 expression is mainly observed in the cortical hem/fimbria,
    the neuroepithelium of the third ventricular zone, midbrain, developing
    cerebellum, and dorsal spinal cord. At P0, with the exception of
    expression in the fimbria, Frizzled10 mRNA expression is limited to
    specific nuclei including the ventral posterior thalamic nucleus (VP)
    and the dorsal lateral geniculate nucleus (DLG) in the developing
    thalamus as well as in the proliferative ventricular zone of the
    developing cerebellum. From P20 to adult, Frizzled10 mRNA is detected
    only in the internal capsule (ic). Our data show that expression of
    Frizzled10 is very strong during embryonic development of the CNS and
    suggest that Frizzled10 may play an essential role in spatial and
    temporal regulation during neural development. (C) 2008 Elsevier B.V.
    All rights reserved.
 C1 [Yan, Yan; Li, Yiping; Hu, Chuanyin; Gu, Xiaochun; Liu, Junhua; Hu, Yu-An; Yang, Yang; Wei, Yiquan; Zhao, Chunjie] Southeast Univ, Sch Med, MOE, Key Lab Dev Genes & Human Dis, Nanjing 210009, Jiangsu, Peoples R China.
    [Yan, Yan; Li, Yiping; Hu, Chuanyin; Gu, Xiaochun; Liu, Junhua; Hu, Yu-An; Yang, Yang; Wei, Yiquan; Zhao, Chunjie] Southeast Univ, Sch Med, Inst Brain Sci, Nanjing 210009, Jiangsu, Peoples R China.
    [Hu, Yu-An] Jinling Hosp, Inst Lab Med, Nanjing 210002, Peoples R China.
 RP Zhao, CJ, Southeast Univ, Sch Med, MOE, Key Lab Dev Genes & Human Dis,
    87 Dingjiaoqiao Rd, Nanjing 210009, Jiangsu, Peoples R China.
 EM zhaocj@seu.edu.cn
 FU National Nature Science Foundation of China [30770696, 30525017];
    Ministry of Education of China and National Basic Research Program of
    China (973 program) [106083]; Ministry of Science and Technology of
    China [2007CB512303]
 FX We thank Samuel J. Pleasure (UCSF) for Frizzled10 EST clone, Li Liu and
    Xiaoxuan Lu for technical assistance and other members of the
    laboratory for valuable discussions. This work was supported by funds
    30770696, 30525017 from National Nature Science Foundation of China,
    106083 from The Ministry of Education of China and National Basic
    Research Program of China (973 program) 2007CB512303 from The Ministry
    of Science and Technology of China to C.Z.
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 NR 16
 TC 0
 PU ELSEVIER SCIENCE BV
 PI AMSTERDAM
 PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
 SN 1567-133X
 J9 GENE EXPR PATTERNS
 JI Gene Expr. Patterns
 PD MAR
 PY 2009
 VL 9
 IS 3
 BP 173
 EP 177
 DI 10.1016/j.gep.2008.11.001
 PG 5
 SC Developmental Biology; Genetics & Heredity
 GA 412GW
 UT ISI:000263714100007
 ER
 
 PT J
 AU Chan, KW
    Yang, CH
    Lin, JW
    Wang, HC
    Lin, FY
    Kuo, ST
    Wong, ML
    Hsu, WL
 AF Chan, Kun-Wei
    Yang, Cheng-Hsiung
    Lin, Jen-Wei
    Wang, Hsien-Chi
    Lin, Fong-Yuan
    Kuo, Shu-Ting
    Wong, Min-Liang
    Hsu, Wei-Li
 TI Phylogenetic analysis of parapoxviruses and the C-terminal
    heterogeneity of viral ATPase proteins
 SO GENE
 LA English
 DT Article
 DE Parapoxviruses; Orf virus; A32L gene; B2L gene; E3L gene
 ID ORF-VIRUS; VACCINIA VIRUS; INTERFERON RESISTANCE; SEQUENCE ALIGNMENT;
    GENE; OUTBREAK; GOATS; IDENTIFICATION; INTEGRINS; HOMOLOG
 AB Two outbreaks of orf virus (a parapoxvirus) infection in goats found in
    Nantou and Taiping of central Taiwan were investigated. The nucleotide
    and the amino acid sequences of viral B2L, E3L and A32L genes in these
    two outbreaks were analyzed, and each of their phylogenetic trees were
    also constructed. In the A32L gene, an unexpected deletion of 24
    nucleotides was found in the Taiping strain. The A32L gene can encode
    an ATPase and is supposed to be involved in virion DNA packaging. The
    24 nucleotides correspond to 8 amino acids residues of the viral
    ATPase, which are located near the C-terminal region of the enzyme.
    Moreover, two copies of the RGD sequence at C-terminal region of ATPase
    were found in the Nantou strain. The 24 nucleotide difference in the
    A32L gene indicated that the Nantou strain and the Taiping strain were
    two separate strains, and it can be used in differential molecular
    diagnosis. Moreover, the C-terminal heterogeneity was found to be a
    general feature of the viral ATPase. Lastly, similar functional motifs
    of the ATPase and the Ras proto-oncoprotein (a GTPase) are discussed.
    (c) 2008 Elsevier B.V. All rights reserved.
 C1 [Chan, Kun-Wei; Lin, Jen-Wei; Wang, Hsien-Chi; Lin, Fong-Yuan; Wong, Min-Liang] Natl Chung Hsing Univ, Coll Vet Med, Dept Vet Med, Taichung 402, Taiwan.
    [Yang, Cheng-Hsiung] Livestock Dis Control Ctr Taichung Cty, Taichung, Taiwan.
    [Hsu, Wei-Li] Natl Chung Hsing Univ, Coll Vet Med, Grad Inst Vet, Taichung 402, Taiwan.
    [Kuo, Shu-Ting] Council Agr, Anim Hlth Res Inst, Tamsui 251, Taiwan.
 RP Wong, ML, Natl Chung Hsing Univ, Coll Vet Med, Dept Vet Med, Taichung
    402, Taiwan.
 EM mlwong@dragon.nchu.edu.tw
    wlhsu@dragon.nchu.edu.tw
 FU Bureau of Animal and Plant Health Inspection and Quarantine (BAPHIQ) ;
    Council of Agriculture, Taiwan 
 FX The authors thank Dr. Sarah M. Richart, Department of Biology and
    Chemistry, Azusa Pacific University, CA, USA for her critical reading
    and suggestion. This work was supported in part by a grant from The
    Bureau of Animal and Plant Health Inspection and Quarantine (BAPHIQ),
    Council of Agriculture, Taiwan.
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 NR 31
 TC 6
 PU ELSEVIER SCIENCE BV
 PI AMSTERDAM
 PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
 SN 0378-1119
 J9 GENE
 JI Gene
 PD MAR 1
 PY 2009
 VL 432
 IS 1-2
 BP 44
 EP 53
 DI 10.1016/j.gene.2008.10.029
 PG 10
 SC Genetics & Heredity
 GA 412GJ
 UT ISI:000263712400006
 ER
 
 PT J
 AU Cui, J
    Yang, H
    Lee, US
 AF Cui, J.
    Yang, H.
    Lee, U. S.
 TI Molecular mechanisms of BK channel activation
 SO CELLULAR AND MOLECULAR LIFE SCIENCES
 LA English
 DT Review
 DE Channel gating; MaxiK; calcium activation; voltage activation; metal
    binding; allosteric
 ID CA2+-ACTIVATED K+ CHANNELS; ADRENAL CHROMAFFIN CELLS; BLADDER
    SMOOTH-MUSCLE; DEPENDENT POTASSIUM CHANNELS; HIPPOCAMPAL PYRAMIDAL
    CELLS; PRESYNAPTIC ACTIVE ZONES; PLANAR LIPID BILAYERS; SACCULAR
    HAIR-CELLS; RAT SKELETAL-MUSCLE; LARGE-CONDUCTANCE
 AB Large conductance, Ca2+-activated potassium (BK) channels are widely
    expressed throughout the animal kingdom and play important roles in
    many physiological processes, such as muscle contraction, neural
    transmission and hearing. These physiological roles derive from the
    ability of BK channels to be synergistically activated by membrane
    voltage, intracellular Ca2+ and other ligands. Similar to voltage-gated
    K+ channels, BK channels possess a pore-gate domain (S5-S6
    transmembrane segments) and a voltage-sensor domain (S1-S4). In
    addition, BK channels contain a large cytoplasmic C-terminal domain
    that serves as the primary ligand sensor. The voltage sensor and the
    ligand sensor allosterically control K+ flux through the pore-gate
    domain in response to various stimuli, thereby linking cellular
    metabolism and membrane excitability. This review summarizes the
    current understanding of these structural domains and their mutual
    interactions in voltage-, Ca2+ - and Mg2+ -dependent activation of the
    channel.
 C1 [Cui, J.] Washington Univ, Dept Biomed Engn, St Louis, MO 63130 USA.
    Washington Univ, Cardiac Bioelect & Arrhythmia Ctr, St Louis, MO 63130 USA.
 RP Cui, J, Washington Univ, Dept Biomed Engn, 1 Brookings Dr, St Louis, MO
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 EM jcui@biomed.wustl.edu
 FU National Institutes of Health [R01-HL70393]
 FX We thank Chris Lingle (Washington University, St. Louis, MO) for
    critical discussions. This work was supported by National Institutes of
    Health grant R01-HL70393 (to J.C.) J.C. is an associate professor of
    biomedical engineering on the Spencer T. Olin Endowment.
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 NR 234
 TC 37
 PU BIRKHAUSER VERLAG AG
 PI BASEL
 PA VIADUKSTRASSE 40-44, PO BOX 133, CH-4010 BASEL, SWITZERLAND
 SN 1420-682X
 J9 CELL MOL LIFE SCI
 JI Cell. Mol. Life Sci.
 PD MAR
 PY 2009
 VL 66
 IS 5
 BP 852
 EP 875
 DI 10.1007/s00018-008-8609-x
 PG 24
 SC Biochemistry & Molecular Biology; Cell Biology
 GA 413XP
 UT ISI:000263826400009
 ER
 
 PT J
 AU Chang, B
    Liu, GZ
    Yang, G
    Mercado-Uribe, I
    Huang, M
    Liu, JS
 AF Chang, Bin
    Liu, Guangzhi
    Yang, Gong
    Mercado-Uribe, Imelda
    Huang, Miao
    Liu, Jinsong
 TI REDD1 is required for RAS-mediated transformation of human ovarian
    epithelial cells
 SO CELL CYCLE
 LA English
 DT Article
 DE REDD1; RAS; ovarian cancer; transformation; anti-apoptosis
 ID GENE-EXPRESSION; HYPOXIA; TUMORS; IDENTIFICATION; MUTATIONS; RTP801;
    PROTOONCOGENE; SUPPRESSION; STRESS; CANCER
 AB REDD1 is a gene induced by hypoxia and stimuli from multiple DNA
    damage. Here we show that REDD1 expression was elevated in
    RAS-transformed ovarian epithelial cells lines and that this
    overexpression increased these cells' growth rate and
    anchorage-independent growth on soft agar. Injection of immortalized
    ovarian epithelial cells overexpressing REDD1 into nude mice resulted
    in tumor growth that developed into papillary serous carcinoma in the
    peritoneal cavity. Knockdown of REDD1 expression blocked the
    RAS-mediated transformation of these cell lines. REDD1 overexpression
    decreased apoptosis and associated with increased expression of Bcl-xL
    or Bcl-2 and decreased expression of FADD, caspase1, caspase8, caspase
    9, caspase 10, BAX, Bad and Bcl-XS. Our data demonstrated that REDD1 is
    a key mediator in RAS-mediated transformation through an effect on
    anti-apoptosis.
 C1 [Liu, Jinsong] Univ Texas MD Anderson Canc Ctr, Dept Pathol, Unit 85, Houston, TX 77030 USA.
    [Chang, Bin] Huazhong Univ Sci & Technol, Tongji Med Coll, Tongji Hosp, Dept Oncol, Wuhan, Hubei, Peoples R China.
    [Chang, Bin] Shihezi Univ, Sch Med, Dept Pathol, Shihezi, Xinjiang, Peoples R China.
 RP Liu, JS, Univ Texas MD Anderson Canc Ctr, Dept Pathol, Unit 85, 1515
    Holcombe Blvd, Houston, TX 77030 USA.
 EM jliu@mdanderson.org
 FU American Cancer Society [RSG-04-0281-CCE]; National Institutes of
    Health/National Cancer Institute (NIH/NCI) [R01 CA131183-01]
 FX J.L. is supported by a Research Scholar Grant (RSG-04-0281-CCE) from
    the American Cancer Society R01 CA131183-01 from the National
    Institutes of Health/National Cancer Institute (NIH/NCI) and an
    institutional research grant.
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 NR 24
 TC 5
 PU LANDES BIOSCIENCE
 PI AUSTIN
 PA 1002 WEST AVENUE, 2ND FLOOR, AUSTIN, TX 78701 USA
 SN 1538-4101
 J9 CELL CYCLE
 JI Cell Cycle
 PD MAR 1
 PY 2009
 VL 8
 IS 5
 BP 780
 EP 786
 PG 7
 SC Cell Biology
 GA 412KJ
 UT ISI:000263723400022
 ER
 
 PT J
 AU Fujita, N
    Miyachi, H
    Tanaka, H
    Takeo, M
    Nakagawa, N
    Kobayashi, Y
    Iwasa, M
    Watanabe, S
    Takei, Y
 AF Fujita, Naoki
    Miyachi, Hirohide
    Tanaka, Hideaki
    Takeo, Masaki
    Nakagawa, Naoki
    Kobayashi, Yoshinao
    Iwasa, Motoh
    Watanabe, Shozo
    Takei, Yoshiyuki
 TI Iron Overload Is Associated with Hepatic Oxidative Damage to DNA in
    Nonalcoholic Steatohepatitis
 SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION
 LA English
 DT Article
 ID FATTY LIVER-DISEASE; INSULIN-RESISTANCE; HEPATOCELLULAR-CARCINOMA;
    GENETIC HEMOCHROMATOSIS; TRANSFERRIN RECEPTORS; STRESS;
    HYPERFERRITINEMIA; REDISTRIBUTION; PHLEBOTOMY; DEPLETION
 AB Several lines of evidence have suggested that oxidative stress plays an
    important role for the pathogenesis of nonalcoholic steatohepatitis
    (NASH). Therefore, by using immunohistochemical staining of liver
    biopsy samples, we measured hepatic 7,8-dihydro-8-oxo-2' deoxyguanosine
    (8-oxodG), a DNA base-modified product generated by hydroxyl radicals,
    of 38 NASH patients and compared with 24 simple steatosis and 10
    healthy subjects. Relation of hepatic 8-oxodG with clinical,
    biochemical, and histologic variables and changes after iron reduction
    therapy (phlebotomy plus iron-restricted diet) were also examined.
    Hepatic 8-oxodG levels were significantly higher in NASH compared with
    simple steatosis (17.5 versus 2.0 8-oxodG -positive cells/10(5) mu
    m(2); P < 0.0001). 8-oxodG was significantly related to iron overload
    condition, glucose-insulin metabolic abnormality, and severities of
    hepatic steatosis in NASH patients. Logistic regression analysis also
    showed that hepatic iron deposit and insulin resistance were
    independent variables associated with elevated hepatic 8-oxodG. After
    the iron reduction therapy, hepatic 8-oxodG levels were significantly
    decreased (from 20.7 to 13.8 positive cells/10(5) mu m(2); P < 0.01)
    with concomitant reductions of serum transaminase levels in NASH
    patients. In conclusion, iron overload may play an important role in
    the pathogenesis of NASH by generating oxidative DNA damage and iron
    reduction therapy may reduce hepatocellular carcinoma incidence in
    patients with NASH. (Cancer Epidemiol Biomarkers Prev 2009;18(2):424-32)
 C1 [Fujita, Naoki; Miyachi, Hirohide; Tanaka, Hideaki; Takeo, Masaki; Nakagawa, Naoki; Kobayashi, Yoshinao; Iwasa, Motoh; Takei, Yoshiyuki] Mie Univ, Dept Gastroenterol & Hepatol, Grad Sch Med, Div Clin Med & Biomed Sci,Inst Med Sci, Tsu, Mie 5148507, Japan.
    [Watanabe, Shozo] Mie Univ, Ctr Phys & Mental Hlth, Tsu, Mie 5148507, Japan.
 RP Fujita, N, Mie Univ, Dept Gastroenterol & Hepatol, Grad Sch Med, Div
    Clin Med & Biomed Sci,Inst Med Sci, 2-174 Edobashi, Tsu, Mie 5148507,
    Japan.
 EM nfujita@clin.medic.mie-u.ac.jp
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 NR 39
 TC 11
 PU AMER ASSOC CANCER RESEARCH
 PI PHILADELPHIA
 PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
 SN 1055-9965
 J9 CANCER EPIDEM BIOMARKER PREV
 JI Cancer Epidemiol. Biomarkers Prev.
 PD FEB
 PY 2009
 VL 18
 IS 2
 BP 424
 EP 432
 DI 10.1158/1055-9965.EPI-08-0725
 PG 9
 SC Oncology; Public, Environmental & Occupational Health
 GA 410AS
 UT ISI:000263547800009
 ER
 
 PT J
 AU Yokoyama, A
    Kumagai, Y
    Yokoyama, T
    Omori, T
    Kato, H
    Igaki, H
    Tsujinaka, T
    Muto, M
    Yokoyama, M
    Watanabe, H
 AF Yokoyama, Akira
    Kumagai, Yoshiya
    Yokoyama, Tetsuji
    Omori, Tai
    Kato, Hoichi
    Igaki, Hiroyasu
    Tsujinaka, Toshimasa
    Muto, Manabu
    Yokoyama, Masako
    Watanabe, Hiroshi
 TI Health Risk Appraisal Models for Mass Screening for Esophageal and
    Pharyngeal Cancer: An Endoscopic Follow-up Study of Cancer-Free
    Japanese Men
 SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION
 LA English
 DT Article
 ID SQUAMOUS-CELL CARCINOMA; UPPER AERODIGESTIVE TRACT; ALDEHYDE
    DEHYDROGENASES; GENETIC POLYMORPHISMS; ALCOHOL; CONSUMPTION; GENOTYPES;
    DRINKING; SMOKING; DIET
 AB Purpose: To assess the performance of our health risk appraisal (HRA)
    models for screening individuals at high risk of esophageal/pharyngeal
    squamous cell carcinoma (EPSCC).
    Methods: Based on the results of our previous case-control study, we
    invented HRA models that enable screening for EPSCC cases in Japanese
    men with high sensitivity and specificity based on either their
    aldehyde dehydrogenase-2 genotype (HRA-G model) or alcohol flushing
    (HRA-F model) and drinking, smoking, and dietary habits. Follow-up
    endoscopy combined with esophageal iodine staining (median follow-up
    period: 5.0 years) was done on 404 Japanese men (50-78 years) who were
    registered as cancer-free controls in the previous study.
    Results: The follow-up endoscopy resulted in a diagnosis of 6
    esophageal SCC (T-is in 5 and T-1 in 1), 1 hypopharyngeal SCC (TO, and
    1 oropharyngeal SCC (T-2). Seven and 6 of the 8 EPSCC cases were in the
    top 10% risk group at baseline according to the HRA-G and HRA-F models,
    respectively. The EPSCC detection rates per 100 person-years in the top
    10% risk groups by the HRA-G and HRA-F models were 4.38 (95% confidence
    interval, 1.76-9.01) and 3.48 (95% confidence interval, 1.28-7.58),
    respectively. Their age-adjusted relative risk was 95.1- and 26.3-fold,
    respectively (P < 0.0001), higher than in the bottom 90% risk groups.
    Conclusions: The high detection rates for EPSCC in the top 10% risk
    group of this preliminary follow-up study were in good agreement with
    those predicted by the HRA models and thus encouraged the screening
    based on our HRA models in larger populations of Japanese men. (Cancer
    Epidemiol Biomarkers Prev 2009;18(2):651-5)
 C1 [Yokoyama, Akira] Kurihama Alcoholism Ctr, Natl Hosp Org, Kanagawa 2390841, Japan.
    [Kumagai, Yoshiya] Kumagai Satellite Clin, Tokyo, Japan.
    [Yokoyama, Masako] Mitsukoshi Hlth & Welf Fdn, Tokyo, Japan.
    [Watanabe, Hiroshi] Keio Univ, Sch Med, Dept Surg, Shinjuku Ku, Tokyo 160, Japan.
    [Yokoyama, Tetsuji] Natl Inst Publ Hlth, Dept Human Resources Dev, Wako, Saitama 3510197, Japan.
    [Omori, Tai] Kawasaki Municipal Hosp, Dept Gastroenterol, Kawasaki, Kanagawa, Japan.
    [Omori, Tai] Kawasaki Municipal Hosp, Dept Surg, Kawasaki, Kanagawa, Japan.
    [Kato, Hoichi] Natl Canc Ctr, Ctr Canc Control & Informat Serv, Tokyo 104, Japan.
    [Kato, Hoichi; Igaki, Hiroyasu] Natl Canc Ctr, Div Surg, Chuo Ku, Tokyo, Japan.
    [Tsujinaka, Toshimasa] Natl Hosp Org Osaka Natl Hosp, Dept Surg, Osaka, Japan.
    [Muto, Manabu] Kyoto Univ, Sch Med, Dept Gastroenterol & Hepatol, Kyoto 606, Japan.
 RP Yokoyama, A, Kurihama Alcoholism Ctr, Natl Hosp Org, 5-3-1 Nobi,
    Kanagawa 2390841, Japan.
 EM a_yokoyama@kurihama1.hosp.go.jp
 FU Ministry of Health, Labour and Welfare of Japan [12-12, 16-11]
 FX Grant support: Ministry of Health, Labour and Welfare of Japan
    Grants-in-Aid for Cancer Research 12-12 and 16-11.
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 NR 23
 TC 3
 PU AMER ASSOC CANCER RESEARCH
 PI PHILADELPHIA
 PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
 SN 1055-9965
 J9 CANCER EPIDEM BIOMARKER PREV
 JI Cancer Epidemiol. Biomarkers Prev.
 PD FEB
 PY 2009
 VL 18
 IS 2
 BP 651
 EP 655
 DI 10.1158/1055-9965.EPI-08-0758
 PG 5
 SC Oncology; Public, Environmental & Occupational Health
 GA 410AS
 UT ISI:000263547800038
 ER
 
 PT J
 AU Yang, H
    Kadia, T
    Xiao, LC
    Bueso-Ramos, CE
    Hoshino, K
    Thomas, DA
    O'Brien, S
    Jabbour, E
    Pierce, S
    Rosner, GL
    Kantarjian, HM
    Garcia-Manero, G
 AF Yang, Hui
    Kadia, Tapan
    Xiao, Lianchun
    Bueso-Ramos, Carlos E.
    Hoshino, Koyu
    Thomas, Deborah Ann
    O'Brien, Susan
    Jabbour, Elias
    Pierce, Sherry
    Rosner, Gary L.
    Kantarjian, Hagop M.
    Garcia-Manero, Guillermo
 TI Residual DNA methylation at remission is prognostic in adult
    Philadelphia chromosome-negative acute lymphocytic leukemia
 SO BLOOD
 LA English
 DT Article
 ID ACUTE LYMPHOBLASTIC-LEUKEMIA; CYCLE REGULATORY PATHWAY; HYPER-CVAD;
    GENES; THERAPY; P57KIP2; REGIMEN; RELAPSE; DISEASE; CANCER
 AB Pretreatment aberrant DNA methylation patterns are stable at time of
    relapse in acute lymphocytic leukemia (ALL). We hypothesized that the
    detection of residual methylation alterations at the time of
    morphologic remission may predict for worse prognosis. We developed a
    real-time bisulfite polymerase chain reaction assay and analyzed the
    methylation levels of p73, p15, and p57(KIP2) at the time of initial
    remission in 199 patients with Philadelphia chromosome-negative and
    MLL- ALL. Residual p73 methylation was detected in 18 (9.5%) patients,
    p15 in 33 (17.4%), and p57KIP2 in 7 (3.7%); 140 (74%) patients had
    methylation of 0 genes and 48 (25%) of more than or equal to 1 gene. In
    123 (65%) patients, matched pretreatment samples were also studied and
    compared with remission ones: in 82 of those with initial aberrant
    methylation of at least one gene, 59 (72%) had no detectable
    methylation at remission and 23 (28%) had detectable residual
    methylation. By multivariate analysis, the presence of residual p73
    methylation was associated with a significant shorter duration of first
    complete remission (hazard ratio = 2.68, P = .003) and overall survival
    (hazard ratio = 2.69, P = .002). In conclusion, detection of epigenetic
    alterations allows the identification of patients with ALL with
    standard risk but with poor prognosis. (Blood. 2009; 113: 1892-1898)
 C1 [Yang, Hui; Kadia, Tapan; Hoshino, Koyu; Thomas, Deborah Ann; O'Brien, Susan; Jabbour, Elias; Pierce, Sherry; Kantarjian, Hagop M.; Garcia-Manero, Guillermo] Univ Texas MD Anderson Canc Ctr, Dept Leukemia, Houston, TX 77030 USA.
    [Xiao, Lianchun; Rosner, Gary L.] Univ Texas MD Anderson Canc Ctr, Dept Biostat, Houston, TX 77030 USA.
    [Bueso-Ramos, Carlos E.] Univ Texas MD Anderson Canc Ctr, Dept Hematopathol, Houston, TX 77030 USA.
 RP Garcia-Manero, G, Univ Texas MD Anderson Canc Ctr, Dept Leukemia, Box
    428,1515 Holcombe Blvd, Houston, TX 77030 USA.
 EM ggarciam@mdanderson.org
 FU National Cancer Institute [CA100067, CA105771]; Commonwealth Foundation 
 FX This work was supported by the National Cancer Institute (grants
    CA100067 and CA105771) and by the University of Texas
    Physician-Scientist Program funded by the Commonwealth Foundation for
    Cancer Research at the University of Texas M. D. Anderson Cancer Center
    and the Leukemia & Lymphoma Society of America (G.G.-M.).
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 NR 21
 TC 2
 PU AMER SOC HEMATOLOGY
 PI WASHINGTON
 PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
 SN 0006-4971
 J9 BLOOD
 JI Blood
 PD FEB 26
 PY 2009
 VL 113
 IS 9
 BP 1892
 EP 1898
 DI 10.1182/blood-2008-02-141002
 PG 7
 SC Hematology
 GA 412KM
 UT ISI:000263723700005
 ER
 
 PT J
 AU Li, ZX
    Beutel, G
    Rhein, M
    Meyer, J
    Koenecke, C
    Neumann, T
    Yang, M
    Krauter, J
    von Neuhoff, N
    Heuser, M
    Diedrich, H
    Gohring, G
    Wilkens, L
    Schlegelberger, B
    Ganser, A
    Baum, C
 AF Li, Zhixiong
    Beutel, Gernot
    Rhein, Mathias
    Meyer, Johann
    Koenecke, Christian
    Neumann, Thomas
    Yang, Min
    Krauter, Juergen
    von Neuhoff, Nils
    Heuser, Michael
    Diedrich, Helmut
    Goehring, Gudrun
    Wilkens, Ludwig
    Schlegelberger, Brigitte
    Ganser, Arnold
    Baum, Christopher
 TI High-affinity neurotrophin receptors and ligands promote leukemogenesis
 SO BLOOD
 LA English
 DT Article
 ID ACUTE MYELOID-LEUKEMIA; NERVE GROWTH-FACTOR; ACUTE
    LYMPHOBLASTIC-LEUKEMIA; ACUTE MYELOGENOUS LEUKEMIA; TYROSINE KINASES;
    TRANSCRIPTION FACTORS; CELL SURVIVAL; EXPRESSION; TRK; FLT3
 AB Neurotrophins (NTs) and their receptors play a key role in neurogenesis
    and survival. The TRK (tropomyosin-related kinase) receptor protein
    tyrosine kinases (TRKA, TRKB, TRKC) are high-affinity NT receptors that
    are expressed in a variety of human tissues. Their role in normal and
    malignant hematopoiesis is poorly understood. In a prospective study
    involving 94 adult patients we demonstrate for the first time
    cell-surface expression of the 3 TRKs and constitutive activation in
    blasts from patients with de novo or secondary acute leukemia. At least
    one TRK was expressed in 55% of the analyzed cases. We establish a
    clear correlation between the TRK expression pattern and FAB
    classification. Although only few point mutations were found in TRK
    sequences by reverse-transcriptase polymerase chain reaction (RT-PCR),
    we observed coexpression of BDNF (ligand for TRKB) in more than 50% of
    TRKB+ cases (16/30). Activation of TRKA or TRKB by NGF and BDNF,
    respectively, efficiently rescued murine myeloid cells from
    irradiation-induced apoptosis. Coexpression of TRKB/BDNF or TRKA/NGF in
    murine hematopoietic cells induced leukemia. Moreover, activation of
    TRKs was important for survival of both human and murine leukemic
    cells. Our findings suggest that TRKs play an important role in
    leukemogenesis and may serve as a new drug target. (Blood. 2009; 113:
    2028-2037)
 C1 [Li, Zhixiong; Rhein, Mathias; Meyer, Johann; Neumann, Thomas; Yang, Min; Baum, Christopher] Hannover Med Sch, Dept Expt Hematol, D-30625 Hannover, Germany.
    [Beutel, Gernot; Koenecke, Christian; Krauter, Juergen; Heuser, Michael; Diedrich, Helmut; Ganser, Arnold] Hannover Med Sch, Dept Hematol, D-30625 Hannover, Germany.
    [Beutel, Gernot; Koenecke, Christian; Krauter, Juergen; Heuser, Michael; Diedrich, Helmut; Ganser, Arnold] Hannover Med Sch, Dept Hemostasis, D-30625 Hannover, Germany.
    [Beutel, Gernot; Koenecke, Christian; Krauter, Juergen; Heuser, Michael; Diedrich, Helmut; Ganser, Arnold] Hannover Med Sch, Dept Oncol, D-30625 Hannover, Germany.
    [Beutel, Gernot; Koenecke, Christian; Krauter, Juergen; Heuser, Michael; Diedrich, Helmut; Ganser, Arnold] Hannover Med Sch, Dept Stem Cell Transplantat, D-30625 Hannover, Germany.
    [von Neuhoff, Nils; Goehring, Gudrun; Wilkens, Ludwig; Schlegelberger, Brigitte] Hannover Med Sch, Inst Cell & Mol Pathol, D-30625 Hannover, Germany.
    [Baum, Christopher] Cincinnati Childrens Hosp, Med Ctr, Div Expt Hematol, Cincinnati, OH 45229 USA.
 RP Li, ZX, Hannover Med Sch, Dept Expt Hematol, OE6960,Carl Neuberg Str 1,
    D-30625 Hannover, Germany.
 EM li.zhixiong@mh-hannover.de
    baum.christopher@mh-hannover.de
 FU Deutsche Krebshilfe (Bonn, Germany) [10-2090-Li I]; Deutsche
    Forschungsgemeinschaft (DFG, Bonn, Germany) [KO 3582/1-1]; National
    Cancer Institute [R01-CA107492-01A2]; Deutsche Jose Carreras
    Leukamie-Stiftung (Munchen, Germany) [DJCLS F05/10]
 FX We are very grateful to Stefan Bartels and Ludwig Hoy for help with
    statistical analysis; Axel Schambach for providing vector backbones;
    Michael Morgan for providing reagents and critical reading of this
    paper; Peter Horn and Martin Sauer for providing cells; Vanessa Prox,
    Christine Garen, Rene Kirstein, Ellen Neumann, Elke Sturmer, Elvira
    Lux, and Cindy Elfers for technical assistance; and Rolf Baumann, Hans
    Grundtke, Jorg Fruhauf, Anne Koop, and Bernd Polivka (all MHH) for
    irradiation of animals and cells. We also thank Dr D. Martin-Zanca for
    providing cDNA of TPM3/TRK.
    This study was supported by the Deutsche Krebshilfe (Bonn, Germany;
    grant: 10-2090-Li I) and by the Deutsche Forschungsgemeinschaft (DFG,
    Bonn, Germany; excellence cluster REBIRTH). C. B. was also supported by
    the National Cancer Institute (R01-CA107492-01A2). M. R. is a student
    of the MD/PhD program at Hannover Medical School (MHH), and received
    support from the Deutsche Jose Carreras Leukamie-Stiftung (Munchen,
    Germany; grant: DJCLS F05/10). C. K. was supported by DFG (KO 3582/1-1).
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 NR 60
 TC 9
 PU AMER SOC HEMATOLOGY
 PI WASHINGTON
 PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
 SN 0006-4971
 J9 BLOOD
 JI Blood
 PD FEB 26
 PY 2009
 VL 113
 IS 9
 BP 2028
 EP 2037
 DI 10.1182/blood-2008-05-155200
 PG 10
 SC Hematology
 GA 412KM
 UT ISI:000263723700021
 ER
 
 PT J
 AU Kessler, JD
    Hasegawa, H
    Brun, SN
    Emmenegger, BA
    Yang, ZJ
    Dutton, JW
    Wang, F
    Wechsler-Reya, RJ
 AF Kessler, Jessica D.
    Hasegawa, Hiroshi
    Brun, Sonja N.
    Emmenegger, Brian A.
    Yang, Zeng-Jie
    Dutton, John W.
    Wang, Fan
    Wechsler-Reya, Robert J.
 TI N-myc alters the fate of preneoplastic cells in a mouse model of
    medulloblastoma (vol 23, pg 157, 2009)
 SO GENES & DEVELOPMENT
 LA English
 DT Correction
 C1 [Kessler, Jessica D.; Brun, Sonja N.; Emmenegger, Brian A.; Yang, Zeng-Jie; Dutton, John W.; Wechsler-Reya, Robert J.] Duke Univ, Med Ctr, Dept Pharmacol & Canc Biol, Durham, NC 27710 USA.
    [Hasegawa, Hiroshi; Wang, Fan] Duke Univ, Med Ctr, Dept Cell Biol, Durham, NC 27710 USA.
 RP Kessler, JD, Duke Univ, Med Ctr, Dept Pharmacol & Canc Biol, Durham, NC
    27710 USA.
 CR KESSLER JD, 2009, GENE DEV, V23, P157, DOI 10.1101/gad.1759909
 NR 1
 TC 0
 PU COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT
 PI WOODBURY
 PA 500 SUNNYSIDE BLVD, WOODBURY, NY 11797-2924 USA
 SN 0890-9369
 J9 GENE DEVELOP
 JI Genes Dev.
 PD FEB 15
 PY 2009
 VL 23
 IS 4
 BP 535
 EP 535
 PG 1
 SC Cell Biology; Developmental Biology; Genetics & Heredity
 GA 410TH
 UT ISI:000263600700013
 ER
 
 PT J
 AU Lau, KK
    Yang, Y
    Cook, GA
    Wyatt, RJ
    Nishimura, H
 AF Lau, Keith K.
    Yang, Yimu
    Cook, George A.
    Wyatt, Robert J.
    Nishimura, Hiroko
 TI Control of aquaporin 2 expression in collecting ducts of quail kidneys
 SO GENERAL AND COMPARATIVE ENDOCRINOLOGY
 LA English
 DT Article
 DE Avian aquaporin; AQP2; Water channel; Urine concentration; Medullary
    collecting duct; Coturnix quail; ADH
 ID IN-SITU HYBRIDIZATION; WATER-CHANNEL; ARGININE VASOTOCIN;
    FUNCTIONAL-CHARACTERIZATION; GENE-EXPRESSION; JAPANESE-QUAIL; AVIAN
    KIDNEY; RAT-KIDNEY; VASOPRESSIN; RECEPTOR
 AB Birds and mammals are the only vertebrates that can concentrate urine.
    Avian kidneys contain structurally primitive loopless nephrons and also
    more advanced looped nephrons, in the cortical and medullary regions,
    respectively. We have identified the gene sequence of an aquaporin 2
    (AQP2)-homologue water channel in collecting ducts of kidneys from
    adult quail, Coturnix japonica. Although immunoreactive quail AQP2
    (qAQP2) was found in both types of nephrons, the expression is enhanced
    more clearly in the medullary regions after water deprivation. We
    therefore hypothesized that regulation of qAQP2 expression in quail
    kidneys via antidiuretic hormone (ADH) may require more advanced
    nephron structure. In this study, we determined the expression of qAQP2
    mRNA in tissues isolated from the cortical and medullary regions before
    and after water deprivation, by conventional reverse
    transcriptase-polymerase chain reaction (RT-PCR) and quantitative
    real-time PCR. In both normally hydrated and water-deprived groups,
    qAQP2 mRNA levels in the medullary regions were significantly higher (P
    < 0.01) than in the cortical regions. In medullary areas, qAQP2 mRNA
    levels (real-time PCR normalized with 18S) were significantly higher (P
    < 0.01, ANOVA) after water deprivation (1.09 +/- 0.10) than in normally
    hydrated controls (0.46 +/- 0.08). In cortical areas, qAQP2 mRNA levels
    were also higher after water deprivation (0.37 +/- 0.05) than in
    controls (0.11 +/- 0.02). qAQP2 mRNA signals determined by in situ
    hybridization of digoxigenin-labeled riboprobe were also enhanced after
    water deprivation in both cortical and medullary collecting ducts. The
    results suggest that, contrary to our hypothesis, the endogenous
    production of ADH by water deprivation stimulates qAQP2 mRNA in both
    loopless and looped nephrons. (C) 2008 Elsevier Inc. All rights
    reserved.
 C1 [Lau, Keith K.; Yang, Yimu; Nishimura, Hiroko] Univ Tennessee, Hlth Sci Ctr, Coll Med, Dept Physiol, Memphis, TN 38163 USA.
    [Cook, George A.] Univ Tennessee, Hlth Sci Ctr, Dept Pharmacol, Memphis, TN 38163 USA.
    [Lau, Keith K.; Wyatt, Robert J.] Univ Tennessee, Hlth Sci Ctr, Dept Pediat, Memphis, TN 38103 USA.
 RP Nishimura, H, Univ Tennessee, Hlth Sci Ctr, Coll Med, Dept Physiol, 894
    Union Ave, Memphis, TN 38163 USA.
 EM nishimur@physio1.utmem.edu
 FU NSF [IBN-9986633]; NIH [HL52881]; NKF [MG61943]; Le Bonheur Small Grant
    ; Accredo Health Care Foundation 
 FX The authors are grateful for support by NSF Grant IBN-9986633 (PI:
    Hiroko Nishimura), NIH Grant HL52881 (PI: Hiroko Nishimura), NKF Grant
    MG61943 (PI: Keith Lau), Le Bonheur Small Grant (PI: Keith Lau), and a
    generous grant from the Accredo Health Care Foundation (PI: Keith Lau).
    We also thank Ms. Guibin Su for her excellent technical assistance
    throughout the experiments. Rabbit anti-rat AQP2 was a generous gift
    from Dr. Sei Sasaki, Tokyo Medical and Dental University, Tokyo, Japan.
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 NR 37
 TC 3
 PU ACADEMIC PRESS INC ELSEVIER SCIENCE
 PI SAN DIEGO
 PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
 SN 0016-6480
 J9 GEN COMP ENDOCRINOL
 JI Gen. Comp. Endocrinol.
 PD FEB
 PY 2009
 VL 160
 IS 3
 BP 288
 EP 294
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 PG 7
 SC Endocrinology & Metabolism
 GA 410JO
 UT ISI:000263573500009
 ER
 
 PT J
 AU Nagayama, S
    Yamada, E
    Kohno, Y
    Aoyama, T
    Fukukawa, C
    Kubo, H
    Watanabe, G
    Katagiri, T
    Nakamura, Y
    Sakai, Y
    Toguchida, J
 AF Nagayama, Satoshi
    Yamada, Eiji
    Kohno, Yoshiki
    Aoyama, Tomoki
    Fukukawa, Chikako
    Kubo, Hajime
    Watanabe, Go
    Katagiri, Toyomasa
    Nakamura, Yusuke
    Sakai, Yoshiharu
    Toguchida, Junya
 TI Inverse correlation of the up-regulation of FZD10 expression and the
    activation of beta-catenin in synchronous colorectal tumors
 SO CANCER SCIENCE
 LA English
 DT Article
 ID SIGNALING PATHWAY; SYNOVIAL SARCOMAS; RETINOIC ACID; COLON-CANCER; NT2
    CELLS; WNT; FRIZZLED-10; INHIBITION
 AB We investigated the immunohistochemical expression patterns of Frizzled
    homolog 10 (FZD10), a cell-surface receptor for molecules in the Wnt
    pathway, in tissue samples derived from 104 patients with colorectal
    cancers (CRCs). There was no immunoreactivity for FZD10 in normal
    colonic mucosa, and only tumor cells in polyps and CRC tissues showed
    spotted immunostaining patterns in apical sides of the cytoplasm. In
    metastatic liver lesions, tumor cells showed cytoplasmic immunostaining
    similar to primary lesions, whereas normal liver parenchyma showed
    almost no immunostaining. Frequencies of FZD10-immunopositive cells in
    tumor tissues were significantly higher in CRCs than those in polyps
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    with those in metastatic liver lesions (33.2 +/- 39.7% vs 26.4 +/-
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    and metastatic liver lesions from the same patient) suggested that a
    subset of CRCs possessed intrinsic genetic mechanisms causing the
    evolution of FZD10-positive clones during tumor progression, making
    FZD10 a promising candidate for molecular imaging and a target for
    therapy. To our surprise, cancer cells immunopositive for FZD10 showed
    significantly less nuclear accumulation of beta-catenin, compared to
    FZD10-immunonegative cancer cells, and there was a strong inverse
    correlation between nuclear immunostaining scores for beta-catenin
    expression and expression patterns of FZD10 (P = 0.0002), suggesting
    that FZD10 has a distinct role from other FZDs in canonical Wnt signal
    transduction. (Cancer Sci 2009; 100: 405-412).
 C1 [Nagayama, Satoshi; Yamada, Eiji; Kubo, Hajime; Watanabe, Go; Sakai, Yoshiharu] Kyoto Univ, Grad Sch Med, Dept Surg, Kyoto 6068507, Japan.
    [Yamada, Eiji; Kohno, Yoshiki; Aoyama, Tomoki; Toguchida, Junya] Kyoto Univ, Inst Frontier Med Sci, Dept Tissue Regenerat, Kyoto 6068507, Japan.
    [Kohno, Yoshiki] Kyoto Univ, Grad Sch Med, Dept Orthopaed Surg, Kyoto 6068507, Japan.
    [Fukukawa, Chikako; Katagiri, Toyomasa; Nakamura, Yusuke] Univ Tokyo, Inst Med Sci, Ctr Human Genome, Mol Med Lab, Tokyo 1088639, Japan.
    [Toguchida, Junya] Kyoto Univ, Ctr iPS Res & Applicat, ICeMS, Kyoto 6068507, Japan.
 RP Nagayama, S, Kyoto Univ, Grad Sch Med, Dept Surg, Kyoto 6068507, Japan.
 EM nagayama@kuhp.kyoto-u.ac.jp
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 NR 21
 TC 4
 PU WILEY-BLACKWELL PUBLISHING, INC
 PI MALDEN
 PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
 SN 1347-9032
 J9 CANCER SCI
 JI Cancer Sci.
 PD MAR
 PY 2009
 VL 100
 IS 3
 BP 405
 EP 412
 DI 10.1111/j.1349-7006.2008.01052.x
 PG 8
 SC Oncology
 GA 408QR
 UT ISI:000263450200007
 ER
 
 PT J
 AU Shimizu, Y
    Takamori, A
    Utsunomiya, A
    Kurimura, M
    Yamano, Y
    Hishizawa, M
    Hasegawa, A
    Kondo, F
    Kurihara, K
    Harashima, N
    Watanabe, T
    Okamura, J
    Masuda, T
    Kannagi, M
 AF Shimizu, Yukiko
    Takamori, Ayako
    Utsunomiya, Atae
    Kurimura, Mayumi
    Yamano, Yoshihisa
    Hishizawa, Masakatsu
    Hasegawa, Atsuhiko
    Kondo, Fumiaki
    Kurihara, Kiyoshi
    Harashima, Nanae
    Watanabe, Toshiki
    Okamura, Jun
    Masuda, Takao
    Kannagi, Mari
 TI Impaired Tax-specific T-cell responses with insufficient control of
    HTLV-1 in a subgroup of individuals at asymptomatic and smoldering
    stages
 SO CANCER SCIENCE
 LA English
 DT Article
 ID VIRUS TYPE-I; TROPICAL SPASTIC PARAPARESIS; PERIPHERAL-BLOOD
    LYMPHOCYTES; LEUKEMIA-LYMPHOMA; PROVIRAL DNA; IMMUNE-RESPONSE;
    CARRIERS; LEUKEMIA/LYMPHOMA; EXPRESSION; LOAD
 AB Human T-cell leukemia virus type-1 (HTLV-1)-specific T-cell immunity, a
    potential antitumor surveillance system in vivo, is impaired in adult
    T-cell leukemia (ATL). In this study, we aimed to clarify whether the
    T-cell insufficiency in ATL is present before the disease onset or
    occurs as a consequence of the disease. We investigated T-cell
    responses against Tax protein in peripheral blood mononuclear cells
    (PBMCs) from individuals at earlier stages of HTLV-1-infection,
    including 21 asymptomatic HTLV-1 carriers (ACs) and four patients with
    smoldering-type ATL (sATL), whose peripheral lymphocyte count was in
    normal range. About 30% of samples tested showed clear Tax-specific
    interferon (IFN)-gamma producing responses. Proviral loads in this
    group were significantly lower than those in the other less-specific
    response group. The latter group was further divided to two subgroups
    with or without emergence of Tax-specific responses following depletion
    of CC chemokine receptor 4 (CCR4)(+) cells that contained
    HTLV-1-infected cells. In the PBMCs with Tax-specific responses, CD8(+)
    cells efficiently suppressed HTLV-1 p19 production in culture. The
    remaining group without the emergence of Tax-specific response after
    CCR4(+) cell-depletion included at least two sATL and one AC samples,
    which spontaneously produced HTLV-1 p19 in culture, where
    tetramer-binding, Tax-specific cytotoxic T-lymphocytes were either
    undetectable or unresponsive. Our results indicated that
    HTLV-1-specific T-cell responsiveness widely differed among HTLV-1
    carriers, and that impairment of HTLV-1-specific T-cell responses was
    observed not only in advanced ATL patients but also in a subpopulation
    at earlier stages, which was associated with insufficient control of
    HTLV-1. (Cancer Sci 2009; 100: 481-489).
 C1 [Shimizu, Yukiko; Takamori, Ayako; Hasegawa, Atsuhiko; Kondo, Fumiaki; Kurihara, Kiyoshi; Harashima, Nanae; Masuda, Takao; Kannagi, Mari] Tokyo Med & Dent Univ, Dept Immunotherapeut, Grad Sch, Bunkyo Ku, Tokyo 1138519, Japan.
    [Utsunomiya, Atae] Imamura Bunin Hosp, Dept Hematol, Kagoshima 8900064, Japan.
    [Kurimura, Mayumi] Kamigotoh Hosp, Shin Kamigoto, Nagasaki, Japan.
    [Yamano, Yoshihisa] St Marianna Univ, Sch Med, Inst Med Sci, Dept Genome Sci,Miyamae Ku, Kawasaki, Kanagawa 2168512, Japan.
    [Hishizawa, Masakatsu] Kyoto Univ, Grad Sch Med, Dept Hematol & Oncol, Sakyo Ku, Kyoto 5058507, Japan.
    [Watanabe, Toshiki] Univ Tokyo, Grad Sch Frontier Sci, Dept Med Genome Sci, Lab Tumor Cell Biol,Minato Ku, Tokyo 1088639, Japan.
    [Okamura, Jun] Kyushu Natl Canc Ctr, Div Clin Res, Minami Ku, Fukuoka 8111395, Japan.
 RP Kannagi, M, Tokyo Med & Dent Univ, Dept Immunotherapeut, Grad Sch,
    Bunkyo Ku, 1-5-45 Yushima, Tokyo 1138519, Japan.
 EM kann.impt@tmd.ac.jp
 FU Ministry of Education, Culture, Sports, Science, and Technology of
    Japan [17013028]; Ministry of Health, Welfare, and Labor of Japan ;
    Public Trust Haraguchi Memorial Cancer Research Fund 
 FX We thank Ms. Minako Nakashima and Ms. Yasuko Tsuji (Imamura Bun-in
    Hospital, Kagoshima, Japan) for coordination of clinical samples. This
    study was supported by Grant 17013028 from the Ministry of Education,
    Culture, Sports, Science, and Technology of Japan; a grant for an
    anticancer project from the Ministry of Health, Welfare, and Labor of
    Japan; and the Public Trust Haraguchi Memorial Cancer Research Fund.
    The authors have no financial conflict of interest.
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 PU WILEY-BLACKWELL PUBLISHING, INC
 PI MALDEN
 PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
 SN 1347-9032
 J9 CANCER SCI
 JI Cancer Sci.
 PD MAR
 PY 2009
 VL 100
 IS 3
 BP 481
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 DI 10.1111/j.1349-7006.2008.01054.x
 PG 9
 SC Oncology
 GA 408QR
 UT ISI:000263450200017
 ER
 
 PT J
 AU Yang, JJ
    Yang, WJ
    Cheng, C
    Devidas, M
    Cao, XY
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    Borowitz, MJ
    Willman, CL
    Bowman, WP
    Reaman, G
    Carroll, WL
    Hunger, SP
    Evans, WE
    Pui, CH
    Relling, MV
 AF Yang, Jun J.
    Yang, Wenjian
    Cheng, Cheng
    Devidas, Meenakshi
    Cao, Xueyuan
    Campana, Dario
    Borowitz, Michael. J.
    Willman, Cheryl L.
    Bowman, William Paul
    Reaman, Gregory
    Carroll, William L.
    Hunger, Stephen P.
    Evans, William E.
    Pui, Ching-Hon
    Relling, Mary V.
 TI Genetically Defined Racial Differences Underlie Risk of Relapse in
    Childhood Acute Lymphoblastic Leukemia
 SO BLOOD
 LA English
 DT Meeting Abstract
 CT 50th Annual Meeting of the American- Society-of-Hematology
 CY DEC 06-09, 2008
 CL San Francisco, CA
 SP Amer Soc Hematol
 C1 [Yang, Jun J.; Yang, Wenjian; Cheng, Cheng; Cao, Xueyuan; Campana, Dario; Evans, William E.; Pui, Ching-Hon; Relling, Mary V.] St Jude Childrens Hosp, Memphis, TN 38105 USA.
    [Devidas, Meenakshi] Univ Florida, Coll Med, Dept Epidemiol & Hlth Policy Res, Gainesville, FL USA.
    [Borowitz, Michael. J.] Johns Hopkins Univ, Baltimore, MD USA.
    [Willman, Cheryl L.] Univ New Mexico, Canc Res & Treatment Ctr, Albuquerque, NM 87131 USA.
    [Bowman, William Paul] Cook Childrens Med Ctr, Ft Worth, TX USA.
    [Reaman, Gregory] Childrens Natl Med Ctr, Washington, DC 20010 USA.
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    [Hunger, Stephen P.] Childrens Hosp, Aurora, CO USA.
    [Hunger, Stephen P.] Univ Colorado, Denver Sch Med, Aurora, CO USA.
 NR 0
 TC 0
 PU AMER SOC HEMATOLOGY
 PI WASHINGTON
 PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
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 J9 BLOOD
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 PD NOV 16
 PY 2008
 VL 112
 IS 11
 BP 11
 EP 12
 PG 2
 SC Hematology
 GA 389OP
 UT ISI:000262104700015
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 PT J
 AU Amn, A
    Lin, J
    Yang, GP
    Stemkowski, S
 AF Amn, Alpesh
    Lin, Jay
    Yang, Guiping
    Stemkowski, Steve
 TI Clinical and Economic Outcomes Following Full or Partial ACCP
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 SO BLOOD
 LA English
 DT Meeting Abstract
 CT 50th Annual Meeting of the American- Society-of-Hematology
 CY DEC 06-09, 2008
 CL San Francisco, CA
 SP Amer Soc Hematol
 C1 [Amn, Alpesh] Univ Calif Irvine, Div Gen Internal Med, Dept Med, Orange, CA 92668 USA.
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    [Yang, Guiping; Stemkowski, Steve] Premier Inc, Charlotte, NC USA.
 NR 0
 TC 0
 PU AMER SOC HEMATOLOGY
 PI WASHINGTON
 PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
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 J9 BLOOD
 JI Blood
 PD NOV 16
 PY 2008
 VL 112
 IS 11
 BP 69
 EP 70
 PG 2
 SC Hematology
 GA 389OP
 UT ISI:000262104700170
 ER
 
 PT J
 AU Chen, SH
    Yang, WJ
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    Evans, WE
    Relling, MV
 AF Chen, Shih-Hsiang
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    Pui, Ching-Hon
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    Relling, Mary V.
 TI A Genome-Wide Approach Identifies Variations in the Aspartate
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 SO BLOOD
 LA English
 DT Meeting Abstract
 CT 50th Annual Meeting of the American- Society-of-Hematology
 CY DEC 06-09, 2008
 CL San Francisco, CA
 SP Amer Soc Hematol
 C1 [Chen, Shih-Hsiang] Chang Gung Mem Hosp, Dept Pediat, Div Hematol Oncol, Tao Yuan, Taiwan.
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    [Fang, Yiping] St Jude Childrens Hosp, Hartwell Ctr Bioinformat & Biotechnol, Memphis, TN 38105 USA.
    [Pui, Ching-Hon] St Jude Childrens Hosp, Dept Oncol, Memphis, TN 38105 USA.
 NR 0
 TC 0
 PU AMER SOC HEMATOLOGY
 PI WASHINGTON
 PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
 SN 0006-4971
 J9 BLOOD
 JI Blood
 PD NOV 16
 PY 2008
 VL 112
 IS 11
 BP 86
 EP 86
 PG 1
 SC Hematology
 GA 389OP
 UT ISI:000262104700214
 ER
 
 PT J
 AU Trevino, LR
    Shimasaki, N
    Yang, WJ
    Panetta, JC
    Cheng, C
    Pei, DQ
    Chan, D
    Sparreboom, A
    Giacomini, KM
    Pui, CH
    Evans, WE
    Relling, MV
 AF Trevino, Lisa R.
    Shimasaki, Noriko
    Yang, Wenjian
    Panetta, John C.
    Cheng, Cheng
    Pei, Deqing
    Chan, Diana
    Sparreboom, Alex
    Giacomini, Kathleen M.
    Pui, Ching-Hon
    Evans, William E.
    Relling, Mary V.
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 SO BLOOD
 LA English
 DT Meeting Abstract
 CT 50th Annual Meeting of the American- Society-of-Hematology
 CY DEC 06-09, 2008
 CL San Francisco, CA
 SP Amer Soc Hematol
 C1 [Trevino, Lisa R.; Shimasaki, Noriko; Yang, Wenjian; Panetta, John C.; Cheng, Cheng; Pei, Deqing; Chan, Diana; Sparreboom, Alex; Pui, Ching-Hon; Evans, William E.; Relling, Mary V.] St Jude Childrens Hosp, Memphis, TN 38105 USA.
    [Giacomini, Kathleen M.] Univ Calif San Francisco, San Francisco, CA 94143 USA.
 NR 0
 TC 0
 PU AMER SOC HEMATOLOGY
 PI WASHINGTON
 PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
 SN 0006-4971
 J9 BLOOD
 JI Blood
 PD NOV 16
 PY 2008
 VL 112
 IS 11
 BP 86
 EP 86
 PG 1
 SC Hematology
 GA 389OP
 UT ISI:000262104700215
 ER
 
 PT J
 AU Yang, Y
    Ritchie, JP
    Swain, T
    Naggi, A
    Torri, G
    Casu, B
    Pisano, C
    Carminati, P
    Vlodavsky, I
    Sanderson, RD
 AF Yang, Yang
    Ritchie, Joseph P.
    Swain, Telisha
    Naggi, Annamaria
    Torri, Giangiacomo
    Casu, Benito
    Pisano, Claudio
    Carminati, Paolo
    Vlodavsky, Israel
    Sanderson, Ralph D.
 TI The Heparanase Inhibitor SST0001 Is a Potent Inhibitor of Myeloma
    Growth In Vivo
 SO BLOOD
 LA English
 DT Meeting Abstract
 CT 50th Annual Meeting of the American- Society-of-Hematology
 CY DEC 06-09, 2008
 CL San Francisco, CA
 SP Amer Soc Hematol
 C1 [Yang, Yang; Ritchie, Joseph P.; Swain, Telisha; Sanderson, Ralph D.] Univ Alabama, Ctr Comprehens Canc, Birmingham, AL 35294 USA.
    [Yang, Yang; Ritchie, Joseph P.; Swain, Telisha; Sanderson, Ralph D.] Univ Alabama, Dept Pathol, Ctr Metab Bone Dis, Birmingham, AL 35294 USA.
    [Naggi, Annamaria; Torri, Giangiacomo; Casu, Benito] GRonzoni Inst Chem & Biochem Res, Milan, Italy.
    [Pisano, Claudio] Sigma Tau Ind Farmaceut Riunite SpA, Pomezia, Italy.
    [Carminati, Paolo] Sigma Tau Res Switzerland SA, Milan, Italy.
    [Vlodavsky, Israel] Technion Israel Inst Technol, Canc & Vasc Biol Res Ctr, Bruce Rappaport Fac Med, IL-32000 Haifa, Israel.
 NR 0
 TC 0
 PU AMER SOC HEMATOLOGY
 PI WASHINGTON
 PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
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 J9 BLOOD
 JI Blood
 PD NOV 16
 PY 2008
 VL 112
 IS 11
 BP 97
 EP 98
 PG 2
 SC Hematology
 GA 389OP
 UT ISI:000262104700247
 ER
 
 PT J
 AU Huang, G
    Elf, S
    Yan, XM
    Wang, L
    Liu, Y
    Sashida, G
    Gural, A
    Menendez, S
    Lee, J
    Yang, YY
    Zhao, XY
    Nimer, SD
 AF Huang, Gang
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    Lee, Jennifer
    Yang, Youyang
    Zhao, Xinyang
    Nimer, Stephen D.
 TI Previously Unknown Interactions Between AML1 and MLL Provide Epigenetic
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 SO BLOOD
 LA English
 DT Meeting Abstract
 CT 50th Annual Meeting of the American- Society-of-Hematology
 CY DEC 06-09, 2008
 CL San Francisco, CA
 SP Amer Soc Hematol
 C1 [Huang, Gang; Elf, Shannon; Yan, Xiaomei; Wang, Lan; Liu, Yan; Sashida, Goro; Gural, Alex; Menendez, Silvia; Lee, Jennifer; Yang, Youyang; Zhao, Xinyang; Nimer, Stephen D.] Mem Sloan Kettering Canc Ctr, New York, NY USA.
 NR 0
 TC 1
 PU AMER SOC HEMATOLOGY
 PI WASHINGTON
 PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
 SN 0006-4971
 J9 BLOOD
 JI Blood
 PD NOV 16
 PY 2008
 VL 112
 IS 11
 BP 110
 EP 110
 PG 1
 SC Hematology
 GA 389OP
 UT ISI:000262104700283
 ER
 
 PT J
 AU Alipio, Z
    Xu, D
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    Ma, YP
 AF Alipio, Zaida
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    Yang, Jianchang
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    Xu, Wilson
    Ward, David C.
    Ma, Yupo
 TI Reprogrammed Murine Fibroblasts Differentiated into Hematopoietic
    Progenitors Are Able to Successfully Engraft and Repopulate the Bone
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 SO BLOOD
 LA English
 DT Meeting Abstract
 CT 50th Annual Meeting of the American- Society-of-Hematology
 CY DEC 06-09, 2008
 CL San Francisco, CA
 SP Amer Soc Hematol
 C1 [Alipio, Zaida; Xu, Dan; Yang, Jianchang; Fink, Louis M.; Xu, Wilson; Ward, David C.; Ma, Yupo] Nevada Canc Inst, Las Vegas, NV USA.
 NR 0
 TC 0
 PU AMER SOC HEMATOLOGY
 PI WASHINGTON
 PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
 SN 0006-4971
 J9 BLOOD
 JI Blood
 PD NOV 16
 PY 2008
 VL 112
 IS 11
 BP 150
 EP 150
 PG 1
 SC Hematology
 GA 389OP
 UT ISI:000262104700390
 ER
 
 PT J
 AU Mullighan, CG
    Su, XP
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    Miller, CB
    Ma, J
    Liu, W
    Cheng, C
    Harvey, RC
    Chen, IM
    Clifford, R
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    Reaman, G
    Devidas, M
    Gerhard, DS
    Yang, WJ
    Bowman, WP
    Shurtleff, SA
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    Hunger, SP
    Willman, CL
    Downing, JR
 AF Mullighan, Charles G.
    Su, Xiaoping
    Zhang, Jinghui
    Radtke, Ina
    Phillips, Letha A.
    Miller, Christopher B.
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    Cheng, Cheng
    Harvey, Richard C.
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    Clifford, Robert
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    Devidas, Meenakshi
    Gerhard, Daniela S.
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 TI Deletion of IKZF1 (Ikaros) Predicts Poor Outcome and Impaired
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 SO BLOOD
 LA English
 DT Meeting Abstract
 CT 50th Annual Meeting of the American-Society-of-Hematology
 CY DEC 06-09, 2008
 CL San Francisco, CA
 SP Amer Soc Hematol
 C1 [Ma, Jing] St Jude Childrens Hosp, Hartwell Ctr, Memphis, TN 38105 USA.
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    [Hunger, Stephen P.] Childrens Hosp, Aurora, CO USA.
 NR 0
 TC 0
 PU AMER SOC HEMATOLOGY
 PI WASHINGTON
 PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
 SN 0006-4971
 J9 BLOOD
 JI Blood
 PD NOV 16
 PY 2008
 VL 112
 IS 11
 BP 163
 EP 163
 PG 1
 SC Hematology
 GA 389OP
 UT ISI:000262104700428
 ER
 
 PT J
 AU Xu, D
    Alipio, Z
    Yang, JC
    Fink, LM
    Xu, W
    Ward, DC
    Ma, YP
 AF Xu, Dan
    Alipio, Zaida
    Yang, Jianchang
    Fink, Louis M.
    Xu, Wilson
    Ward, David C.
    Ma, Yupo
 TI Phenotypic Correction of Hemophilia a Using An Ips-Based Cellular
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 SO BLOOD
 LA English
 DT Meeting Abstract
 CT 50th Annual Meeting of the American-Society-of-Hematology
 CY DEC 06-09, 2008
 CL San Francisco, CA
 SP Amer Soc Hematol
 C1 [Xu, Dan; Alipio, Zaida; Yang, Jianchang; Fink, Louis M.; Xu, Wilson; Ward, David C.; Ma, Yupo] Nevada Canc Inst, Las Vegas, NV USA.
 NR 0
 TC 0
 PU AMER SOC HEMATOLOGY
 PI WASHINGTON
 PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
 SN 0006-4971
 J9 BLOOD
 JI Blood
 PD NOV 16
 PY 2008
 VL 112
 IS 11
 BP 194
 EP 194
 PG 1
 SC Hematology
 GA 389OP
 UT ISI:000262104700515
 ER
 
 PT J
 AU Lopes, EC
    Cerchietti, L
    Yang, SN
    Melnick, A
    Chiosis, G
 AF Lopes, Eloisi Caldas
    Cerchietti, Leandro
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    Melnick, Ari
    Chiosis, Gabriela
 TI Antitumor Efficacy of the Purine-Scaffold Hsp90 Inhibitor PU-H71 in
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 SO BLOOD
 LA English
 DT Meeting Abstract
 CT 50th Annual Meeting of the American- Society-of-Hematology
 CY DEC 06-09, 2008
 CL San Francisco, CA
 SP Amer Soc Hematol
 C1 [Lopes, Eloisi Caldas; Chiosis, Gabriela] Mem Sloan Kettering Canc Ctr, New York, NY 10021 USA.
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 NR 0
 TC 0
 PU AMER SOC HEMATOLOGY
 PI WASHINGTON
 PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
 SN 0006-4971
 J9 BLOOD
 JI Blood
 PD NOV 16
 PY 2008
 VL 112
 IS 11
 BP 225
 EP 225
 PG 1
 SC Hematology
 GA 389OP
 UT ISI:000262104700603
 ER
 
 PT J
 AU Yang, J
    Cao, YB
    Hong, SY
    Li, HY
    Kwak, LW
    Yi, Q
 AF Yang, Jing
    Cao, Yabing
    Hong, Sungyongl
    Li, Haiyan
    Kwak, Larry W.
    Yi, Qing
 TI Human-Like Mouse Models for Testing the Efficacy and Safety of
    Anti-beta(2)-Microglobulin Monoclonal Antibodies to Treat Myeloma
 SO BLOOD
 LA English
 DT Meeting Abstract
 CT 50th Annual Meeting of the American- Society-of-Hematology
 CY DEC 06-09, 2008
 CL San Francisco, CA
 SP Amer Soc Hematol
 C1 [Yang, Jing; Cao, Yabing; Hong, Sungyongl; Li, Haiyan; Kwak, Larry W.; Yi, Qing] Univ Texas MD Anderson Canc Ctr, Houston, TX 77030 USA.
 NR 0
 TC 0
 PU AMER SOC HEMATOLOGY
 PI WASHINGTON
 PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
 SN 0006-4971
 J9 BLOOD
 JI Blood
 PD NOV 16
 PY 2008
 VL 112
 IS 11
 BP 239
 EP 239
 PG 1
 SC Hematology
 GA 389OP
 UT ISI:000262104700642
 ER
 
 PT J
 AU Yang, XV
    Banerjee, Y
    Femandez, JA
    Deguchi, H
    Xu, X
    Mosnier, LO
    Urbanus, R
    Degroot, PG
    White, TC
    McCarty, OJT
    Griffin, JH
 AF Yang, Xia V.
    Banerjee, Yajnavalka
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    Mosnier, Laurent O.
    Urbanus, Roift
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    White, Tara C.
    McCarty, Owen J. T.
    Griffin, John H.
 TI Activation of the PI3K-Akt Pathway by Activated Protein C Occurs Via a
    Novel Receptor, Apolipoprotein E Receptor 2 (ApoER2)
 SO BLOOD
 LA English
 DT Meeting Abstract
 CT 50th Annual Meeting of the American- Society-of-Hematology
 CY DEC 06-09, 2008
 CL San Francisco, CA
 SP Amer Soc Hematol
 C1 [Yang, Xia V.; Banerjee, Yajnavalka; Femandez, Jose A.; Deguchi, Hiroshi; Xu, Xiao; Mosnier, Laurent O.; Griffin, John H.] Scripps Res Inst, La Jolla, CA 92037 USA.
    [Degroot, Phillip G.] Univ Med Ctr Utrecht, Lab Clin Chem & Haemataol, Utrecht, Netherlands.
    [White, Tara C.; McCarty, Owen J. T.] Oregon Hlth & Sci Univ, Sch Med, Div Biomed Engn, Portland, OR 97201 USA.
 NR 0
 TC 0
 PU AMER SOC HEMATOLOGY
 PI WASHINGTON
 PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
 SN 0006-4971
 J9 BLOOD
 JI Blood
 PD NOV 16
 PY 2008
 VL 112
 IS 11
 BP 259
 EP 259
 PG 1
 SC Hematology
 GA 389OP
 UT ISI:000262104700696
 ER
 
 PT J
 AU Zhuang, JL
    Yang, L
    Lwin, ST
    Edwards, CM
    Edwards, JR
    Mundy, GR
 AF Zhuang, Junling
    Yang, Li
    Lwin, Seint T.
    Edwards, Claire M.
    Edwards, James R.
    Mundy, Gregory R.
 TI Osteoclasts in Myeloma Are Derived from Gr-1(+)CD11b(+) Myeloid Immune
    Suppressor Cells of the Bone Marrow Niche in Vivo
 SO BLOOD
 LA English
 DT Meeting Abstract
 CT 50th Annual Meeting of the American- Society-of-Hematology
 CY DEC 06-09, 2008
 CL San Francisco, CA
 SP Amer Soc Hematol
 C1 [Yang, Li] Vanderbilt Univ, Med Ctr, Nashville, TN USA.
 NR 0
 TC 2
 PU AMER SOC HEMATOLOGY
 PI WASHINGTON
 PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
 SN 0006-4971
 J9 BLOOD
 JI Blood
 PD NOV 16
 PY 2008
 VL 112
 IS 11
 BP 273
 EP 273
 PG 1
 SC Hematology
 GA 389OP
 UT ISI:000262104700737
 ER
 
 PT J
 AU Yang, L
    Orlowski, RZ
 AF Yang, Lin
    Orlowski, Robert Z.
 TI ZKSCAN3, a Novel Zinc Finger Transcription Factor, Regulates Cyclin D2
    Expression in Multiple Myeloma (MM) Cells
 SO BLOOD
 LA English
 DT Meeting Abstract
 CT 50th Annual Meeting of the American- Society-of-Hematology
 CY DEC 06-09, 2008
 CL San Francisco, CA
 SP Amer Soc Hematol
 C1 [Yang, Lin] Univ Texas Houston, MD Anderson Canc Ctr, Houston, TX 77030 USA.
    [Orlowski, Robert Z.] Univ Texas MD Anderson Canc Ctr, Houston, TX 77030 USA.
 NR 0
 TC 0
 PU AMER SOC HEMATOLOGY
 PI WASHINGTON
 PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
 SN 0006-4971
 J9 BLOOD
 JI Blood
 PD NOV 16
 PY 2008
 VL 112
 IS 11
 BP 278
 EP 278
 PG 1
 SC Hematology
 GA 389OP
 UT ISI:000262104700750
 ER
 
 PT J
 AU Wang, JB
    Wu, T
    Yang, JF
    Zhang, JP
    Cao, XY
    Yin, YM
    Sun, Y
    Luo, RM
    Lu, DP
    Tong, CR
 AF Wang, Jing-Bo
    Wu, Tong
    Yang, Jun-Fang
    Zhang, Jian-Ping
    Cao, Xing-Yu
    Yin, Yu-Ming
    Sun, Yuan
    Luo, Rong-Mu
    Lu, Dao-Pei
    Tong, Chun-Rong
 TI Management of Early Leukemia Relapse after Allogeneic Hematopoietic
    Stem Cell Transplantation by Donor's Dendritic Cell-Primed
    Cytokine-Induced Killer Cells
 SO BLOOD
 LA English
 DT Meeting Abstract
 CT 50th Annual Meeting of the American- Society-of-Hematology
 CY DEC 06-09, 2008
 CL San Francisco, CA
 SP Amer Soc Hematol
 C1 [Wang, Jing-Bo; Wu, Tong; Yang, Jun-Fang; Zhang, Jian-Ping; Cao, Xing-Yu; Yin, Yu-Ming; Sun, Yuan; Luo, Rong-Mu; Lu, Dao-Pei; Tong, Chun-Rong] Beijing Daopei Hosp, Beijing, Peoples R China.
 NR 0
 TC 0
 PU AMER SOC HEMATOLOGY
 PI WASHINGTON
 PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
 SN 0006-4971
 J9 BLOOD
 JI Blood
 PD NOV 16
 PY 2008
 VL 112
 IS 11
 BP 307
 EP 308
 PG 2
 SC Hematology
 GA 389OP
 UT ISI:000262104701053
 ER
 
 PT J
 AU Yang, Y
    Ritchie, JP
    Suva, LJ
    Sanderson, RD
 AF Yang, Yang
    Ritchie, Joseph P.
    Suva, Larry J.
    Sanderson, Ralph D.
 TI Heparanase Promotes the Osteolytic Phenotype in Multiple Myeloma
 SO BLOOD
 LA English
 DT Meeting Abstract
 CT 50th Annual Meeting of the American-Society-of-Hematology
 CY DEC 06-09, 2008
 CL San Francisco, CA
 SP Amer Soc Hematol
 C1 [Yang, Yang; Ritchie, Joseph P.; Sanderson, Ralph D.] Univ Alabama, Dept Pathol, Ctr Metab Bone Dis, Birmingham, AL 35294 USA.
    [Yang, Yang; Ritchie, Joseph P.; Sanderson, Ralph D.] Univ Alabama, Ctr Comprehens Canc, Birmingham, AL 35294 USA.
    [Suva, Larry J.] Univ Arkansas Med Sci, Dept Orthopaed Surg, Ctr Orthopaed Res, Little Rock, AR 72205 USA.
 NR 0
 TC 0
 PU AMER SOC HEMATOLOGY
 PI WASHINGTON
 PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
 SN 0006-4971
 J9 BLOOD
 JI Blood
 PD NOV 16
 PY 2008
 VL 112
 IS 11
 BP 311
 EP 312
 PG 2
 SC Hematology
 GA 389OP
 UT ISI:000262104701065
 ER
 
 PT J
 AU Rao, R
    Fiskus, W
    Yang, YH
    Joshi, R
    Fernandez, P
    Lee, P
    Jillella, A
    Tao, JG
    Atadja, P
    Sotomayor, E
    Bhalla, KN
 AF Rao, Rekha
    Fiskus, Warren
    Yang, Yonghua
    Joshi, Rajeshree
    Fernandez, Pravina
    Lee, Pearl
    Jillella, Anand
    Tao, Jianguo
    Atadja, Peter
    Sotomayor, Eduardo
    Bhalla, Kapil N.
 TI Co-Treatment with Panobinostat Enhances Bortezomib-Induced Unfolded
    Protein Response, Endoplasmic Reticulum Stress and Apoptosis of Human
    Mantle Cell Lymphoma Cells
 SO BLOOD
 LA English
 DT Meeting Abstract
 CT 50th Annual Meeting of the American- Society-of-Hematology
 CY DEC 06-09, 2008
 CL San Francisco, CA
 SP Amer Soc Hematol
 C1 [Rao, Rekha; Fiskus, Warren; Yang, Yonghua; Joshi, Rajeshree; Fernandez, Pravina; Lee, Pearl; Jillella, Anand; Bhalla, Kapil N.] Med Coll Georgia, MCG Canc Ctr, Augusta, GA 30912 USA.
    [Tao, Jianguo; Sotomayor, Eduardo] Univ S Florida, Coll Med, H Lee Moffitt Canc Ctr & Res Inst, Tampa, FL 33612 USA.
    [Atadja, Peter] Novartis Inst Biomed Res, Cambridge, MA USA.
 NR 0
 TC 0
 PU AMER SOC HEMATOLOGY
 PI WASHINGTON
 PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
 SN 0006-4971
 J9 BLOOD
 JI Blood
 PD NOV 16
 PY 2008
 VL 112
 IS 11
 BP 327
 EP 328
 PG 2
 SC Hematology
 GA 389OP
 UT ISI:000262104701111
 ER
 
 PT J
 AU Lange, B
    Yang, RK
    Gan, J
    Hank, JA
    Sievers, E
    Gerbing, R
    Alonzo, T
    Sondel, PM
 AF Lange, Beverly
    Yang, Richard K.
    Gan, Jacek
    Hank, Jaqueline A.
    Sievers, Eric
    Gerbing, Robert
    Alonzo, Todd
    Sondel, Paul M.
 TI Clinical and Serologic Interleukin 2 Receptor alpha Response to
    Interleukin-2 in CCG-2961, a Ranomized Phase 3 Trial for Pediatric
    Acute Myeloid Leukemia.
 SO BLOOD
 LA English
 DT Meeting Abstract
 CT 50th Annual Meeting of the American- Society-of-Hematology
 CY DEC 06-09, 2008
 CL San Francisco, CA
 SP Amer Soc Hematol
 C1 [Lange, Beverly] Childrens Hosp Philadelphia, Philadelphia, PA 19104 USA.
    [Yang, Richard K.; Gan, Jacek; Hank, Jaqueline A.; Sondel, Paul M.] Univ Wisconsin, Sch Med, Madison, WI 53706 USA.
    [Sievers, Eric] Seattle Genet Inc, Bothell, WA USA.
    [Gerbing, Robert] Childrens Oncol Grp, Arcadia, CA USA.
    [Alonzo, Todd] Univ So Calif, Keck Sch Med, Arcadia, CA USA.
 NR 0
 TC 0
 PU AMER SOC HEMATOLOGY
 PI WASHINGTON
 PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
 SN 0006-4971
 J9 BLOOD
 JI Blood
 PD NOV 16
 PY 2008
 VL 112
 IS 11
 BP 353
 EP 353
 PG 1
 SC Hematology
 GA 389OP
 UT ISI:000262104701183
 ER
 
 PT J
 AU Yang, LK
    Sun, MF
    Manithody, C
    Gailani, D
    Rezaie, AR
 AF Yang, Likui
    Sun, Mao-fu
    Manithody, Chandrashekhara
    Gailani, David
    Rezaie, Alireza R.
 TI Characterization of Heparin Binding Site Residues on the Catalytic
    Domain of Factor XIa.
 SO BLOOD
 LA English
 DT Meeting Abstract
 CT 50th Annual Meeting of the American- Society-of-Hematology
 CY DEC 06-09, 2008
 CL San Francisco, CA
 SP Amer Soc Hematol
 C1 [Yang, Likui; Manithody, Chandrashekhara; Rezaie, Alireza R.] St Louis Univ, Sch Med, St Louis, MO USA.
    [Sun, Mao-fu; Gailani, David] Vanderbilt Univ, Nashville, TN USA.
 NR 0
 TC 0
 PU AMER SOC HEMATOLOGY
 PI WASHINGTON
 PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
 SN 0006-4971
 J9 BLOOD
 JI Blood
 PD NOV 16
 PY 2008
 VL 112
 IS 11
 BP 374
 EP 375
 PG 2
 SC Hematology
 GA 389OP
 UT ISI:000262104701242
 ER
 
 PT J
 AU Chen, HR
    Si, YJ
    He, XP
    Yang, K
    Hu, B
    Du, ZL
    Zhang, XM
    Zhang, CC
 AF Chen, Huiren
    Si, Yingjian
    He, Xuepeng
    Yang, Kai
    Hu, Bo
    Du, Zhenlan
    Zhang, Xiaomei
    Zhang, Chuancang
 TI HLA-Mismatched Hematopoietic Stem Cell Transplantation for Treatment of
    Chronic Myelogenous Leukemia
 SO BLOOD
 LA English
 DT Meeting Abstract
 CT 50th Annual Meeting of the American- Society-of-Hematology
 CY DEC 06-09, 2008
 CL San Francisco, CA
 SP Amer Soc Hematol
 C1 [Chen, Huiren; Si, Yingjian; He, Xuepeng; Yang, Kai; Hu, Bo; Du, Zhenlan; Zhang, Xiaomei; Zhang, Chuancang] Gen Hosp Beijing Millitary Reg, Beijing, Peoples R China.
 NR 0
 TC 0
 PU AMER SOC HEMATOLOGY
 PI WASHINGTON
 PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
 SN 0006-4971
 J9 BLOOD
 JI Blood
 PD NOV 16
 PY 2008
 VL 112
 IS 11
 BP 406
 EP 407
 PG 2
 SC Hematology
 GA 389OP
 UT ISI:000262104701337
 ER
 
 PT J
 AU Ye, JY
    Chan, GC
    Chan, S
    Luo, JC
    Yang, M
 AF Ye, Jie Yu
    Chan, Godfrey ChiFung
    Chan, Shing
    Luo, Jue Cong
    Yang, Mo
 TI Recombinant PDGF-BB Enhances Platelet Recovery in Mice with Radiation
    Induced Thromobocytopenia.
 SO BLOOD
 LA English
 DT Meeting Abstract
 CT 50th Annual Meeting of the American-Society-of-Hematology
 CY DEC 06-09, 2008
 CL San Francisco, CA
 SP Amer Soc Hematol
 C1 [Ye, Jie Yu; Chan, Shing; Luo, Jue Cong; Yang, Mo] Univ Hong Kong, Dept Paediat & Adolescent Med, Hong Kong, Hong Kong, Peoples R China.
    [Chan, Godfrey ChiFung] Queen Mary Hosp, Hong Kong, Hong Kong, Peoples R China.
 NR 0
 TC 0
 PU AMER SOC HEMATOLOGY
 PI WASHINGTON
 PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
 SN 0006-4971
 J9 BLOOD
 JI Blood
 PD NOV 16
 PY 2008
 VL 112
 IS 11
 BP 448
 EP 448
 PG 1
 SC Hematology
 GA 389OP
 UT ISI:000262104701454
 ER
 
 PT J
 AU Yang, M
    Chan, GC
    Ye, JY
    Liu, C
 AF Yang, Mo
    Chan, Godfrey ChiFung
    Ye, Jie Yu
    Liu, Chang
 TI Angelica Polysaccharides Promotes Thrombopoiesis through the
    Phosphatidylinositol 3-Kinase/Akt Pathway.
 SO BLOOD
 LA English
 DT Meeting Abstract
 CT 50th Annual Meeting of the American- Society-of-Hematology
 CY DEC 06-09, 2008
 CL San Francisco, CA
 SP Amer Soc Hematol
 C1 [Yang, Mo; Ye, Jie Yu] Univ Hong Kong, Dept Pediat & Adolescent Med, Hong Kong, Hong Kong, Peoples R China.
    [Chan, Godfrey ChiFung] Queen Mary Hosp, Hong Kong, Hong Kong, Peoples R China.
    [Liu, Chang] Univ Hong Kong, Mol Chinese Med Lab, Hong Kong, Hong Kong, Peoples R China.
 NR 0
 TC 0
 PU AMER SOC HEMATOLOGY
 PI WASHINGTON
 PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
 SN 0006-4971
 J9 BLOOD
 JI Blood
 PD NOV 16
 PY 2008
 VL 112
 IS 11
 BP 450
 EP 451
 PG 2
 SC Hematology
 GA 389OP
 UT ISI:000262104701462
 ER
 
 PT J
 AU Yang, M
    Zhou, M
    Ye, JY
    Cheung, YF
    Chan, S
    Ha, SY
    Chan, GC
 AF Yang, Mo
    Zhou, Min
    Ye, Jie Yu
    Cheung, Yiu Fai
    Chan, Shing
    Ha, Shau Yin
    Chan, Godfrey ChiFung
 TI The Effect and Underlying Mechanism of Melatonin on Platelet Formation
    and Survival in a Thrombocytopenic Model.
 SO BLOOD
 LA English
 DT Meeting Abstract
 CT 50th Annual Meeting of the American- Society-of-Hematology
 CY DEC 06-09, 2008
 CL San Francisco, CA
 SP Amer Soc Hematol
 C1 [Yang, Mo; Ye, Jie Yu; Cheung, Yiu Fai; Chan, Shing; Ha, Shau Yin] Univ Hong Kong, Dept Pediat & Adolescent Med, Hong Kong, Hong Kong, Peoples R China.
    [Zhou, Min] Chengdu Childres Hosp, Dept Hematol, Chengdu, Peoples R China.
    [Chan, Godfrey ChiFung] Queen Mary Hosp, Hong Kong, Hong Kong, Peoples R China.
 NR 0
 TC 0
 PU AMER SOC HEMATOLOGY
 PI WASHINGTON
 PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
 SN 0006-4971
 J9 BLOOD
 JI Blood
 PD NOV 16
 PY 2008
 VL 112
 IS 11
 BP 451
 EP 451
 PG 1
 SC Hematology
 GA 389OP
 UT ISI:000262104701463
 ER
 
 PT J
 AU Yang, SJ
    Hong, SH
    Lee, GY
    Jung, JY
    Oh, IH
 AF Yang, Seung-Jip
    Hong, Seong-Hyun
    Lee, Ga-Young
    Jung, Ju-Young
    Oh, Il-Hoan
 TI HoxB4 Effects on Hematopoietic Stem Cells Are Dependent on STAT3
    Activity; A Potential Convergence of Self-Renewing Signals.
 SO BLOOD
 LA English
 DT Meeting Abstract
 CT 50th Annual Meeting of the American- Society-of-Hematology
 CY DEC 06-09, 2008
 CL San Francisco, CA
 SP Amer Soc Hematol
 C1 [Yang, Seung-Jip; Hong, Seong-Hyun; Lee, Ga-Young; Jung, Ju-Young] Catholic Univ Korea, Catholic Cell Therapy Ctr, Seoul, South Korea.
    [Oh, Il-Hoan] Catholic Univ Korea, Cell Therapy Ctr, Seoul, South Korea.
 NR 0
 TC 0
 PU AMER SOC HEMATOLOGY
 PI WASHINGTON
 PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
 SN 0006-4971
 J9 BLOOD
 JI Blood
 PD NOV 16
 PY 2008
 VL 112
 IS 11
 BP 494
 EP 495
 PG 2
 SC Hematology
 GA 389OP
 UT ISI:000262104701600
 ER
 
 PT J
 AU Mani, M
    Venkatasubrahmanyam, S
    Sanyal, M
    Yang, YJ
    Huang, J
    Levy, S
    Butte, A
    Weinberg, KI
    Jahn, T
 AF Mani, Maheswaran
    Venkatasubrahmanyam, Shivkumar
    Sanyal, Mrinmoy
    Yang, Yujun
    Huang, Jing
    Levy, Shoshana
    Butte, Atul
    Weinberg, Kenneth I.
    Jahn, Thomas
 TI Wiskott-Aldrich Syndrome Protein (WASP) Is An Effector of Kit Signaling.
 SO BLOOD
 LA English
 DT Meeting Abstract
 CT 50th Annual Meeting of the American- Society-of-Hematology
 CY DEC 06-09, 2008
 CL San Francisco, CA
 SP Amer Soc Hematol
 C1 [Mani, Maheswaran; Yang, Yujun; Huang, Jing; Weinberg, Kenneth I.; Jahn, Thomas] Stanford Univ, Sch Med, Pediat Stem Cell Transplantat, Stanford, CA 94305 USA.
    [Venkatasubrahmanyam, Shivkumar; Butte, Atul] Stanford Univ, Sch Med, Ctr Biomed Informat Res, Stanford, CA 94305 USA.
    [Sanyal, Mrinmoy; Levy, Shoshana] Stanford Univ, Sch Med, Div Oncol, Stanford, CA 94305 USA.
 NR 0
 TC 0
 PU AMER SOC HEMATOLOGY
 PI WASHINGTON
 PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
 SN 0006-4971
 J9 BLOOD
 JI Blood
 PD NOV 16
 PY 2008
 VL 112
 IS 11
 BP 503
 EP 503
 PG 1
 SC Hematology
 GA 389OP
 UT ISI:000262104701632
 ER
 
 PT J
 AU Kalra, VK
    Patel, N
    Gonsalves, C
    Yang, MY
    Malik, P
 AF Kalra, Vijay K.
    Patel, Nitin
    Gonsalves, Caryn
    Yang, Minyang
    Malik, Punam
 TI Placenta Growth Factor Induces 5-Lipoxygenase-Activating Protein Via
    Hypoxia-Inducible Factor-1 alpha and Contributes to Increased
    Leukotrienes in Sickle Cell Disease
 SO BLOOD
 LA English
 DT Meeting Abstract
 CT 50th Annual Meeting of the American- Society-of-Hematology
 CY DEC 06-09, 2008
 CL San Francisco, CA
 SP Amer Soc Hematol
 C1 [Kalra, Vijay K.; Patel, Nitin; Gonsalves, Caryn] USC Keck Sch Med, Los Angeles, CA USA.
    [Yang, Minyang; Malik, Punam] Cincinnati Childrens Hosp, Med Ctr, Dept Pediat, Div Expt Hematol & Canc Biol, Cincinnati, OH USA.
 NR 0
 TC 0
 PU AMER SOC HEMATOLOGY
 PI WASHINGTON
 PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
 SN 0006-4971
 J9 BLOOD
 JI Blood
 PD NOV 16
 PY 2008
 VL 112
 IS 11
 BP 516
 EP 516
 PG 1
 SC Hematology
 GA 389OP
 UT ISI:000262104701669
 ER
 
 PT J
 AU Yang, DT
    Wuerzberger-Davis, S
    Chen, YH
    Yu, M
    Zeng, H
    Bates, P
    Wen, RR
    Wang, D
    Miyamoto, S
 AF Yang, David T.
    Wuerzberger-Davis, Shelly
    Chen, Yuhong
    Yu, Mei
    Zeng, Hu
    Bates, Paul
    Wen, Renren
    Wang, Demin
    Miyamoto, Shigeki
 TI The Critical Role of I kappa b alpha Dependent Nuclear Export of
    NF-kappa b in B-Cell Development
 SO BLOOD
 LA English
 DT Meeting Abstract
 CT 50th Annual Meeting of the American-Society-of-Hematology
 CY DEC 06-09, 2008
 CL San Francisco, CA
 SP Amer Soc Hematol
 C1 [Yang, David T.; Wuerzberger-Davis, Shelly; Bates, Paul; Miyamoto, Shigeki] Univ Wisconsin, Sch Med & Publ Hlth, Madison, WI USA.
    [Chen, Yuhong; Yu, Mei; Zeng, Hu; Wen, Renren; Wang, Demin] Blood Ctr Wisconsin, Blood Res Inst, Milwaukee, WI USA.
 NR 0
 TC 0
 PU AMER SOC HEMATOLOGY
 PI WASHINGTON
 PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
 SN 0006-4971
 J9 BLOOD
 JI Blood
 PD NOV 16
 PY 2008
 VL 112
 IS 11
 BP 545
 EP 545
 PG 1
 SC Hematology
 GA 389OP
 UT ISI:000262104701754
 ER
 
 PT J
 AU Yang, ZZ
    Novak, A
    Witzig, TE
    Ansell, SM
 AF Yang, Zhi-Zhang
    Novak, Anne
    Witzig, Thomas E.
    Ansell, Stephen M.
 TI Malignant B Cell-Derived TGF-beta Controls the Generation of T(H)1,
    T(H)17 and T-reg Cells in the Tumor Microenvironment of B-Cell
    Non-Hodgkin Lymohoma (NHL)
 SO BLOOD
 LA English
 DT Meeting Abstract
 CT 50th Annual Meeting of the American- Society-of-Hematology
 CY DEC 06-09, 2008
 CL San Francisco, CA
 SP Amer Soc Hematol
 C1 [Yang, Zhi-Zhang; Witzig, Thomas E.; Ansell, Stephen M.] Mayo Clin, Rochester, MN USA.
    [Novak, Anne] Mayo Clin & Mayo Fdn, Rochester, MN 55905 USA.
 NR 0
 TC 0
 PU AMER SOC HEMATOLOGY
 PI WASHINGTON
 PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
 SN 0006-4971
 J9 BLOOD
 JI Blood
 PD NOV 16
 PY 2008
 VL 112
 IS 11
 BP 550
 EP 551
 PG 2
 SC Hematology
 GA 389OP
 UT ISI:000262104701772
 ER
 
 PT J
 AU Buhmann, R
    Yang, T
    Schifferer, M
    Obermeier, M
    Jaeger, G
    Kolb, HJ
 AF Buhmann, Raymund
    Yang, Ting
    Schifferer, Monica
    Obermeier, Martin
    Jaeger, Gundula
    Kolb, Hans-Jochem
 TI Therapeutic Nucleic Acids: A Potential Source of Resistance to Cancer,
    Antiviral and Immunosuppressive Therapy
 SO BLOOD
 LA English
 DT Meeting Abstract
 CT 50th Annual Meeting of the American-Society-of-Hematology
 CY DEC 06-09, 2008
 CL San Francisco, CA
 SP Amer Soc Hematol
 C1 [Buhmann, Raymund; Kolb, Hans-Jochem] Univ Munich, Klinikum Grosshadern, Med Clin 3, KGMC, D-8000 Munich, Germany.
    [Yang, Ting] Fujian Med Univ, Union Hosp, Dept Hematol, Fuzhou, Fujian, Peoples R China.
    [Schifferer, Monica] Helmholtz Zentrum Munchen, Munich, Germany.
    [Obermeier, Martin; Jaeger, Gundula] Max Von Pettenkofer Inst, D-8000 Munich, Germany.
 NR 0
 TC 0
 PU AMER SOC HEMATOLOGY
 PI WASHINGTON
 PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
 SN 0006-4971
 J9 BLOOD
 JI Blood
 PD NOV 16
 PY 2008
 VL 112
 IS 11
 BP 571
 EP 571
 PG 1
 SC Hematology
 GA 389OP
 UT ISI:000262104701835
 ER
 
 PT J
 AU Brown, RD
    Kabani, K
    Yang, S
    Esther, A
    Ho, PJ
    Gibson, J
    Joshua, DE
 AF Brown, Ross D.
    Kabani, Karieshma
    Yang, Shihong
    Esther, Aklilu
    Ho, Phoebe Joy
    Gibson, John
    Joshua, Douglas E.
 TI Trogocytosis in Multiple Myeloma
 SO BLOOD
 LA English
 DT Meeting Abstract
 CT 50th Annual Meeting of the American- Society-of-Hematology
 CY DEC 06-09, 2008
 CL San Francisco, CA
 SP Amer Soc Hematol
 C1 [Brown, Ross D.; Kabani, Karieshma; Yang, Shihong; Esther, Aklilu; Ho, Phoebe Joy; Gibson, John; Joshua, Douglas E.] Royal Prince Alfred Hosp, Camperdown, NSW 2050, Australia.
 NR 0
 TC 0
 PU AMER SOC HEMATOLOGY
 PI WASHINGTON
 PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
 SN 0006-4971
 J9 BLOOD
 JI Blood
 PD NOV 16
 PY 2008
 VL 112
 IS 11
 BP 594
 EP 594
 PG 1
 SC Hematology
 GA 389OP
 UT ISI:000262104702015
 ER
 
 PT J
 AU Zhang, W
    Yang, M
    Chan, S
    Chan, GC
 AF Zhang, Wei
    Yang, Mo
    Chan, Shing
    Chan, Godfrey ChiFung
 TI TPO Exerts a Protective Effect on Iron-Induced Apoptosis Via Erk1/2
    Signaling in Human Mesenchymal Stem Cells
 SO BLOOD
 LA English
 DT Meeting Abstract
 CT 50th Annual Meeting of the American- Society-of-Hematology
 CY DEC 06-09, 2008
 CL San Francisco, CA
 SP Amer Soc Hematol
 C1 [Zhang, Wei] Tianjin Univ, Coll Med, Sch Lab Med, Tianjin 300072, Peoples R China.
    [Yang, Mo; Chan, Shing] Univ Hong Kong, Dept Pediat & Adolescent Med, Hong Kong, Hong Kong, Peoples R China.
    [Chan, Godfrey ChiFung] Queen Mary Hosp, Hong Kong, Hong Kong, Peoples R China.
 NR 0
 TC 0
 PU AMER SOC HEMATOLOGY
 PI WASHINGTON
 PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
 SN 0006-4971
 J9 BLOOD
 JI Blood
 PD NOV 16
 PY 2008
 VL 112
 IS 11
 BP 656
 EP 656
 PG 1
 SC Hematology
 GA 389OP
 UT ISI:000262104702204
 ER
 
 PT J
 AU Yang, M
    Chan, S
    Cheung, YF
    Hai, SY
    Chan, GC
 AF Yang, Mo
    Chan, Shing
    Cheung, Yiu Fai
    Hai, Shau Yin
    Chan, Godfrey ChiFung
 TI Iron-Overload Induces Apoptosis in Cardiomyocytes and Hepatocytes Via
    Mitochondrial/Caspase-3 Pathways
 SO BLOOD
 LA English
 DT Meeting Abstract
 CT 50th Annual Meeting of the American- Society-of-Hematology
 CY DEC 06-09, 2008
 CL San Francisco, CA
 SP Amer Soc Hematol
 C1 [Yang, Mo; Chan, Shing; Cheung, Yiu Fai; Hai, Shau Yin] Univ Hong Kong, Dept Pediat & Adolescent Med, Hong Kong, Hong Kong, Peoples R China.
    [Chan, Godfrey ChiFung] Queen Mary Hosp, Hong Kong, Hong Kong, Peoples R China.
 NR 0
 TC 0
 PU AMER SOC HEMATOLOGY
 PI WASHINGTON
 PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
 SN 0006-4971
 J9 BLOOD
 JI Blood
 PD NOV 16
 PY 2008
 VL 112
 IS 11
 BP 656
 EP 656
 PG 1
 SC Hematology
 GA 389OP
 UT ISI:000262104702205
 ER
 
 PT J
 AU Wang, CH
    Lin, CY
    Yang, CC
    Chuang, YJ
 AF Wang, Chieh-Hue
    Lin, Chia-Yi
    Yang, Chung-Chi
    Chuang, Yung-Jen
 TI Placenta Endothelial Protein 1 Is a Novel Neural Guidance Molecule on
    Angiogenesis.
 SO BLOOD
 LA English
 DT Meeting Abstract
 CT 50th Annual Meeting of the American- Society-of-Hematology
 CY DEC 06-09, 2008
 CL San Francisco, CA
 SP Amer Soc Hematol
 C1 [Wang, Chieh-Hue; Lin, Chia-Yi; Chuang, Yung-Jen] Inst Bioinformat & Struct Biol, Dept Life Sci, Hsinchu, Taiwan.
    [Yang, Chung-Chi] Tao Yuan Armed Forces Gen Hosp, Dept Med, Div Cardiol, Tao Yuan, Taiwan.
 NR 0
 TC 0
 PU AMER SOC HEMATOLOGY
 PI WASHINGTON
 PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
 SN 0006-4971
 J9 BLOOD
 JI Blood
 PD NOV 16
 PY 2008
 VL 112
 IS 11
 BP 663
 EP 664
 PG 2
 SC Hematology
 GA 389OP
 UT ISI:000262104702231
 ER
 
 PT J
 AU Douer, D
    Watkins, K
    Mark, L
    Ann, M
    Yang, AS
    Avramis, VI
 AF Douer, Dan
    Watkins, Kristy
    Mark, Lisa
    Ann, Mohrbacher
    Yang, Allen S.
    Avramis, Vassilios I.
 TI Sustained and Prolonged Asparagine Depletion by Multiple Doses of
    Intravenous Pegylated Asparaginase in the Treatment of Adults with
    Newly Diagnosed Acute Lymphoblastic Leukemia.
 SO BLOOD
 LA English
 DT Meeting Abstract
 CT 50th Annual Meeting of the American- Society-of-Hematology
 CY DEC 06-09, 2008
 CL San Francisco, CA
 SP Amer Soc Hematol
 C1 [Douer, Dan; Watkins, Kristy; Mark, Lisa; Ann, Mohrbacher; Yang, Allen S.] Univ So Calif, Kenneth Norris Jr Comprehens Canc Ctr, Los Angeles, CA 90033 USA.
    [Avramis, Vassilios I.] Childrens Hosp Los Angeles, Los Angeles, CA 90027 USA.
 NR 0
 TC 0
 PU AMER SOC HEMATOLOGY
 PI WASHINGTON
 PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
 SN 0006-4971
 J9 BLOOD
 JI Blood
 PD NOV 16
 PY 2008
 VL 112
 IS 11
 BP 673
 EP 673
 PG 1
 SC Hematology
 GA 389OP
 UT ISI:000262104702261
 ER
 
 PT J
 AU Wang, JM
    Lue, SQ
    Yang, JM
    Song, XM
    Chen, L
    Hou, J
    Zhang, WP
    Huan, CM
    Ni, X
    Qiu, HY
 AF Wang, Jianmin
    Lue, Shuqing
    Yang, Jianmin
    Song, Xianmin
    Chen, Li
    Hou, Jun
    Zhang, Weiping
    Huan, Chongmei
    Ni, Xiong
    Qiu, Huiying
 TI A Homoharringtonine-Based Protocol Is Superior to Daunorubicin and
    Idarubicin-Based Protocols in Elderly Patients with Newly-Diagnosed
    Acute Myeloid Leukemia with Comparable Effects and Low Toxicities:
    Experience in a Chinese Center.
 SO BLOOD
 LA English
 DT Meeting Abstract
 CT 50th Annual Meeting of the American- Society-of-Hematology
 CY DEC 06-09, 2008
 CL San Francisco, CA
 SP Amer Soc Hematol
 C1 [Wang, Jianmin; Lue, Shuqing; Yang, Jianmin; Song, Xianmin; Chen, Li; Hou, Jun; Zhang, Weiping; Huan, Chongmei; Ni, Xiong; Qiu, Huiying] Mil Med Coll 2, Changhai Hosp, Dept Hematol, Shanghai, Peoples R China.
 NR 0
 TC 0
 PU AMER SOC HEMATOLOGY
 PI WASHINGTON
 PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
 SN 0006-4971
 J9 BLOOD
 JI Blood
 PD NOV 16
 PY 2008
 VL 112
 IS 11
 BP 679
 EP 679
 PG 1
 SC Hematology
 GA 389OP
 UT ISI:000262104702279
 ER
 
 PT J
 AU Yang, DH
    Ahn, JS
    Kim, YK
    Lee, JJ
    Choi, YJ
    Shin, HJ
    Chung, JS
    Moon, JH
    Chae, YS
    Kim, JG
    Sohn, SK
    Kim, HJ
 AF Yang, Deok-Hwan
    Ahn, Jae Sook
    Kim, Yeo-Kyeoung
    Lee, Je-Jung
    Choi, Young Jin
    Shin, Ho Jin
    Chung, Joo-Seop
    Moon, Joon Ho
    Chae, Yee Soo
    Kim, Jong Gwang
    Sohn, Sang Kyun
    Kim, Hyeoung-Joon
 TI Comparing Standard IPI with Revised-IPI in Patients with Diffuse Large
    B-Cell Lymphoma: Which Has a More Differential Potential for Predicting
    the Outcomes after R-CHOP Chemotherapy
 SO BLOOD
 LA English
 DT Meeting Abstract
 CT 50th Annual Meeting of the American-Society-of-Hematology
 CY DEC 06-09, 2008
 CL San Francisco, CA
 SP Amer Soc Hematol
 C1 [Yang, Deok-Hwan; Ahn, Jae Sook] Chonnam Natl Univ, Hwasun Hosp, Jeollanam Do, South Korea.
    [Ahn, Jae Sook; Kim, Yeo-Kyeoung; Kim, Hyeoung-Joon] Chonnam Natl Univ, Sch Med, Jeollanam Do, South Korea.
    [Choi, Young Jin; Shin, Ho Jin; Chung, Joo-Seop] Pusan Natl Univ, Sch Med, Pusan, South Korea.
    [Moon, Joon Ho; Chae, Yee Soo; Kim, Jong Gwang] Kyungpook Natl Univ Hosp, Taegu, South Korea.
    [Sohn, Sang Kyun] Korean Soc Hematol, Seoul, South Korea.
 NR 0
 TC 0
 PU AMER SOC HEMATOLOGY
 PI WASHINGTON
 PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
 SN 0006-4971
 J9 BLOOD
 JI Blood
 PD NOV 16
 PY 2008
 VL 112
 IS 11
 BP 698
 EP 699
 PG 2
 SC Hematology
 GA 389OP
 UT ISI:000262104702336
 ER
 
 PT J
 AU Lin, CN
    Kao, CY
    Hong, CL
    Ye, PQ
    Miao, CH
    Hamaguchi, N
    Wu, HL
    Shi, GY
    Yang, YL
    Yu, IS
    Tao, MH
    Fang, CC
    Liu, YL
    High, KA
    Lin, SW
 AF Lin, Chia-Ni
    Kao, Chung-Yang
    Hong, Chia-Lun
    Ye, Peiqing
    Miao, Carol H.
    Hamaguchi, Nobuko
    Wu, Hua-Lin
    Shi, Guey-Yueh
    Yang, Yung-Li
    Yu, I-Shing
    Tao, Mi-Hua
    Fang, Cheng-Chieh
    Liu, Yi-Lin
    High, Katherine A.
    Lin, Shu-Wha
 TI Engineered Factor IX with Augmented Clotting Activities in a Hemophilia
    B Mouse Model.
 SO BLOOD
 LA English
 DT Meeting Abstract
 CT 50th Annual Meeting of the American- Society-of-Hematology
 CY DEC 06-09, 2008
 CL San Francisco, CA
 SP Amer Soc Hematol
 C1 [Lin, Chia-Ni; Kao, Chung-Yang; Hong, Chia-Lun; Yu, I-Shing; Lin, Shu-Wha] Natl Taiwan Univ, Coll Med, Dept Clin Sci & Med Biotechnol, Taipei 10764, Taiwan.
    [Ye, Peiqing; Miao, Carol H.] Seattle Childrens Hosp Res Inst, Seattle, WA USA.
    [Miao, Carol H.] Univ Washington, Dept Pediat, Seattle, WA 98195 USA.
    [Hamaguchi, Nobuko] Brandeis Univ, Dept Biochem, Waltham, MA 02254 USA.
    [Wu, Hua-Lin; Shi, Guey-Yueh] Natl Cheng Kung Univ, Coll Med, Dept Biochem, Tainan 70101, Taiwan.
    [Yang, Yung-Li] Natl Taiwan Univ Hosp, Dept Lab Med, Taipei, Taiwan.
    [Tao, Mi-Hua; Fang, Cheng-Chieh] Acad Sinica, Inst Biomed Sci, Taipei, Taiwan.
    [Liu, Yi-Lin] Childrens Hosp Philadelphia, Dept Hematol, Philadelphia, PA 19104 USA.
    [High, Katherine A.] Childrens Hosp Philadelphia, Howard Hughes Med Inst, Philadelphia, PA 19104 USA.
 NR 0
 TC 0
 PU AMER SOC HEMATOLOGY
 PI WASHINGTON
 PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
 SN 0006-4971
 J9 BLOOD
 JI Blood
 PD NOV 16
 PY 2008
 VL 112
 IS 11
 BP 706
 EP 706
 PG 1
 SC Hematology
 GA 389OP
 UT ISI:000262104702358
 ER
 
 PT J
 AU Yang, YW
    Wrench, DJ
    Lister, TA
    Fitzgibbon, J
 AF Yang, Youwen
    Wrench, David J.
    Lister, T. Andrew
    Fitzgibbon, Jude
 TI Recurrent Chromosomal Intermingling Interactions at the BCL2 Locus in
    T(14;18) +Ve and -Ve Cell Lines
 SO BLOOD
 LA English
 DT Meeting Abstract
 CT 50th Annual Meeting of the American- Society-of-Hematology
 CY DEC 06-09, 2008
 CL San Francisco, CA
 SP Amer Soc Hematol
 C1 [Yang, Youwen; Wrench, David J.; Lister, T. Andrew; Fitzgibbon, Jude] Barts & London Queen Marys Sch Med & Dent, London, England.
 NR 0
 TC 0
 PU AMER SOC HEMATOLOGY
 PI WASHINGTON
 PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
 SN 0006-4971
 J9 BLOOD
 JI Blood
 PD NOV 16
 PY 2008
 VL 112
 IS 11
 BP 713
 EP 713
 PG 1
 SC Hematology
 GA 389OP
 UT ISI:000262104702381
 ER
 
 PT J
 AU Ang, AL
    Wang, ZP
    Yang, LY
    Natesan, V
    Poon, M
    Koh, LP
    Goh, YT
    Chowbay, B
    Chuah, C
 AF Ang, Ai Leen
    Wang, Zhen Ping
    Yang, Li Yi
    Natesan, Vallalan
    Poon, Michelle
    Koh, Liang Piu
    Goh, Yeow Tee
    Chowbay, Balram
    Chuah, Charles
 TI The M351T BCR-ABL Kinase Mutation Is Uncommon in Asian Patients with
    Imatinib-Resistant Chronic Myeloid Leukemia: Possible Relationship with
    Imatinib Plasma Levels.
 SO BLOOD
 LA English
 DT Meeting Abstract
 CT 50th Annual Meeting of the American-Society-of-Hematology
 CY DEC 06-09, 2008
 CL San Francisco, CA
 SP Amer Soc Hematol
 C1 [Ang, Ai Leen; Yang, Li Yi; Natesan, Vallalan; Goh, Yeow Tee] Singapore Gen Hosp, Singapore 0316, Singapore.
    [Wang, Zhen Ping; Chowbay, Balram] Natl Canc Ctr, Singapore, Singapore.
    [Poon, Michelle; Koh, Liang Piu] Natl Univ Singapore Hosp, Singapore 0511, Singapore.
    [Chuah, Charles] Singapore Gen Hosp Duke NUS, Grad Sch Med, Singapore, Singapore.
 NR 0
 TC 0
 PU AMER SOC HEMATOLOGY
 PI WASHINGTON
 PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
 SN 0006-4971
 J9 BLOOD
 JI Blood
 PD NOV 16
 PY 2008
 VL 112
 IS 11
 BP 739
 EP 739
 PG 1
 SC Hematology
 GA 389OP
 UT ISI:000262104702455
 ER
 
 PT J
 AU Cataland, S
    Yang, SB
    Horne, A
    Lin, SL
    George, J
    Wu, HF
 AF Cataland, Spero
    Yang, Shangbin
    Horne, April
    Lin, Shili
    George, James
    Wu, Haifeng
 TI Lower ADAMTS13 Activity and Higher Bethesda Units of Antibody Inhibitor
    in Early Remission Are Associated with a Higher Probability of TTP
    Exacerbation.
 SO BLOOD
 LA English
 DT Meeting Abstract
 CT 50th Annual Meeting of the American-Society-of-Hematology
 CY DEC 06-09, 2008
 CL San Francisco, CA
 SP Amer Soc Hematol
 C1 [Cataland, Spero; Yang, Shangbin; Horne, April; Lin, Shili; Wu, Haifeng] Ohio State Univ, Columbus, OH 43210 USA.
    [George, James] Univ Oklahoma, Hlth Sci Ctr, Oklahoma City, OK USA.
 NR 0
 TC 0
 PU AMER SOC HEMATOLOGY
 PI WASHINGTON
 PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
 SN 0006-4971
 J9 BLOOD
 JI Blood
 PD NOV 16
 PY 2008
 VL 112
 IS 11
 BP 802
 EP 802
 PG 1
 SC Hematology
 GA 389OP
 UT ISI:000262104702632
 ER
 
 PT J
 AU Dierov, JK
    Kim, TK
    Yang, XW
    Perl, A
    Burke, BA
    Wang, Z
    Gu, TL
    Gewirtz, AM
    Corey, SJ
    Polakiewicz, R
    Carroll, M
 AF Dierov, Jamil K.
    Kim, Tae Kon
    Yang, Xiaowei
    Perl, Alexander
    Burke, Beth A.
    Wang, Zhu
    Gu, Ting-Lei
    Gewirtz, Alan M.
    Corey, Seth J.
    Polakiewicz, Roberto
    Carroll, Martin
 TI Phosphoproteomic Analysis of Primary Acute Myeloid Leukemia Cells
    Reveals Redundant Roles for Src Family Kinases in AML Survival
 SO BLOOD
 LA English
 DT Meeting Abstract
 CT 50th Annual Meeting of the American- Society-of-Hematology
 CY DEC 06-09, 2008
 CL San Francisco, CA
 SP Amer Soc Hematol
 C1 [Dierov, Jamil K.; Yang, Xiaowei; Wang, Zhu] Univ Penn, Dept Med, Philadelphia, PA 19104 USA.
    [Kim, Tae Kon] Univ Miami, Dept Med, Stem Cell Transplant Program, Miami, FL USA.
    [Perl, Alexander] Univ Penn, Abramson Canc Ctr, Philadelphia, PA 19104 USA.
    [Gu, Ting-Lei; Polakiewicz, Roberto] Cell Signaling Technol Inc, Danvers, MA USA.
    [Gewirtz, Alan M.] Univ Penn, Sch Med, Philadelphia, PA 19104 USA.
    [Corey, Seth J.] Northwestern Univ, Feinberg Sch Med, Div Hematol Oncol & Transplanat Pediat, Chicago, IL 60611 USA.
    [Carroll, Martin] Univ Penn, Div Hematol & Oncol, Philadelphia, PA 19104 USA.
 NR 0
 TC 0
 PU AMER SOC HEMATOLOGY
 PI WASHINGTON
 PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
 SN 0006-4971
 J9 BLOOD
 JI Blood
 PD NOV 16
 PY 2008
 VL 112
 IS 11
 BP 917
 EP 917
 PG 1
 SC Hematology
 GA 389OP
 UT ISI:000262104703090
 ER
 
 PT J
 AU Yang, ML
    Yang, GQ
    Jia, JH
    Ostrov, D
    May, WS
 AF Yang, Mingli
    Yang, George Q.
    Jia, Jinghua
    Ostrov, David
    May, W. Stratford
 TI JAZ "Targeting" Compounds Induce G1 Cell Cycle Arrest Followed by Cell
    Death in Human Leukemia Cells
 SO BLOOD
 LA English
 DT Meeting Abstract
 CT 50th Annual Meeting of the American- Society-of-Hematology
 CY DEC 06-09, 2008
 CL San Francisco, CA
 SP Amer Soc Hematol
 C1 [Yang, Mingli; Yang, George Q.; Jia, Jinghua; May, W. Stratford] Univ Florida, Dept Med, Gainesville, FL USA.
    [Yang, Mingli; Yang, George Q.; Jia, Jinghua; May, W. Stratford] Univ Florida, UF Shands Canc Ctr, Gainesville, FL USA.
    [Ostrov, David] Univ Florida, Dept Pathol Immunol & Lab Med, Gainesville, FL USA.
 NR 0
 TC 0
 PU AMER SOC HEMATOLOGY
 PI WASHINGTON
 PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
 SN 0006-4971
 J9 BLOOD
 JI Blood
 PD NOV 16
 PY 2008
 VL 112
 IS 11
 BP 919
 EP 919
 PG 1
 SC Hematology
 GA 389OP
 UT ISI:000262104703098
 ER
 
 PT J
 AU Kirk, CJ
    Jiang, J
    Muchamuel, T
    Dajee, M
    Swinarski, D
    Aujay, M
    Bennett, MK
    Yang, JF
    Lewis, E
    Laidig, G
    Molineaux, CJ
 AF Kirk, Christopher J.
    Jiang, Jing
    Muchamuel, Tony
    Dajee, Maya
    Swinarski, Deborah
    Aujay, Monette
    Bennett, Mark K.
    Yang, Jinfu
    Lewis, Evan
    Laidig, Guy
    Molineaux, Christopher J.
 TI The Selective Proteasome Inhibitor Carfilzomib Is Well Tolerated in
    Experimental Animals with Dose Intensive Administration.
 SO BLOOD
 LA English
 DT Meeting Abstract
 CT 50th Annual Meeting of the American- Society-of-Hematology
 CY DEC 06-09, 2008
 CL San Francisco, CA
 SP Amer Soc Hematol
 C1 [Kirk, Christopher J.; Jiang, Jing; Muchamuel, Tony; Dajee, Maya; Swinarski, Deborah; Aujay, Monette; Bennett, Mark K.; Yang, Jinfu; Lewis, Evan; Laidig, Guy] Proteolix Inc, Res, San Francisco, CA USA.
 NR 0
 TC 0
 PU AMER SOC HEMATOLOGY
 PI WASHINGTON
 PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
 SN 0006-4971
 J9 BLOOD
 JI Blood
 PD NOV 16
 PY 2008
 VL 112
 IS 11
 BP 954
 EP 954
 PG 1
 SC Hematology
 GA 389OP
 UT ISI:000262104703204
 ER
 
 PT J
 AU Rhein, M
    Yang, M
    Kaever, V
    Meyer, J
    Baum, C
    Li, ZX
 AF Rhein, Mathias
    Yang, Min
    Kaever, Volkhard
    Meyer, Johann
    Baum, Christopher
    Li, Zhixiong
 TI Leukemia Induced by Altered TRK-Signaling Is Sensitive to Rapamycin
    Treatment in a Preclinical Model.
 SO BLOOD
 LA English
 DT Meeting Abstract
 CT 50th Annual Meeting of the American- Society-of-Hematology
 CY DEC 06-09, 2008
 CL San Francisco, CA
 SP Amer Soc Hematol
 C1 [Kaever, Volkhard] Hannover Med Sch, Inst Pharmacol, D-3000 Hannover, Germany.
 NR 0
 TC 0
 PU AMER SOC HEMATOLOGY
 PI WASHINGTON
 PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
 SN 0006-4971
 J9 BLOOD
 JI Blood
 PD NOV 16
 PY 2008
 VL 112
 IS 11
 BP 984
 EP 984
 PG 1
 SC Hematology
 GA 389OP
 UT ISI:000262104703290
 ER
 
 PT J
 AU Yang, H
    Lang, S
    Zhai, ZM
    Spring, CM
    Reheman, A
    Chen, PG
    Flick, MJ
    Degen, JL
    Li, L
    Kahr, WHA
    Freedman, J
    Ni, HY
 AF Yang, Hong
    Lang, Sean
    Zhai, Zhimin
    Spring, Christopher M.
    Reheman, Adili
    Chen, Pingguo
    Flick, Matthew J.
    Degen, Jay L.
    Li, Ling
    Kahr, Walter H. A.
    Freedman, John
    Ni, Heyu
 TI Engagement of Fibrinogen and beta 3 Integrin Is Required for
    Maintenance of Platelet Intracellular and Cell Surface P-Selectin
    Expression.
 SO BLOOD
 LA English
 DT Meeting Abstract
 CT 50th Annual Meeting of the American- Society-of-Hematology
 CY DEC 06-09, 2008
 CL San Francisco, CA
 SP Amer Soc Hematol
 C1 [Yang, Hong; Lang, Sean; Reheman, Adili; Ni, Heyu] Univ Toronto, St Michaels Hosp, Dept Lab Med & Pathobiol, Toronto, ON M5B 1W8, Canada.
    [Yang, Hong; Lang, Sean; Spring, Christopher M.; Chen, Pingguo; Ni, Heyu] Canadian Blood Serv, Toronto, ON, Canada.
    [Zhai, Zhimin] Anhui Med Univ, Affiliated Hosp 2, Anhui Prov Hosp, Canc Lab, Hefei, Peoples R China.
    [Spring, Christopher M.; Chen, Pingguo] St Michaels Hosp, Dept Lab Med, Toronto, ON M5B 1W8, Canada.
    [Flick, Matthew J.; Degen, Jay L.] Childrens Hosp Res Fdn, Cincinnati, OH 45229 USA.
    [Flick, Matthew J.; Degen, Jay L.] Univ Cincinnati, Cincinnati, OH USA.
    [Li, Ling] Hosp Sick Children, Cell Biol Program, Toronto, ON M5G 1X8, Canada.
    [Kahr, Walter H. A.] Hosp Sick Children, Div Hematol Oncol, Toronto, ON M5G 1X8, Canada.
    [Ni, Heyu] Univ Toronto, St Michaels Hosp, Dept Med & Physiol, Toronto, ON M5B 1W8, Canada.
    [Freedman, John] St Michaels Hosp, Dept Med, Toronto, ON M5B 1W8, Canada.
    [Freedman, John] St Michaels Hosp, Dept Lab Med & Pathobiol, Toronto, ON M5B 1W8, Canada.
 NR 0
 TC 0
 PU AMER SOC HEMATOLOGY
 PI WASHINGTON
 PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
 SN 0006-4971
 J9 BLOOD
 JI Blood
 PD NOV 16
 PY 2008
 VL 112
 IS 11
 BP 989
 EP 989
 PG 1
 SC Hematology
 GA 389OP
 UT ISI:000262104703307
 ER
 
 PT J
 AU Xing, DX
    Ramsay, AG
    Gribben, JG
    Decker, WK
    Burt, JK
    Li, SF
    Simon, SN
    Yang, H
    Cooper, L
    McMannis, JD
    Champlin, RE
    Shpall, EJ
    Zweidler-McKay, P
    Bollard, CM
 AF Xing, Dongxia
    Ramsay, Alan G.
    Gribben, John G.
    Decker, William K.
    Burt, Jared K.
    Li, Sufang
    Simon, Simon N.
    Yang, Hong
    Cooper, Laurence
    McMannis, John D.
    Champlin, Richard E.
    Shpall, Elizabeth J.
    Zweidler-McKay, Patrick
    Bollard, Catherine M.
 TI Ex Vivo Expansion of Cord Blood Natural Killer Cells Overcomes Impaired
    Immune Synapse Formation and Effector Function in Acute Myeloid Leukemia
 SO BLOOD
 LA English
 DT Meeting Abstract
 CT 50th Annual Meeting of the American- Society-of-Hematology
 CY DEC 06-09, 2008
 CL San Francisco, CA
 SP Amer Soc Hematol
 C1 [Xing, Dongxia; Decker, William K.; Burt, Jared K.; Li, Sufang; Simon, Simon N.; Yang, Hong; Cooper, Laurence; McMannis, John D.; Champlin, Richard E.; Shpall, Elizabeth J.; Zweidler-McKay, Patrick] Univ Texas MD Anderson Canc Ctr, Houston, TX 77030 USA.
    [Ramsay, Alan G.; Gribben, John G.] Barts & London Queen Marys Sch Med & Dent, Ctr Med Oncol, London, England.
    [Bollard, Catherine M.] Baylor Coll Med, Houston, TX 77030 USA.
 NR 0
 TC 0
 PU AMER SOC HEMATOLOGY
 PI WASHINGTON
 PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
 SN 0006-4971
 J9 BLOOD
 JI Blood
 PD NOV 16
 PY 2008
 VL 112
 IS 11
 BP 999
 EP 999
 PG 1
 SC Hematology
 GA 389OP
 UT ISI:000262104703342
 ER
 
 PT J
 AU Jiang, EZ
    Yu, M
    Hsieh, YT
    DeLaTorre, B
    Kadavallore, A
    Scharman, C
    Park, E
    Yang, AS
    Muschen, M
    Groffen, J
    Heisterkamp, N
    Kim, YM
 AF Jiang, Enzi
    Yu, Min
    Hsieh, Yao-Te
    DeLaTorre, Brian
    Kadavallore, Asha
    Scharman, Carlton
    Park, Eugene
    Yang, Allen S.
    Muschen, Markus
    Groffen, John
    Heisterkamp, Nora
    Kim, Yong-Mi
 TI Preclinical Evaluation of Adjuvant Therapy with AMD3100 for Drug
    Resistant Philadelphia Chromosome Positive and Negative ALL
 SO BLOOD
 LA English
 DT Meeting Abstract
 CT 50th Annual Meeting of the American- Society-of-Hematology
 CY DEC 06-09, 2008
 CL San Francisco, CA
 SP Amer Soc Hematol
 C1 [Jiang, Enzi; Yu, Min; Hsieh, Yao-Te; DeLaTorre, Brian; Kadavallore, Asha; Scharman, Carlton; Park, Eugene; Muschen, Markus; Groffen, John; Heisterkamp, Nora; Kim, Yong-Mi] CHLA USC, Los Angeles, CA USA.
    [Yang, Allen S.] Univ So Calif, Jane Anne Nohl Div Hematol, Los Angeles, CA USA.
 NR 0
 TC 0
 PU AMER SOC HEMATOLOGY
 PI WASHINGTON
 PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
 SN 0006-4971
 J9 BLOOD
 JI Blood
 PD NOV 16
 PY 2008
 VL 112
 IS 11
 BP 1005
 EP 1005
 PG 1
 SC Hematology
 GA 389OP
 UT ISI:000262104703359
 ER
 
 PT J
 AU Yang, BY
    Sheehan, JP
 AF Yang, Buyue
    Sheehan, John P.
 TI Depolymerized Holothurian Glycosaminoglycan Inhibits Plasma Thrombin
    Generation Via Interaction with the Factor IXa Heparin-Binding Exosite
 SO BLOOD
 LA English
 DT Meeting Abstract
 CT 50th Annual Meeting of the American- Society-of-Hematology
 CY DEC 06-09, 2008
 CL San Francisco, CA
 SP Amer Soc Hematol
 C1 [Sheehan, John P.] Univ Wisconsin, Dept Med Hematol Oncol, Madison, WI USA.
 NR 0
 TC 0
 PU AMER SOC HEMATOLOGY
 PI WASHINGTON
 PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
 SN 0006-4971
 J9 BLOOD
 JI Blood
 PD NOV 16
 PY 2008
 VL 112
 IS 11
 BP 1058
 EP 1058
 PG 1
 SC Hematology
 GA 389OP
 UT ISI:000262104703518
 ER
 
 PT J
 AU Koh, Y
    Kim, DY
    Kwon, HC
    Kim, MK
    Kim, BS
    Kim, YK
    Kim, I
    Kim, JS
    Kim, JS
    Kim, CS
    Kim, HJ
    Kwak, JY
    Lee, NR
    Min, YH
    Park, CW
    Sohn, SK
    Shin, HJ
    Oh, SJ
    Yoon, SS
    Lee, JH
    Zang, DY
    Chung, J
    Cheong, JW
    Jung, CW
    Jo, DY
    Chung, YJ
    Jung, SH
    Xu, HD
    Byun, HM
    Yang, AS
    Park, S
 AF Koh, Youngil
    Kim, Dae-Young
    Kwon, Hyuk-Chan
    Kim, Min Kyoung
    Kim, Byung-Soo
    Kim, Yu-Kyung
    Kim, Inho
    Kim, Jae Seog
    Kim, Jin Seog
    Kim, Chul Soo
    Kim, Hyeoung-Joon
    Kwak, Jae-Yong
    Lee, Na-Ri
    Min, Yoo-Hong
    Park, Chong Won
    Sohn, Sang Kyun
    Shin, Ho-Jin
    Oh, Suk Joong
    Yoon, Sung-Soo
    Lee, Jung-Hee
    Zang, Dae Young
    Chung, Jooseop
    Cheong, Jun-Won
    Jung, Chul W.
    Jo, Deog-Yeon
    Chung, Yeun-Jun
    Jung, Seung-Hyun
    Xu, Hai-Dong
    Byun, Hyang-Min
    Yang, Allen S.
    Park, Seonyang
 TI Molecular Predictive Markers in Dose Escalation Treatment for
    Suboptimal Responders to Standard Dose Imatinib in CML
 SO BLOOD
 LA English
 DT Meeting Abstract
 CT 50th Annual Meeting of the American- Society-of-Hematology
 CY DEC 06-09, 2008
 CL San Francisco, CA
 SP Amer Soc Hematol
 C1 [Koh, Youngil; Kwon, Hyuk-Chan; Kim, Min Kyoung; Kim, Yu-Kyung; Kim, Inho; Kim, Jae Seog; Kim, Jin Seog; Kim, Hyeoung-Joon; Kwak, Jae-Yong; Min, Yoo-Hong; Park, Chong Won; Sohn, Sang Kyun; Shin, Ho-Jin; Oh, Suk Joong; Zang, Dae Young; Chung, Jooseop; Cheong, Jun-Won; Jung, Chul W.; Jo, Deog-Yeon] Korean Soc Hematol, CML Working Party, Seoul, South Korea.
    [Kim, Dae-Young] Univ Ulsan, Coll Med, Asan Med Ctr, Dept Hematol, Seoul, South Korea.
    [Kim, Byung-Soo] Korea Univ, Med Ctr, Seoul, South Korea.
    [Kim, Chul Soo] Inha Univ, Seoul, South Korea.
    [Lee, Na-Ri] Cheonbuk Natl Univ, Sch Med, Cheonju, South Korea.
    [Park, Seonyang] Seoul Natl Univ, Coll Med, Dept Internal Med, Seoul 151, South Korea.
    [Chung, Yeun-Jun; Jung, Seung-Hyun; Xu, Hai-Dong] Catholic Univ, Coll Med, Integrated Res Ctr Genome Polymorphism, Dept Microbiol, Seoul, South Korea.
    [Byun, Hyang-Min] Univ So Calif, Norris Canc Ctr, Los Angeles, CA USA.
    [Yang, Allen S.] Univ So Calif, Jane Anne Nohl Div Hematol, Los Angeles, CA USA.
 NR 0
 TC 0
 PU AMER SOC HEMATOLOGY
 PI WASHINGTON
 PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
 SN 0006-4971
 J9 BLOOD
 JI Blood
 PD NOV 16
 PY 2008
 VL 112
 IS 11
 BP 1105
 EP 1106
 PG 2
 SC Hematology
 GA 389OP
 UT ISI:000262104703658
 ER
 
 PT J
 AU Cortes, J
    O'Brien, S
    Ault, P
    Borthakur, G
    Jabbour, E
    Bradley-Garelik, B
    Debreczeni, K
    Yang, D
    Liu, D
    Kantarjian, H
 AF Cortes, Jorge
    O'Brien, Susan
    Ault, Patricia
    Borthakur, Gautam
    Jabbour, Elias
    Bradley-Garelik, Brigid
    Debreczeni, Krisztina
    Yang, Daniel
    Liu, David
    Kantarjian, Hagop
 TI Pregnancy Outcomes among Patients with Chronic Myeloid Leukemia Treated
    with Dasatinib
 SO BLOOD
 LA English
 DT Meeting Abstract
 CT 50th Annual Meeting of the American-Society-of-Hematology
 CY DEC 06-09, 2008
 CL San Francisco, CA
 SP Amer Soc Hematol
 C1 [Cortes, Jorge; O'Brien, Susan; Ault, Patricia; Borthakur, Gautam; Jabbour, Elias; Kantarjian, Hagop] Univ Texas MD Anderson Canc Ctr, Houston, TX 77030 USA.
    [Bradley-Garelik, Brigid; Yang, Daniel; Liu, David] Bristol Myers Squibb Co, Wallingford, CT 06492 USA.
    [Debreczeni, Krisztina] Bristol Myers Squibb Co, Pennington, NJ USA.
 NR 0
 TC 0
 PU AMER SOC HEMATOLOGY
 PI WASHINGTON
 PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
 SN 0006-4971
 J9 BLOOD
 JI Blood
 PD NOV 16
 PY 2008
 VL 112
 IS 11
 BP 1109
 EP 1109
 PG 1
 SC Hematology
 GA 389OP
 UT ISI:000262104703667
 ER
 
 PT J
 AU Lipton, JH
    le Coutre, PD
    Wang, J
    Yang, M
    Szczudlo, T
    Giles, F
 AF Lipton, Jeffrey H.
    le Coutre, Philipp D.
    Wang, Jim
    Yang, Mindy
    Szczudlo, Tomasz
    Giles, Francis
 TI Nilotinib in Elderly Chronic Myeloid Leukemia Patients in Chronic Phase
    (CML-CP) with Imatinib Resistance or Intolerance: Efficacy and Safety
    Analysis
 SO BLOOD
 LA English
 DT Meeting Abstract
 CT 50th Annual Meeting of the American- Society-of-Hematology
 CY DEC 06-09, 2008
 CL San Francisco, CA
 SP Amer Soc Hematol
 C1 [Lipton, Jeffrey H.] Princess Margaret Hosp, Toronto, ON M4X 1K9, Canada.
    [le Coutre, Philipp D.] Humboldt Univ, Charite, Dept Hematol & Oncol, Berlin, Germany.
    [Wang, Jim] Novartis Pharmaceut, E Hanover, NJ USA.
    [Yang, Mindy; Szczudlo, Tomasz] Novartis Pharmaceut, E Hanover, NJ USA.
    [Giles, Francis] Univ Texas Hlth Sci Ctr San Antonio, CTRC, Inst Drug Dev, San Antonio, TX 78229 USA.
 NR 0
 TC 0
 PU AMER SOC HEMATOLOGY
 PI WASHINGTON
 PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
 SN 0006-4971
 J9 BLOOD
 JI Blood
 PD NOV 16
 PY 2008
 VL 112
 IS 11
 BP 1110
 EP 1110
 PG 1
 SC Hematology
 GA 389OP
 UT ISI:000262104703670
 ER
 
 PT J
 AU Maddipoti, SC
    Bueso-Ramos, C
    Yang, H
    Fernandez, M
    Kuang, SQ
    Fang, ZH
    Stevenson, W
    Wei, Y
    Pierce, S
    Garcia-Manero, G
 AF Maddipoti, Sirisha C.
    Bueso-Ramos, Carlos
    Yang, Hui
    Fernandez, Michael
    Kuang, Shaoquing
    Fang, Zihong
    Stevenson, William
    Wei, Yue
    Pierce, Sherry
    Garcia-Manero, Guillermo
 TI Epigenetic Silencing of the RUNX3 Gene by Promoter Hypermethylation in
    Patients with Acute Myeloid Leukemia
 SO BLOOD
 LA English
 DT Meeting Abstract
 CT 50th Annual Meeting of the American- Society-of-Hematology
 CY DEC 06-09, 2008
 CL San Francisco, CA
 SP Amer Soc Hematol
 C1 [Maddipoti, Sirisha C.; Yang, Hui; Kuang, Shaoquing; Fang, Zihong; Stevenson, William; Wei, Yue; Pierce, Sherry; Garcia-Manero, Guillermo] Univ Texas MD Anderson Canc Ctr, Dept Leukemia, Houston, TX 77030 USA.
    [Bueso-Ramos, Carlos; Fernandez, Michael] Univ Texas MD Anderson Canc Ctr, Dept Hematopathol, Houston, TX 77030 USA.
 NR 0
 TC 0
 PU AMER SOC HEMATOLOGY
 PI WASHINGTON
 PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
 SN 0006-4971
 J9 BLOOD
 JI Blood
 PD NOV 16
 PY 2008
 VL 112
 IS 11
 BP 1148
 EP 1148
 PG 1
 SC Hematology
 GA 389OP
 UT ISI:000262104703777
 ER
 
 PT J
 AU Bhojwani, D
    Wang, J
    Yang, JJ
    Morrison, D
    Devidas, M
    Raetz, E
    Hunger, SP
    Relling, MV
    Carroll, WL
 AF Bhojwani, Deepa
    Wang, Jinhua
    Yang, Jun J.
    Morrison, Debra
    Devidas, Meenakshi
    Raetz, Elizabeth
    Hunger, Stephen P.
    Relling, Mary V.
    Carroll, William L.
 TI Evolution of Gene Expression Signatures in Relapsed Childhood Acute
    Lymphoblastic Leukemia Differs Based on Timing of Relapse
 SO BLOOD
 LA English
 DT Meeting Abstract
 CT 50th Annual Meeting of the American- Society-of-Hematology
 CY DEC 06-09, 2008
 CL San Francisco, CA
 SP Amer Soc Hematol
 C1 [Bhojwani, Deepa; Yang, Jun J.; Relling, Mary V.] St Jude Childrens Hosp, Memphis, TN 38105 USA.
    [Wang, Jinhua; Morrison, Debra; Raetz, Elizabeth] NYU, Med Ctr, New York, NY 10016 USA.
    [Devidas, Meenakshi] Univ Florida, Coll Med, Dept Epidemiol & Hlth Policy Res, Gainesville, FL USA.
    [Hunger, Stephen P.] Childrens Hosp, Aurora, CO USA.
    [Hunger, Stephen P.] Univ Colorado, Sch Dent Med, Aurora, CO USA.
    [Carroll, William L.] NYU, Inst Canc, New York, NY USA.
 NR 0
 TC 0
 PU AMER SOC HEMATOLOGY
 PI WASHINGTON
 PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
 SN 0006-4971
 J9 BLOOD
 JI Blood
 PD NOV 16
 PY 2008
 VL 112
 IS 11
 BP 1149
 EP 1149
 PG 1
 SC Hematology
 GA 389OP
 UT ISI:000262104703781
 ER
 
 PT J
 AU Kuang, SQ
    Zweidler-McKay, P
    Yang, H
    Fang, ZH
    Tong, WG
    Garcia-Mancro, G
 AF Kuang, Shaoqing
    Zweidler-McKay, Patrick
    Yang, Hui
    Fang, Zhi Hong
    Tong, Weigang
    Garcia-Mancro, Guillermo
 TI Epigenetic Inactivation of Notch Signaling Target Genes RES in B Cell
    Acute Lymphoblastic Leukemia
 SO BLOOD
 LA English
 DT Meeting Abstract
 CT 50th Annual Meeting of the American- Society-of-Hematology
 CY DEC 06-09, 2008
 CL San Francisco, CA
 SP Amer Soc Hematol
 C1 [Kuang, Shaoqing; Yang, Hui; Fang, Zhi Hong; Tong, Weigang; Garcia-Mancro, Guillermo] Univ Texas MD Anderson Canc Ctr, Dept Leukemia, Houston, TX 77030 USA.
    [Zweidler-McKay, Patrick] Univ Texas MD Anderson Canc Ctr, Div Pediat, Houston, TX 77030 USA.
 NR 0
 TC 0
 PU AMER SOC HEMATOLOGY
 PI WASHINGTON
 PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
 SN 0006-4971
 J9 BLOOD
 JI Blood
 PD NOV 16
 PY 2008
 VL 112
 IS 11
 BP 1157
 EP 1157
 PG 1
 SC Hematology
 GA 389OP
 UT ISI:000262104703808
 ER
 
 PT J
 AU Zhou, RF
    Ou-Yang, J
    Chang, DY
    Xu, JY
    Chen, B
    Yang, YG
    Zhang, QG
    Shao, XY
 AF Zhou, Rong-Fu
    Ou-yang, Jian
    Chang, Da-Yu
    Xu, Jing-Yan
    Chen, Bing
    Yang, Yong-Gong
    Zhang, Qi-Guo
    Shao, Xiao-Yan
 TI Profiles of Th1, Th2, Th17 and Treg Cells in Patients with Chronic
    Idiopathic Thrombocytopenic Purpura
 SO BLOOD
 LA English
 DT Meeting Abstract
 CT 50th Annual Meeting of the American- Society-of-Hematology
 CY DEC 06-09, 2008
 CL San Francisco, CA
 SP Amer Soc Hematol
 C1 [Zhou, Rong-Fu; Ou-yang, Jian; Chang, Da-Yu; Xu, Jing-Yan; Chen, Bing; Yang, Yong-Gong; Zhang, Qi-Guo; Shao, Xiao-Yan] Nanjing Univ, Nanjing Drum Tower Hosp, Nanjing, Peoples R China.
 NR 0
 TC 0
 PU AMER SOC HEMATOLOGY
 PI WASHINGTON
 PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
 SN 0006-4971
 J9 BLOOD
 JI Blood
 PD NOV 16
 PY 2008
 VL 112
 IS 11
 BP 1168
 EP 1168
 PG 1
 SC Hematology
 GA 389OP
 UT ISI:000262104704022
 ER
 
 PT J
 AU Zhang, XL
    Chen, SH
    Yang, LJ
    Zhu, K
    Li, YQ
 AF Zhang, Xueli
    Chen, Shaohua
    Yang, Lijian
    Zhu, Kanger
    Li, Yangqiu
 TI The Feature of TCR V gamma And TCR V delta Repertoire Distribution and
    Clonality in Patients with Immune Thrombocytopeine Purpura
 SO BLOOD
 LA English
 DT Meeting Abstract
 CT 50th Annual Meeting of the American-Society-of-Hematology
 CY DEC 06-09, 2008
 CL San Francisco, CA
 SP Amer Soc Hematol
 C1 [Zhang, Xueli; Zhu, Kanger] Jinan Univ, Dept Hematol, Affiliated Hosp 1, Guangzhou, Guangdong, Peoples R China.
    [Chen, Shaohua; Yang, Lijian] Jinan Univ, Inst Hematol, Coll Med, Guangzhou, Guangdong, Peoples R China.
 NR 0
 TC 0
 PU AMER SOC HEMATOLOGY
 PI WASHINGTON
 PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
 SN 0006-4971
 J9 BLOOD
 JI Blood
 PD NOV 16
 PY 2008
 VL 112
 IS 11
 BP 1169
 EP 1169
 PG 1
 SC Hematology
 GA 389OP
 UT ISI:000262104704027
 ER
 
 PT J
 AU Kundu, M
    Yang, CY
    McCastlain, K
    Wu, JM
    Zhang, J
    Lindsten, T
    Ney, P
    Thompson, CB
 AF Kundu, Mondira
    Yang, Chia-Ying
    McCastlain, Kelly
    Wu, Junmin
    Zhang, Ji
    Lindsten, Tullia
    Ney, Paul
    Thompson, Craig B.
 TI Hsp90 regulates Ulk1-mediated autophagic clearance of mitochondria
 SO BLOOD
 LA English
 DT Meeting Abstract
 CT 50th Annual Meeting of the American- Society-of-Hematology
 CY DEC 06-09, 2008
 CL San Francisco, CA
 SP Amer Soc Hematol
 C1 [Kundu, Mondira; McCastlain, Kelly; Zhang, Ji] Dept Pathol, Memphis, TN USA.
    [Wu, Junmin; Lindsten, Tullia] Abramson Family Canc IRes Inst, Philadelphia, PA USA.
    [Ney, Paul] St Jude Childrens Rsch Hosp, Memphis, TN USA.
    [Thompson, Craig B.] Univ Penn, Sch Med, Myeloma Program, Abramson Canc Ctr, Philadelphia, PA 19104 USA.
 NR 0
 TC 0
 PU AMER SOC HEMATOLOGY
 PI WASHINGTON
 PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
 SN 0006-4971
 J9 BLOOD
 JI Blood
 PD NOV 16
 PY 2008
 VL 112
 IS 11
 BP 1186
 EP 1186
 PG 1
 SC Hematology
 GA 389OP
 UT ISI:000262104704076
 ER
 
 PT J
 AU Chang, MH
    Kim, SJ
    Kim, WS
    Choi, CW
    Suh, C
    Kim, SH
    Yang, DH
    Won, JH
    Il Lee, S
 AF Chang, Myung Hee
    Kim, Seck Jin
    Kim, Won Seog
    Choi, Chul Won
    Suh, Cheolwon
    Kim, Sung Hyun
    Yang, Deok-Hwan
    Won, Jong-Ho
    Il Lee, Soon
 TI Treatment Outcome and Prognostic Factors in Patients with Precursor B
    and T Lymphoblastic Lymphoma.
 SO BLOOD
 LA English
 DT Meeting Abstract
 CT 50th Annual Meeting of the American- Society-of-Hematology
 CY DEC 06-09, 2008
 CL San Francisco, CA
 SP Amer Soc Hematol
 C1 [Chang, Myung Hee; Kim, Seck Jin; Kim, Won Seog] Sungkyunkwan Univ, Sch Med, Samsung Med Ctr, Seoul, South Korea.
    [Choi, Chul Won] Korea Univ, Guro Hosp, Seoul, South Korea.
    [Suh, Cheolwon] Asan Med Ctr, Seoul, South Korea.
    [Kim, Sung Hyun] Dong A Univ Hosp, Dept Hem Onc, Pusan, South Korea.
    [Yang, Deok-Hwan] Chonnam Natl Univ, Hwasun Hosp, Jeollanam Do, South Korea.
    [Won, Jong-Ho] Soon Chun Hyang Univ Hosp, Seoul, South Korea.
    [Il Lee, Soon] Dankook Univ, Coll Med, Cheonan, South Korea.
 NR 0
 TC 0
 PU AMER SOC HEMATOLOGY
 PI WASHINGTON
 PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
 SN 0006-4971
 J9 BLOOD
 JI Blood
 PD NOV 16
 PY 2008
 VL 112
 IS 11
 BP 1232
 EP 1232
 PG 1
 SC Hematology
 GA 389OP
 UT ISI:000262104704219
 ER
 
 PT J
 AU Muchamuel, T
    Aujay, M
    Bennett, MK
    Dajee, M
    Demo, S
    Kirk, CJ
    Fang, Y
    Jiang, J
    Lewis, E
    Lu, Y
    Laidig, G
    Parlati, F
    Shields, J
    Sun, CM
    Yang, JF
    Zhou, HJ
 AF Muchamuel, Tony
    Aujay, Monette
    Bennett, Mark K.
    Dajee, Maya
    Demo, Susan
    Kirk, Christopher J.
    Fang, Ying
    Jiang, Jing
    Lewis, Evan
    Lu, Yan
    Laidig, Guy
    Parlati, Francesco
    Shields, Jamie
    Sun, Congcong m
    Yang, Jinfiu
    Zhou, Han-Jie
 TI Preclinical Pharmacology and in Vitro Characterization of PR-047, An
    Oral Inhibitor of the 20S Proteasome
 SO BLOOD
 LA English
 DT Meeting Abstract
 CT 50th Annual Meeting of the American- Society-of-Hematology
 CY DEC 06-09, 2008
 CL San Francisco, CA
 SP Amer Soc Hematol
 C1 [Muchamuel, Tony; Aujay, Monette; Bennett, Mark K.; Dajee, Maya; Demo, Susan; Kirk, Christopher J.; Fang, Ying; Jiang, Jing; Lewis, Evan; Lu, Yan; Laidig, Guy; Parlati, Francesco; Shields, Jamie; Sun, Congcong m; Yang, Jinfiu; Zhou, Han-Jie] Proteolix Inc, Res, San Francisco, CA USA.
 NR 0
 TC 0
 PU AMER SOC HEMATOLOGY
 PI WASHINGTON
 PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
 SN 0006-4971
 J9 BLOOD
 JI Blood
 PD NOV 16
 PY 2008
 VL 112
 IS 11
 BP 1257
 EP 1257
 PG 1
 SC Hematology
 GA 389OP
 UT ISI:000262104704289
 ER
 
 PT J
 AU Kim, YK
    Lee, JJ
    Sohn, SK
    Shin, HJ
    Chung, JS
    Choi, YJ
    Moon, JH
    Chae, YS
    Kim, JG
    Ahn, JS
    Yang, DH
    Kim, HJ
 AF Kim, Yeo-Kyeoung
    Lee, Je-Jung
    Sohn, Sang-Kyun
    Shin, Ho-Jin
    Chung, Joo-Seop
    Choi, Young-Jin
    Moon, Joon-Ho
    Chae, Yee-Soo
    Kim, Jong-Gwang
    Ahn, Jae-Sook
    Yang, Deok-Hwan
    Kim, Hyeoung-Joon
 CA KMMWP
 TI Results of a Phase II Multicenter Study of Immunochemotherapy with
    Fludarabine, Cyclophosphamide and Rituximab (FCR) for Symptomatic
    Waldenstrom's Macroglobulinemia.
 SO BLOOD
 LA English
 DT Meeting Abstract
 CT 50th Annual Meeting of the American- Society-of-Hematology
 CY DEC 06-09, 2008
 CL San Francisco, CA
 SP Amer Soc Hematol
 C1 [Kim, Yeo-Kyeoung; Lee, Je-Jung; Ahn, Jae-Sook; Yang, Deok-Hwan; Kim, Hyeoung-Joon] Chonnam Natl Univ, Sch Med, Kwangju, South Korea.
    [Sohn, Sang-Kyun; Moon, Joon-Ho; Chae, Yee-Soo; Kim, Jong-Gwang] Kyungpook Natl Univ, Sch Med, Taegu, South Korea.
    [Shin, Ho-Jin; Chung, Joo-Seop; Choi, Young-Jin] Pusan Natl Univ, Sch Med, Pusan, South Korea.
    [KMMWP] KMMWP, Seoul, South Korea.
 NR 0
 TC 1
 PU AMER SOC HEMATOLOGY
 PI WASHINGTON
 PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
 SN 0006-4971
 J9 BLOOD
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 PD NOV 16
 PY 2008
 VL 112
 IS 11
 BP 1265
 EP 1265
 PG 1
 SC Hematology
 GA 389OP
 UT ISI:000262104704311
 ER
 
 PT J
 AU Yang, Z
    Kondo, T
    Voorhorst, CS
    Nabinger, SC
    Ndong, L
    Yin, FQ
    Chan, EM
    Wurstlin, O
    Kratz, C
    Niemeyer, CM
    Flotho, C
    Hashino, E
    Chan, R
 AF Yang, Zhenyun
    Kondo, Takako
    Voorhorst, Cara S.
    Nabinger, Sarah C.
    Ndong, Leila
    Yin, Fuqin
    Chan, Edward M.
    Wurstlin, Oliver
    Kratz, Christian
    Niemeyer, Charlotte Marie
    Flotho, Christian
    Hashino, Eri
    Chan, Rebecca
 TI Increased C-Jun and Reduced GATA2 Expression Promotes Aberrant
    Monocytic Differentiation and Expansion Induced by Activating PTPN11
    Mutants
 SO BLOOD
 LA English
 DT Meeting Abstract
 CT 50th Annual Meeting of the American- Society-of-Hematology
 CY DEC 06-09, 2008
 CL San Francisco, CA
 SP Amer Soc Hematol
 C1 [Yang, Zhenyun; Kondo, Takako; Voorhorst, Cara S.; Nabinger, Sarah C.; Ndong, Leila; Yin, Fuqin; Hashino, Eri; Chan, Rebecca] Indiana Univ, Sch Med, Indianapolis, IN USA.
    [Chan, Edward M.] Eli Lilly & Co, Indianapolis, IN 46285 USA.
    [Wurstlin, Oliver; Kratz, Christian; Niemeyer, Charlotte Marie; Flotho, Christian] Univ Freiburg, Freiburg, Germany.
 NR 0
 TC 0
 PU AMER SOC HEMATOLOGY
 PI WASHINGTON
 PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
 SN 0006-4971
 J9 BLOOD
 JI Blood
 PD NOV 16
 PY 2008
 VL 112
 IS 11
 BP 1275
 EP 1276
 PG 2
 SC Hematology
 GA 389OP
 UT ISI:000262104704338
 ER
 
 PT J
 AU Chan, G
    Kalaitzidis, D
    Usenko, T
    Kutok, J
    Yang, WT
    Mohi, G
    Neel, B
 AF Chan, Goedon
    Kalaitzidis, Demetrios
    Usenko, Tatiana
    Kutok, Jeffery
    Yang, Wentian
    Mohi, Golam
    Neel, Benjamin
 TI Expression of Leukemogenic Ptpn11 Causes a Fatal Myeloproliferative
    Disorder by Affecting Multiple Stages of Hematopoiesis.
 SO BLOOD
 LA English
 DT Meeting Abstract
 CT 50th Annual Meeting of the American- Society-of-Hematology
 CY DEC 06-09, 2008
 CL San Francisco, CA
 SP Amer Soc Hematol
 C1 [Chan, Goedon; Usenko, Tatiana] Ontario Canc Inst, Dept Stem Cell & Dev Biol, Toronto, ON M4X 1K9, Canada.
    [Neel, Benjamin] Beth Israel Deaconess Med Ctr, Canc Biol Program, Boston, MA 02215 USA.
    [Kutok, Jeffery] Harvard Univ, Brigham & Womens Hosp, Sch Med, Boston, MA 02115 USA.
    [Yang, Wentian] Brown Univ, Alpert Med Sch, Dept Orthoped, Providence, RI 02912 USA.
    [Mohi, Golam] Upstate Med Univ, Dept Pharmacol, Syracuse, NY USA.
 NR 0
 TC 0
 PU AMER SOC HEMATOLOGY
 PI WASHINGTON
 PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
 SN 0006-4971
 J9 BLOOD
 JI Blood
 PD NOV 16
 PY 2008
 VL 112
 IS 11
 BP 1280
 EP 1280
 PG 1
 SC Hematology
 GA 389OP
 UT ISI:000262104704351
 ER
 
 PT J
 AU Ansell, SM
    Novak, A
    Yang, ZZ
    Fredericksen, ZS
    Wang, AH
    Kay, N
    Liebow, M
    Dogan, A
    Call, TG
    Witzig, T
    Habermann, TM
    Slager, SL
    Cerhan, JR
 AF Ansell, Stephen M.
    Novak, Anne
    Yang, Zhi-Zhang
    Fredericksen, Zachary S.
    Wang, Alice H.
    Kay, Neil
    Liebow, Mark
    Dogan, Ahmet
    Call, Timothy G.
    Witzig, Thomas
    Habermann, Thomas M.
    Slager, Susan L.
    Cerhan, James R.
 TI Genetic Variation in Genes That Regulate T-Cell Differentiation and
    Function Is Associated with An Increased Risk of Developing B-Cell
    Non-Hodgkin Lymphoma.
 SO BLOOD
 LA English
 DT Meeting Abstract
 CT 50th Annual Meeting of the American- Society-of-Hematology
 CY DEC 06-09, 2008
 CL San Francisco, CA
 SP Amer Soc Hematol
 C1 [Ansell, Stephen M.; Novak, Anne; Yang, Zhi-Zhang; Fredericksen, Zachary S.; Wang, Alice H.; Kay, Neil; Liebow, Mark; Dogan, Ahmet; Call, Timothy G.; Witzig, Thomas; Habermann, Thomas M.; Slager, Susan L.; Cerhan, James R.] Mayo Clin, Rochester, MN USA.
 NR 0
 TC 0
 PU AMER SOC HEMATOLOGY
 PI WASHINGTON
 PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
 SN 0006-4971
 J9 BLOOD
 JI Blood
 PD NOV 16
 PY 2008
 VL 112
 IS 11
 BP 1288
 EP 1289
 PG 2
 SC Hematology
 GA 389OP
 UT ISI:000262104704380
 ER
 
 PT J
 AU Yang, J
    Liu, X
    Nyland, S
    Zhang, R
    Thomas, K
    Jarbadan, RN
    Loughran, TP
 AF Yang, Jun
    Liu, Xin
    Nyland, Susan
    Zhang, Ranran
    Thomas, Kendall
    Jarbadan, Ruth Nancy
    Loughran, Thomas P., Jr.
 TI Platelet-Derived Growth Factor (PDGF)-BB Mediates Survival of Leukemic
    Large Granular Lymphocyte Via An Autocrine Regulatory Pathway
 SO BLOOD
 LA English
 DT Meeting Abstract
 CT 50th Annual Meeting of the American- Society-of-Hematology
 CY DEC 06-09, 2008
 CL San Francisco, CA
 SP Amer Soc Hematol
 C1 [Yang, Jun; Liu, Xin; Zhang, Ranran; Thomas, Kendall; Jarbadan, Ruth Nancy; Loughran, Thomas P., Jr.] Penn State Hershey Canc Inst, Hershey, PA USA.
    [Nyland, Susan] NIH, Rare Dis Clin Res Network, Bone Marrow Failure Dis Consortium, Bethesda, MD USA.
 NR 0
 TC 0
 PU AMER SOC HEMATOLOGY
 PI WASHINGTON
 PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
 SN 0006-4971
 J9 BLOOD
 JI Blood
 PD NOV 16
 PY 2008
 VL 112
 IS 11
 BP 1301
 EP 1301
 PG 1
 SC Hematology
 GA 389OP
 UT ISI:000262104704421
 ER
 
 PT J
 AU Chen, XL
    Huang, YH
    Yan, L
    Brault, M
    Wang, ZZ
    Arildsen, MT
    Yang, E
 AF Chen, Xiaolan
    Huang, Yuhui
    Yan, Ling
    Brault, Marie
    Wang, Zhizhang
    Arildsen, Maryann T.
    Yang, Elizabeth
 TI p19Arf Cooperates with Shp2 in Lymphoid Leukemogenesis
 SO BLOOD
 LA English
 DT Meeting Abstract
 CT 50th Annual Meeting of the American- Society-of-Hematology
 CY DEC 06-09, 2008
 CL San Francisco, CA
 SP Amer Soc Hematol
 C1 [Chen, Xiaolan; Huang, Yuhui; Yan, Ling; Brault, Marie; Wang, Zhizhang; Arildsen, Maryann T.; Yang, Elizabeth] Vanderbilt Univ, Nashville, TN USA.
 NR 0
 TC 0
 PU AMER SOC HEMATOLOGY
 PI WASHINGTON
 PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
 SN 0006-4971
 J9 BLOOD
 JI Blood
 PD NOV 16
 PY 2008
 VL 112
 IS 11
 BP 1302
 EP 1302
 PG 1
 SC Hematology
 GA 389OP
 UT ISI:000262104704426
 ER
 
 PT J
 AU Kim, KT
    Borgstein, NG
    Yang, YJ
    Haltom, E
    Mook, L
    Ababa, MD
    Reddy, SK
    Sherman, ML
 AF Kim, Kenneth T.
    Borgstein, Niels G.
    Yang, Yijun
    Haltom, Eric
    Mook, Louisa
    Ababa, Michelle D.
    Reddy, Sandeep K.
    Sherman, Matthew Leigh
 TI ACE-011, a Soluble Activin Receptor Type IIa IgG-Fc Fusion Protein,
    Increases Hemoglobin and Hematocrit Levels in Postmenopausal Healthy
    Women
 SO BLOOD
 LA English
 DT Meeting Abstract
 CT 50th Annual Meeting of the American- Society-of-Hematology
 CY DEC 06-09, 2008
 CL San Francisco, CA
 SP Amer Soc Hematol
 C1 [Kim, Kenneth T.; Ababa, Michelle D.] W Coast Clin Trials, Cypress, CA USA.
    [Borgstein, Niels G.; Yang, Yijun; Haltom, Eric; Mook, Louisa; Sherman, Matthew Leigh] Acceleron Pharma, Cambridge, MA USA.
 NR 0
 TC 0
 PU AMER SOC HEMATOLOGY
 PI WASHINGTON
 PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
 SN 0006-4971
 J9 BLOOD
 JI Blood
 PD NOV 16
 PY 2008
 VL 112
 IS 11
 BP 1316
 EP 1316
 PG 1
 SC Hematology
 GA 389OP
 UT ISI:000262104704473
 ER
 
 PT J
 AU Maillard, I
    Chen, YX
    Friedman, A
    Yang, YQ
    Tubbs, AT
    Shestova, O
    Pear, WS
    Hua, XX
 AF Maillard, Ivan
    Chen, Ya-Xiong
    Friedman, Ann
    Yang, Yuqing
    Tubbs, Anthony T.
    Shestova, Olga
    Pear, Warren S.
    Hua, Xianxin
 TI Menin regulates the function of hematopoietic stem cells and lymphoid
    progenitors
 SO BLOOD
 LA English
 DT Article
 ID HISTONE METHYLTRANSFERASE COMPLEX; HOX GENE-EXPRESSION; MLL-MUTANT
    MICE; TRANSFORMATION; LEUKEMIA; DEFECTS; PROLIFERATION; TARGETS; BMI-1;
    LOCUS
 AB Men1 is a tumor suppressor gene mutated in endocrine neoplasms. Besides
    its endocrine role, the Men1 gene product menin interacts with the
    mixed lineage leukemia (MLL) protein, a histone H3 lysine 4
    methyltransferase. Although menin and MLL fusion proteins cooperate to
    activate Homeobox (Hox) gene expression during transformation, little
    is known about the normal hematopoietic functions of menin. Here, we
    studied hematopoiesis after Men1 ablation. Menin loss modestly impaired
    blood neutrophil, lymphocyte, and platelet counts. Without
    hematopoietic stress, multilineage and myelo-erythroid bone marrow
    progenitor numbers were preserved, while B lymphoid progenitors were
    decreased. In contrast, competitive transplantation revealed a marked
    functional defect of long-term hematopoietic stem cells (HSC) in the
    absence of menin, despite normal initial homing of progenitors to the
    bone marrow. HoxA9 gene expression was only modestly decreased in
    menin-deficient HSCs. These observations reveal a novel and essential
    role for menin in HSC homeostasis that was most apparent during
    situations of hematopoietic recovery, suggesting that menin regulates
    molecular pathways that are essential during the adaptive HSC response
    to stress. (Blood. 2009; 113: 1661-1669)
 C1 [Maillard, Ivan; Friedman, Ann] Univ Michigan, Inst Life Sci, Ctr Stem Cell Biol, Ann Arbor, MI 48109 USA.
    [Maillard, Ivan] Univ Michigan, Dept Internal Med, Div Hematol Oncol, Ann Arbor, MI 48109 USA.
    [Maillard, Ivan] Univ Michigan, Dept Cell & Dev Biol, Ann Arbor, MI 48109 USA.
    [Maillard, Ivan] Univ Penn, Div Hematol Oncol, Philadelphia, PA 19104 USA.
    [Maillard, Ivan; Chen, Ya-Xiong; Yang, Yuqing; Tubbs, Anthony T.; Shestova, Olga; Pear, Warren S.; Hua, Xianxin] Univ Penn, Abramson Family Canc Res Inst, Philadelphia, PA 19104 USA.
    [Chen, Ya-Xiong; Yang, Yuqing; Tubbs, Anthony T.; Pear, Warren S.; Hua, Xianxin] Univ Penn, Dept Canc Biol, Philadelphia, PA 19104 USA.
    [Shestova, Olga] Univ Penn, Dept Pathol & Lab Med, Philadelphia, PA 19104 USA.
    [Pear, Warren S.] Univ Penn, Inst Med & Engn, Philadelphia, PA 19104 USA.
 RP Maillard, I, Univ Michigan, Inst Life Sci, Ctr Stem Cell Biol, Ann
    Arbor, MI 48109 USA.
 EM imaillar@umich.edu
    huax@mail.med.upenn.edu
 FU National Institutes of Health (Bethesda, MD) ; Leukemia & Lymphoma
    Society (White Plains, NY) ; Specialized Center of Research (SCOR) [R01
    CA113962, R01CA100912]; Damon Runyon Cancer Research Foundation (New
    York, NY) [DRG-102-05]; University of Michigan's Biological Sciences
    Scholar Program (Ann Arbor, MI) 
 FX We thank Dr Sean Morrison and Dr Jay Hess for advice and critical
    reading of the manuscript.
    This work was supported by grants from the National Institutes of
    Health (Bethesda, MD) and a Leukemia & Lymphoma Society (White Plains,
    NY) Specialized Center of Research (SCOR) grant (R01 CA113962 and
    R01CA100912, X. H. and W. S. P.). I. M. was supported by a grant from
    the Damon Runyon Cancer Research Foundation (New York, NY; DRG-102-05)
    and by the University of Michigan's Biological Sciences Scholar Program
    (Ann Arbor, MI).
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 NR 32
 TC 6
 PU AMER SOC HEMATOLOGY
 PI WASHINGTON
 PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
 SN 0006-4971
 J9 BLOOD
 JI Blood
 PD FEB 19
 PY 2009
 VL 113
 IS 8
 BP 1661
 EP 1669
 DI 10.1182/blood-2008-01-135012
 PG 9
 SC Hematology
 GA 410GS
 UT ISI:000263566100008
 ER
 
 PT J
 AU Reheman, A
    Yang, H
    Zhu, GH
    Jin, WX
    He, F
    Spring, CM
    Bai, XF
    Gross, PL
    Freedman, J
    Ni, HY
 AF Reheman, Adili
    Yang, Hong
    Zhu, Guangheng
    Jin, Wuxun
    He, Feng
    Spring, Christopher M.
    Bai, Xufang
    Gross, Peter L.
    Freedman, John
    Ni, Heyu
 TI Plasma fibronectin depletion enhances platelet aggregation and thrombus
    formation in mice lacking fibrinogen and von Willebrand factor
 SO BLOOD
 LA English
 DT Article
 ID PROTEIN-DISULFIDE-ISOMERASE; IN-VIVO; MONOCLONAL-ANTIBODY; INJURED
    ARTERIOLES; MURINE MODEL; GAMMA-CHAIN; HEMOSTASIS; INHIBITION;
    COLLAGEN; THROMBOSPONDIN-1
 AB We previously showed that platelet aggregation and thrombus formation
    occurred in mice lacking both fibrinogen (Fg) and von Willebrand factor
    (VWF) and that plasma fibronectin (pFn) promoted thrombus growth and
    stability in injured arterioles in wild-type mice. To examine whether
    pFn is required for Fg/VWF-independent thrombosis, we generated
    Fg/VWF/conditional pFn triple-deficient (TKO; Cre(+), Fn(flox/flox),
    Fg/VWF-/-) mice and littermate control (Cre(-), Fn(flox/flox),
    Fg/VWF-/-) mice. Surprisingly, TKO platelet aggregation was not
    abolished, but instead was enhanced in both heparinized platelet-rich
    plasma and gel-filtered platelets. This enhancement was diminished when
    TKO platelets were aggregated in pFn-positive control platelet-poor
    plasma (PPP), whereas aggregation was enhanced when control platelets
    were aggregated in pFn-depleted TKO PPP. The TKO platelet aggregation
    can be completely inhibited by our newly developed mouse anti-mouse
    beta(3) integrin antibodies but was not affected by anti-mouse GPIb
    alpha antibodies. Enhanced platelet aggregation was also observed when
    heparinized TKO blood was perfused in collagen-coated perfusion
    chambers. Using intravital microscopy, we further showed that
    thrombogenesis in TKO mice was enhanced in both FeCl3-injured
    mesenteric arterioles and laser-injured cremaster arterioles. Our data
    indicate that pFn is not essential for Fg/VWF-independent thrombosis
    and that soluble pFn is probably an important inhibitory factor for
    platelet aggregation. (Blood. 2009; 113: 1809-1817)
 C1 [Ni, Heyu] Univ Toronto, Canadian Blood Serv, Toronto, ON M5B 1W8, Canada.
    [Reheman, Adili; Yang, Hong; Freedman, John; Ni, Heyu] Univ Toronto, Dept Lab Med & Pathol, Toronto, ON M5B 1W8, Canada.
    [Reheman, Adili; Yang, Hong; Zhu, Guangheng; Jin, Wuxun; He, Feng; Spring, Christopher M.; Bai, Xufang; Gross, Peter L.; Freedman, John; Ni, Heyu] St Michaels Hosp, Toronto Platelet Immunobiol Grp, Toronto, ON M5B 1W8, Canada.
    [Reheman, Adili; Yang, Hong; Zhu, Guangheng; Jin, Wuxun; He, Feng; Spring, Christopher M.; Bai, Xufang; Gross, Peter L.; Freedman, John; Ni, Heyu] St Michaels Hosp, Dept Lab Med, Keenan Res Ctr, Li Ka Shing Knowledge Inst, Toronto, ON M5B 1W8, Canada.
    [Bai, Xufang; Gross, Peter L.] McMaster Univ, Dept Med, Henderson Res Ctr, Hamilton, ON, Canada.
    [Freedman, John; Ni, Heyu] Univ Toronto, Dept Med, Toronto, ON M5B 1W8, Canada.
    [Ni, Heyu] Univ Toronto, Dept Physiol, Toronto, ON M5B 1W8, Canada.
 RP Ni, HY, Univ Toronto, Canadian Blood Serv, 30 Bond St,Room 2-006,Bond
    Wing, Toronto, ON M5B 1W8, Canada.
 EM nih@smh.toronto.on.ca
 FU Heart and Stroke Foundation of Canada (Ontario) ; Canadian Blood
    Services and Canadian Institutes of Health Research ; St Michael's
    Hospital ; Canadian Blood Services ; Canada Foundation for Innovation ;
    Heart and Stroke/Richard Lewar Excellence Award ; Canadian Blood
    Services postdoctoral fellowship award 
 FX We thank Drs Reinhard Farssler, Jay L. Degen, Denisa D. Wagner, and
    Cecile V. Denis for their earlier work preparing pFn conditional
    knockout mice, Fg and VWF gene-deficient mice. We thank Dr Pingguo Chen
    for his assistance with genotyping and backcrossing GPIb
    alpha<SUP>-/-</SUP> and beta 3<SUP>-/-</SUP> mice onto BALB/c
    background and Michelle Lee Webster and Sean Lang for assistance with
    preparation of the manuscript.
    This work was supported by the Heart and Stroke Foundation of Canada
    (Ontario), Canadian Blood Services and Canadian Institutes of Health
    Research, and by equipment funds from St Michael's Hospital, Canadian
    Blood Services, and Canada Foundation for Innovation. H. Y. is a
    recipient of the Heart and Stroke/Richard Lewar Excellence Award and a
    Canadian Blood Services postdoctoral fellowship award.
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 NR 51
 TC 7
 PU AMER SOC HEMATOLOGY
 PI WASHINGTON
 PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
 SN 0006-4971
 J9 BLOOD
 JI Blood
 PD FEB 19
 PY 2009
 VL 113
 IS 8
 BP 1809
 EP 1817
 DI 10.1182/blood-2008-04-148361
 PG 9
 SC Hematology
 GA 410GS
 UT ISI:000263566100025
 ER
 
 PT J
 AU Cui, X
    Xu, SM
    Mu, DS
    Yang, ZM
 AF Cui, Xiao
    Xu, Si Min
    Mu, Dao Shuai
    Yang, Zhi Min
 TI Genomic analysis of rice microRNA promoters and clusters
 SO GENE
 LA English
 DT Article
 DE miRNA gene; Rice; Promoter; miRNA cluster
 ID COMPUTATIONAL IDENTIFICATION; MOLECULAR EVOLUTION; NUCLEAR EXPORT; CORE
    PROMOTERS; SMALL RNAS; ARABIDOPSIS; EXPRESSION; TARGETS; GENES;
    BIOGENESIS
 AB MicroRNAs (miRNAs) are endogenous single-stranded non-coding small RNAs
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    transcriptional regulation of miRNA genes. In this study, we performed
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    promoter/transcription start site (TSS) and TATA-box, and organization
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    miRNA genes have a greater proportion of promoters than the
    non-conserved miRNA genes. We further globally analyzed the genomic
    organization of pri-miRNAs and found that 52 rice miRNA genes appear in
    18 clusters. Alignment of the miRNA sequences in these clusters shows a
    number of miRNA paralogs within the cluster. The data obtained may aid
    our understanding of the specific sequences upstream of pre-miRNAs and
    the functional implications of miRNA clusters in rice plants. (C) 2008
    Elsevier B.V. All rights reserved.
 C1 [Cui, Xiao; Xu, Si Min; Mu, Dao Shuai; Yang, Zhi Min] Nanjing Agr Univ, Coll Life Sci, Dept Biochem & Mol Biol, Nanjiang 210095, Peoples R China.
 RP Yang, ZM, Nanjing Agr Univ, Coll Life Sci, Dept Biochem & Mol Biol,
    Nanjiang 210095, Peoples R China.
 EM zmyang@njau.edu.cn
 FU National Natural Science Foundation of China [30671249]; Natural
    Science Foundation of Jiang Su, China [BK2006137]; NAU 
 FX This research was supported by the National Natural Science Foundation
    of China (30671249) and the Natural Science Foundation of Jiang Su,
    China (BK2006137), as well as the Student Research Training program
    from NAU.
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 NR 42
 TC 11
 PU ELSEVIER SCIENCE BV
 PI AMSTERDAM
 PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
 SN 0378-1119
 J9 GENE
 JI Gene
 PD FEB 15
 PY 2009
 VL 431
 IS 1-2
 BP 61
 EP 66
 DI 10.1016/j.gene.2008.11.016
 PG 6
 SC Genetics & Heredity
 GA 407XG
 UT ISI:000263397000009
 ER
 
 PT J
 AU Zhao, Q
    Yam, R
    Zhang, BQ
    Yang, YK
    Cheng, XJ
    Li, R
 AF Zhao, Qiang
    Yam, Richard C. M.
    Zhang, Baoqing
    Yang, Yingkui
    Cheng, Xinjian
    Li, Robert K. Y.
 TI Novel all-cellulose ecocomposites prepared in ionic liquids
 SO CELLULOSE
 LA English
 DT Article
 DE Cellulose; Rice husk (RH); Ionic liquid (IL); Ecocomposite
 ID SELF-REINFORCED COMPOSITES; RICE HUSK; POLYMER COMPOSITES; POROUS
    CARBON; FIBER; DISSOLUTION; SILICA; NANOCOMPOSITE; DERIVATIVES; SOLVENT
 AB In this study, a kind of novel all-cellulose ecocomposites based on
    cellulose and rice husk (RH) has been prepared by using green solvent,
    ionic liquid (IL), as processing medium. Due to the presence of the RH,
    these ecocomposites also contain an inorganic component, silica. The
    content and distribution of the silica in the ecocomposite have been
    investigated by energy dispersive X-ray (EDX) and X-ray photoelectron
    spectroscopy (XPS) analyses. The mechanical properties of these
    ecocomposites, including both static and dynamic, have been determined
    by using tensile test and dynamic mechanical analysis (DMA),
    respectively. The effect of processing conditions on the interfacial
    bonding and therefore the mechanical performance of the final
    ecocomposites has been investigated further. Results show that the
    incorporation of the RH can provide stiffening effect for cellulose
    matrix, and the pretreatment of RH fillers by IL can enhance the
    filler/matrix interfacial bonding, thus further improving the
    mechanical performance of the ecocomposite. By selecting suitable
    composition ratios and processing conditions optimal mechanical
    performance with the balance among stiffness, strength and elongation
    at break can be obtained.
 C1 [Zhao, Qiang; Zhang, Baoqing; Yang, Yingkui; Cheng, Xinjian; Li, Robert K. Y.] City Univ Hong Kong, Dept Phys & Mat Sci, Kowloon, Hong Kong, Peoples R China.
    [Zhao, Qiang; Yam, Richard C. M.; Zhang, Baoqing] City Univ Hong Kong, Dept Mfg Engn & Engn Management, Kowloon, Hong Kong, Peoples R China.
 RP Li, R, City Univ Hong Kong, Dept Phys & Mat Sci, Tat Chee Ave, Kowloon,
    Hong Kong, Peoples R China.
 EM aprkyl@cityu.edu.hk
 FU City University of Hong Kong [ARG 9667009]
 FX This work was supported by a grant from the City University of Hong
    Kong (Project No. ARG 9667009).
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 NR 40
 TC 13
 PU SPRINGER
 PI DORDRECHT
 PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
 SN 0969-0239
 J9 CELLULOSE
 JI Cellulose
 PD APR
 PY 2009
 VL 16
 IS 2
 BP 217
 EP 226
 DI 10.1007/s10570-008-9251-3
 PG 10
 SC Materials Science, Paper & Wood; Materials Science, Textiles; Polymer
    Science
 GA 407GZ
 UT ISI:000263352900007
 ER
 
 PT J
 AU Chiu, HY
    Tsao, LY
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 AF Chiu, Han-Yao
    Tsao, Lon-Yen
    Yang, Rei-Cheng
 TI Heat-shock response protects peripheral blood mononuclear cells (PBMCs)
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 SO CELL STRESS & CHAPERONES
 LA English
 DT Article
 DE Heat-shock response; Rat; Superoxide; Oxidative stress; Mitochondrion
 ID OXIDATIVE STRESS; CYTOCHROME-C; SEPTIC LIVER; DNA-DAMAGE; DEATH;
    PRETREATMENT; APOPTOSIS; EXERCISE; DYSFUNCTION; ACTIVATION
 AB The present study was designed to investigate ex vivo the protective
    mechanisms of heat-shock response against H2O2-induced oxidative stress
    in peripheral blood mononuclear cells (PBMCs) of rats. Twenty-four
    hours later, heat-shock treatment was executed in vivo; rat PBMCs were
    collected and treated with H2O2. The accumulation of reactive oxygen
    species and the mitochondrial membrane potential were evaluated by
    intracellular fluorescent dHE and JC-1 dye staining, respectively, and
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    analysis. Cellular apoptosis was assayed by TUNEL staining and double
    staining of Annexin V and PI. The results showed that H2O2-induced
    oxidative stress leads to intracellular superoxide accumulation and
    collapse of the mitochondrial membrane potential in rat PBMCs.
    Moreover, cellular apoptosis was detected after H2O2 treatment, and the
    release of mitochondrial cytochrome c from mitochondria to cytosol was
    significantly enhanced. Heat-shock pretreatment decreases the
    accumulation of intracellular superoxide in PBMCs during H2O2-induced
    oxidative stress. Moreover, heat-shock treatment prevents the collapse
    of the mitochondrial membrane potential and cytochrome c release from
    mitochondria during H2O2-induced oxidative stress. In conclusion,
    mitochondria are critical organelles of the protective effects of
    heat-shock treatment. Cellular apoptosis during H2O2-induced oxidative
    stress is decreased by heat-shock treatment through a decrease in
    superoxide induction and preservation of the mitochondrial membrane
    potential.
 C1 [Yang, Rei-Cheng] Kaohsiung Med Univ, Coll Med, Dept Pediat, Kaohsiung, Taiwan.
    [Chiu, Han-Yao; Tsao, Lon-Yen] Changhua Christian Hosp, Dept Pediat, Changhua, Taiwan.
    [Chiu, Han-Yao; Tsao, Lon-Yen] Chang Jung Christian Univ, Dept Resp Care, Tainan, Taiwan.
 RP Yang, RC, Kaohsiung Med Univ, Coll Med, Dept Pediat, 100 Shih Chuan 1st
    Rd, Kaohsiung, Taiwan.
 EM rechya@kmu.edu.tw
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 TC 4
 PU SPRINGER
 PI DORDRECHT
 PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
 SN 1355-8145
 J9 CELL STRESS CHAPERONES
 JI Cell Stress Chaperones
 PD MAR
 PY 2009
 VL 14
 IS 2
 BP 207
 EP 217
 DI 10.1007/s12192-008-0075-8
 PG 11
 SC Cell Biology
 GA 407GY
 UT ISI:000263352800011
 ER
 
 PT J
 AU Li, CL
    Yang, Y
    Gu, JJ
    Ma, Y
    Jin, Y
 AF Li, Chunliang
    Yang, Ying
    Gu, Junjie
    Ma, Yu
    Jin, Ying
 TI Derivation and transcriptional profiling analysis of pluripotent stem
    cell lines from rat blastocysts
 SO CELL RESEARCH
 LA English
 DT Article
 DE embryonic stem cells; blastocysts; primitive endoderm; teratomas
 ID SELF-RENEWAL; EFFICIENT DERIVATION; PRIMITIVE ENDODERM; FACTOR OCT-4;
    MOUSE; DIFFERENTIATION; ESTABLISHMENT; CULTURE; GROWTH; FGF
 AB Embryonic stem (ES) cells are derived from blastocyst-stage embryos.
    Their unique properties of self-renewal and pluripotency make them an
    attractive tool for basic research and a potential cell resource for
    therapy. ES cells of mouse and human have been successfully generated
    and applied in a wide range of research. However, no genuine ES cell
    lines have been obtained from rat to date. In this study, we identified
    pluripotent cells in early rat embryos using specific antibodies
    against markers of pluripotent stem cells. Subsequently, by modifying
    the culture medium for rat blastocysts, we derived pluripotent rat
    ES-like cell lines, which expressed pluripotency markers and formed
    embryoid bodies (EBs) in vitro. Importantly, these rat ES-like cells
    were able to produce teratomas. Both EBs and teratomas contained
    tissues from all three embryonic germ layers. In addition, from the rat
    ES-like cells, we derived a rat primitive endoderm (PrE) cell line.
    Furthermore, we conducted transcriptional profiling of the rat ES-like
    cells and identified the unique molecular signature of the rat
    pluripotent stem cells. Our analysis demonstrates that multiple
    signaling pathways, including the BMP, Activin and mTOR pathways, may
    be involved in keeping the rat ES-like cells in an undifferentiated
    state. The cell lines and information obtained in this study will
    accelerate our understanding of the molecular regulation underlying
    pluripotency and guide us in the appropriate manipulation of ES cells
    from a particular species.
 C1 [Li, Chunliang; Yang, Ying; Gu, Junjie; Ma, Yu; Jin, Ying] Shanghai Jiao Tong Univ, Sch Med, Chinese Acad Sci,Key Lab Stem Cell Biol, Shanghai Inst Biol Sci,Inst Hlth Sci, Shanghai 200025, Peoples R China.
    [Gu, Junjie; Ma, Yu; Jin, Ying] Shanghai Jiao Tong Univ, Sch Med, Shanghai Stem Cell Inst, Shanghai 200025, Peoples R China.
    [Gu, Junjie; Ma, Yu; Jin, Ying] Shanghai Jiao Tong Univ, Sch Med, Chinese Minist Educ, Key Lab Cell Differentiat & Apoptosis, Shanghai 200025, Peoples R China.
    [Li, Chunliang; Yang, Ying] Chinese Acad Sci, Grad Sch, Beijing 100049, Peoples R China.
 RP Jin, Y, Shanghai Jiao Tong Univ, Sch Med, Chinese Acad Sci,Key Lab Stem
    Cell Biol, Shanghai Inst Biol Sci,Inst Hlth Sci, 225 S Chongqing Rd,
    Shanghai 200025, Peoples R China.
 EM yjin@sibs.ac.cn
 FU Shanghai Science & Technology Developmental Foundations [06dj14001];
    National High Technology Research and Development Program of China
    [2006AA02Z197, 2006CB943901, 2007CB947904, 2007CB948004]; Shanghai
    JiaoTong University School of Medicine and Shanghai Institutes for
    Biological Sciences, CAS 
 FX Authors express appreciation to Erbo Xu (Boston College) for his help
    in preparation of this manuscript and to Yuan Guan (Institute of Health
    Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy
    of Sciences) for his help in subretinal injection. The study was
    supported by the financial support of the Grants from the Shanghai
    Science & Technology Developmental Foundations (Grant number:
    06dj14001), the National High Technology Research and Development
    Program of China (2006AA02Z197, 2006CB943901, 2007CB947904, and
    2007CB948004), Shanghai JiaoTong University School of Medicine and
    Shanghai Institutes for Biological Sciences, CAS.
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 NR 38
 TC 9
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 PI NEW YORK
 PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
 SN 1001-0602
 J9 CELL RES
 JI Cell Res.
 PD FEB
 PY 2009
 VL 19
 IS 2
 BP 173
 EP 186
 DI 10.1038/cr.2008.301
 PG 14
 SC Cell Biology
 GA 406IF
 UT ISI:000263287500004
 ER
 
 PT J
 AU Guo, W
    Zhang, KM
    Tu, K
    Li, YX
    Zhu, L
    Xiao, HS
    Yang, Y
    Wu, JR
 AF Guo, Wei
    Zhang, Kun-Ming
    Tu, Kang
    Li, Yi-Xue
    Zhu, Li
    Xiao, Hua-Sheng
    Yang, Ying
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 TI Adipogenesis licensing and execution are disparately linked to cell
    proliferation
 SO CELL RESEARCH
 LA English
 DT Article
 DE adipogenesis; proliferation; contact inhibition; DNA methylation; C/EBP
    alpha
 ID MITOTIC CLONAL EXPANSION; 3T3-L1 PREADIPOCYTE DIFFERENTIATION;
    ADIPOCYTE DIFFERENTIATION; LEUKEMIC-CELLS; GROWTH ARREST; STEM-CELL;
    RECEPTOR; CYCLE; INHIBITION; PHASE
 AB Coordination of cell differentiation and proliferation is a key issue
    in the development process of multi-cellular organisms and stem cells.
    Here we provide evidence that the establishment of adipocyte
    differentiation of 3T3-L1 cells requires two processes: the licensing
    of an adipogenesis gene-expression program within a particular
    growth-arrest stage, i.e., the contact-inhibition stage, and then the
    execution of this program in a cell-cycle-independent manner, by which
    the licensed progenitors are differentiated into adipocytes in the
    presence of inducing factors. Our results showed that differentiation
    licensing of 3T3-L1 cells during the contact-inhibition stage involved
    epigenetic modifications such as DNA methylation and histone
    modifications, whereas disturbing these epigenetic modifications by DNA
    methylation inhibitors or RNAi during the contact-inhibition stage
    significantly reduced adipogenesis efficiency. More importantly, when
    these licensed 3T3-L1 cells were re-cultured under non-differentiating
    conditions or treated only with insulin, this adipogenesis commitment
    could be maintained from one cell generation to the next, whereby the
    licensed program could be activated in a cell-cycle-independent manner
    once these cells were subjected to adipogenesis-inducing conditions.
    This result suggests that differentiation licensing and differentiation
    execution can be uncoupled and disparately linked to cell
    proliferation. Our findings deliver a new concept that cell-fate
    decision can be subdivided into at least two stages, licensing and
    execution, which might have different regulatory relationships with
    cell proliferation. In addition, this new concept may provide a clue
    for developing new strategies against obesity.
 C1 [Guo, Wei; Zhang, Kun-Ming; Tu, Kang; Li, Yi-Xue; Zhu, Li; Xiao, Hua-Sheng; Yang, Ying; Wu, Jia-Rui] Chinese Acad Sci, Shanghai Inst Biol Sci, Inst Biochem & Cell Biol, Key Lab Syst Biol, Shanghai 200031, Peoples R China.
    [Guo, Wei; Zhang, Kun-Ming; Yang, Ying; Wu, Jia-Rui] Chinese Acad Sci, Shanghai Inst Biol Sci, Inst Biochem & Cell Biol, State Key Lab Mol Biol, Shanghai 200031, Peoples R China.
    [Xiao, Hua-Sheng] Natl Engn Ctr Biochip Shanghai, Shanghai 201203, Peoples R China.
    [Wu, Jia-Rui] Univ Sci & Technol China, Hefei Natl Lab Phys Sci Microscale, Hefei 230027, Peoples R China.
    [Wu, Jia-Rui] Univ Sci & Technol China, Sch Life Sci, Hefei 230027, Peoples R China.
 RP Wu, JR, Chinese Acad Sci, Shanghai Inst Biol Sci, Inst Biochem & Cell
    Biol, Key Lab Syst Biol, 320 Yue Yang Rd, Shanghai 200031, Peoples R
    China.
 EM wujr@sibs.ac.cn
 FU National Natural Science Foundation of China [2006CB503900, 30230110,
    30521005]; Chinese Academy of Sciences [KSCX1-YW-02]
 FX We thank DS Li (Chinese Academy of Scienses, China) for critically
    reading this article. This work was supported by the "973 Program" No.
    2006CB503900, grants from the National Natural Science Foundation of
    China No. 30230110 and No. 30521005, and a grant from the Knowledge
    Innovation Program of the Chinese Academy of Sciences KSCX1-YW-02 to
    JRW.
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 SN 1001-0602
 J9 CELL RES
 JI Cell Res.
 PD FEB
 PY 2009
 VL 19
 IS 2
 BP 216
 EP 223
 DI 10.1038/cr.2008.319
 PG 8
 SC Cell Biology
 GA 406IF
 UT ISI:000263287500008
 ER
 
 PT J
 AU Zhu, CY
    Li, CY
    Li, Y
    Zhan, YQ
    Li, YH
    Xu, CW
    Xu, WX
    Sun, HB
    Yang, XM
 AF Zhu, C-Y
    Li, C-Y
    Li, Y.
    Zhan, Y-Q
    Li, Y-H
    Xu, C-W
    Xu, W-X
    Sun, H. B.
    Yang, X-M
 TI Cell growth suppression by thanatos-associated protein 11(THAP11) is
    mediated by transcriptional downregulation of c-Myc
 SO CELL DEATH AND DIFFERENTIATION
 LA English
 DT Article
 DE THAP11; c-Myc; growth suppression; transcriptional repressor
 ID ORNITHINE-DECARBOXYLASE GENE; EMBRYONIC STEM-CELLS; CYCLIN D1; HISTONE
    ACETYLATION; BINDING PROTEIN; TARGET GENES; THAP DOMAIN; P2 PROMOTER;
    REPRESSION; PROLIFERATION
 AB Thanatos-associated proteins (THAPs) are zinc-dependent,
    sequence-specific DNA-binding factors involved in cell proliferation,
    apoptosis, cell cycle, chromatin modification and transcriptional
    regulation. THAP11 is the most recently described member of this human
    protein family. In this study, we show that THAP11 is ubiquitously
    expressed in normal tissues and frequently downregulated in several
    human tumor tissues. Overexpression of THAP11 markedly inhibits growth
    of a number of different cells, including cancer cells and
    non-transformed cells. Silencing of THAP11 by RNA interference in HepG2
    cells results in loss of cell growth repression. These results suggest
    that human THAP11 may be an endogenous physiologic regulator of cell
    proliferation. We also provide evidence that the function of THAP11 is
    mediated by its ability to repress transcription of c-Myc. Promoter
    reporter assays indicate a DNA binding-dependent c-Myc transcriptional
    repression. Chromatin immunoprecipitations and EMSA assay suggest that
    THAP11 directly binds to the c-Myc promoter. The findings that
    expression of c-Myc rescues significantly cells from THAP11-mediated
    cell growth suppression and that THAP11 expression only slightly
    inhibits c-Myc null fibroblasts cells growth reveal that THAP11
    inhibits cell growth through downregulation of c-Myc expression. Taken
    together, these suggest that THAP11 functions as a cell growth
    suppressor by negatively regulating the expression of c-Myc.
 C1 [Yang, X-M] Beijing Inst Radiat Med, Dept Biochem & Mol Biol, Beijing 100850, Peoples R China.
    [Li, C-Y; Zhan, Y-Q; Xu, W-X] Key Lab Prote & Geom, Beijing, Peoples R China.
    [Li, Y.] Anhui Med Univ, Dept Pathophysiol, Hefei, Peoples R China.
    [Li, Y-H; Sun, H. B.] Mt Sinai Sch Med, New York, NY USA.
 RP Yang, XM, Beijing Inst Radiat Med, Dept Biochem & Mol Biol, 27 Taiping
    Rd, Beijing 100850, Peoples R China.
 EM xmyang2@nic.bmi.ac.cn
 FU Special Funds for Major State Basic Research of China [2006CB910802];
    Chinese National Natural Science Fund for the Popularization of Science
    [30321003]; Chinese National Nature Foundation Key Program Project
    [30630035]; Chinese National Natural Science Foundation project
    [30480659, 30870958]; Beijing National Natural Science Foundation
    project 
 FX We are grateful to Dr. Ken Kinzler and Bert Vogelstein (The Sidney
    Kimmel Comprehensive Cancer Center, Johns Hopkins University School of
    Medicine) for providing c-Myc promoter luciferase reporter, and
    appreciate Dr. Tong- Chuan He for advice. This work was partially
    supported by the Special Funds for Major State Basic Research of China
    (2006CB910802), Chinese National Natural Science Fund for the
    Popularization of Science (30321003), Chinese National Nature
    Foundation Key Program Project (30630035), Chinese National Natural
    Science Foundation project (30480659, 30870958), and Beijing National
    Natural Science Foundation project.
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 NR 44
 TC 4
 PU NATURE PUBLISHING GROUP
 PI LONDON
 PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
 SN 1350-9047
 J9 CELL DEATH DIFFERENTIATION
 JI Cell Death Differ.
 PD MAR
 PY 2009
 VL 16
 IS 3
 SI Sp. Iss. SI
 BP 395
 EP 405
 DI 10.1038/cdd.2008.160
 PG 11
 SC Biochemistry & Molecular Biology; Cell Biology
 GA 407JT
 UT ISI:000263360100006
 ER
 
 PT J
 AU Ye, J
    Li, JZ
    Liu, Y
    Li, XH
    Yang, TS
    Ma, XD
    Li, Q
    Yao, ZM
    Li, P
 AF Ye, Jing
    Li, John Zhong
    Liu, Yang
    Li, Xuanhe
    Yang, Tianshu
    Ma, Xiaodong
    Li, Qing
    Yao, Zemin
    Li, Peng
 TI Cideb, an ER- and Lipid Droplet-Associated Protein, Mediates VLDL
    Lipidation and Maturation by Interacting with Apolipoprotein B
 SO CELL METABOLISM
 LA English
 DT Article
 ID LOW-DENSITY LIPOPROTEIN; TRIGLYCERIDE TRANSFER PROTEIN; DIET-INDUCED
    OBESITY; ENDOPLASMIC-RETICULUM; PROTEASOMAL DEGRADATION; INSULIN
    SENSITIVITY; GOLGI-APPARATUS; MOUSE-LIVER; MICE; SECRETION
 AB Secretion of triacylglycerol-enriched very-low-density lipoproteins
    (VLDLs) from the liver is vital for maintaining plasma lipid
    homeostasis. However, the process of VLDL assembly and lipidation is
    not well characterized. Here, we observed that liver of Cideb null mice
    had higher levels of triacylglycerols accompanied by low level of VLDL
    secretion. Furthermore, VLDL particles secreted from hepatocytes of
    Cideb null mice have low levels of triacylglycerols but normal levels
    of apoB. We also observed that Cideb is localized to endoplasmic
    reticulum and lipid droplets. Importantly, we have identified apoB as a
    Cideb-inter-acting protein. By infecting adenoviruses expressing
    various Cideb truncations into hepatocytes of Cideb null mice, we found
    that Cideb requires both its apoB-binding and lipid droplet association
    domains to restore the secretion of triacyl glycerol-enriched VLDL
    particles. Our data suggest that Cideb promotes the formation of
    triacylglycerol-enriched VLDL particles and provides a molecular
    insight into VLDL lipidation and maturation in hepatocytes.
 C1 [Ye, Jing; Li, John Zhong; Liu, Yang; Li, Xuanhe; Yang, Tianshu; Ma, Xiaodong; Li, Peng] Tsinghua Univ, Dept Biol Sci & Biotechnol, Minist Educ, Prot Sci Lab, Beijing 100084, Peoples R China.
    [Ye, Jing; Li, Qing] Fourth Mil Med Univ, Xijing Hosp, Dept Pathol, Xian 710032, Shaanxi, Peoples R China.
    [Yao, Zemin] Univ Ottawa, Dept Biochem Microbiol & Immunol, Ottawa, ON K1H 8M5, Canada.
 RP Li, P, Tsinghua Univ, Dept Biol Sci & Biotechnol, Minist Educ, Prot Sci
    Lab, Beijing 100084, Peoples R China.
 EM li-peng@mail.tsinghua.edu.cn
 FU National Natural Science Foundation of China [30429001, 30530350,
    30700268]; Ministry of Education of China [704002]; National Basic
    Research Program of China [2006CB5039009, 2007CB914404]; Ministry of
    Science and Technology of China ; Canadian Institute of Health Research
    [MT-15486]
 FX We thank members of Peng Li's laboratory at Tsinghua University for
    technical assistance and helpful discussion and Doctor S.C. Lin for
    critical editing of the manuscript. This work was supported by grants
    from the National Natural Science Foundation of China (30429001 and
    30530350 to P.L. and 30700268 to J.Y.), the Ministry of Education of
    China (704002 to P.L.), the National Basic Research Program of China
    (2006CB5039009 and 2007CB914404), the Ministry of Science and
    Technology of China, and the Canadian Institute of Health Research
    (MT-15486 to Z.Y.). We are grateful to the technical help provided by
    Mr. Mingxi Li at Tsinghua University and Ms. Shumei Zhong at University
    of Ottawa. This work was also supported by the Program for Changjiang
    Scholars and Innovative Research Team in University from the Ministry
    of Education in China. We thank Doctor Wanjin Hong at the Institute of
    Molecular and Cell Biology in Singapore for providing GS28 antibody and
    Doctor Senfang Sui at Tsinghua University for help with EM analysis.
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 NR 32
 TC 18
 PU CELL PRESS
 PI CAMBRIDGE
 PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
 SN 1550-4131
 J9 CELL METAB
 JI Cell Metab.
 PD FEB 4
 PY 2009
 VL 9
 IS 2
 BP 177
 EP 190
 DI 10.1016/j.cmet.2008.12.013
 PG 14
 SC Cell Biology; Endocrinology & Metabolism
 GA 406BG
 UT ISI:000263269400009
 ER
 
 PT J
 AU Koto, K
    Horie, N
    Kimura, S
    Murata, H
    Sakabe, T
    Matsui, T
    Watanabe, M
    Adachi, S
    Maekawa, T
    Fushiki, S
    Kubo, T
 AF Koto, Kazutaka
    Horie, Naoyuki
    Kimura, Shinya
    Murata, Hiroaki
    Sakabe, Tomoya
    Matsui, Takaaki
    Watanabe, Motonobu
    Adachi, Souichi
    Maekawa, Taira
    Fushiki, Shinji
    Kubo, Toshikazu
 TI Clinically relevant dose of zoledronic acid inhibits spontaneous lung
    metastasis in a murine osteosarcoma model
 SO CANCER LETTERS
 LA English
 DT Article
 DE Zoledronic acid; Osteosarcoma; Metastasis; Neovascularization
 ID NITROGEN-CONTAINING BISPHOSPHONATES; CANCER-CELL GROWTH; 3RD-GENERATION
    BISPHOSPHONATE; IN-VITRO; PROSTATE-CANCER; BONE METASTASES; ANTICANCER
    AGENTS; BLADDER-CANCER; VIVO; APOPTOSIS
 AB Clinically obtainable concentrations of zoledronic acid (ZOL) inhibited
    the production of vascular endothelial growth factor and reduced the
    migration, adhesion, and invasiveness of osteosarcoma (OS) cells in
    vitro. The in vivo effects of ZOL were investigated by using a murine
    model of spontaneous lung metastasis. The higher dose of ZOL (80 mu
    g/kg three times/week) inhibited the growth of OS at the primary site,
    accompanied by inhibition of neovascularization in the tumor.
    Interestingly, while the lower dose of ZOL (80 mu g/kg once a week)
    could not inhibit the growth of CS at the primary site, it
    significantly prevented lung metastasis. (C) 2008 Elsevier Ireland Ltd.
    All rights reserved.
 C1 [Kimura, Shinya; Maekawa, Taira] Kyoto Univ Hosp, Dept Transfus Med & Cell Therapy, Sakyo Ku, Kyoto 6068507, Japan.
    [Koto, Kazutaka; Horie, Naoyuki; Murata, Hiroaki; Sakabe, Tomoya; Matsui, Takaaki; Kubo, Toshikazu] Kyoto Prefectural Univ Med, Grad Sch Med Sci, Dept Orthoped, Kamigyo Ku, Kyoto 6028566, Japan.
    [Horie, Naoyuki; Fushiki, Shinji] Kyoto Prefectural Univ Med, Grad Sch Med Sci, Dept Pathol & Appl Neurobiol, Kamigyo Ku, Kyoto 6028566, Japan.
    [Watanabe, Motonobu; Adachi, Souichi] Kyoto Univ Hosp, Dept Pediat, Sakyo Ku, Kyoto 6068507, Japan.
 RP Kimura, S, Kyoto Univ Hosp, Dept Transfus Med & Cell Therapy, Sakyo Ku,
    Kyoto 6068507, Japan.
 EM shkimu@kuhp.kyoto-u.ac.jp
 FU Ministry of Education, Culture, Sports, Science and Technology of Japan
    [15790796, 18591056]
 FX We are grateful to Dr. Jonathan Green (Novartis Pharma AG, Basel,
    Switzerland) for critically reading the manuscript and to Ms. Yoko
    Nakagawa for her excellent technical support. This study is partially
    supported by Grants-inAid for Scientific Research from the Ministry of
    Education, Culture, Sports, Science and Technology of Japan (15790796
    to H.M. and 18591056 to S.K.).
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 NR 43
 TC 12
 PU ELSEVIER IRELAND LTD
 PI CLARE
 PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
    IRELAND
 SN 0304-3835
 J9 CANCER LETT
 JI Cancer Lett.
 PD FEB 18
 PY 2009
 VL 274
 IS 2
 BP 271
 EP 278
 DI 10.1016/j.canlet.2008.09.026
 PG 8
 SC Oncology
 GA 405ER
 UT ISI:000263206100014
 ER
 
 PT J
 AU Luo, XM
    Maarschalk, E
    O'Connell, RM
    Wang, P
    Yang, L
    Baltimore, D
 AF Luo, Xin M.
    Maarschalk, Emily
    O'Connell, Ryan M.
    Wang, Pin
    Yang, Lili
    Baltimore, David
 TI Engineering human hematopoietic stem/progenitor cells to produce a
    broadly neutralizing anti-HIV antibody after in vitro maturation to
    human B lymphocytes
 SO BLOOD
 LA English
 DT Article
 ID HUMAN MONOCLONAL-ANTIBODY; PBL-SCID MICE; IMMUNODEFICIENCY-VIRUS;
    STEM-CELLS; TRANSGENE EXPRESSION; PASSIVE-IMMUNIZATION; LENTIVIRAL
    VECTORS; RETROVIRAL VECTOR; SECRETING CELLS; AIDS VACCINE
 AB Broadly neutralizing anti-HIV antibodies are rare and have proved hard
    to elicit with any immunogen. We have tested in vitro the notion that
    such antibodies or other antiviral proteins could be made by
    lentivirus-mediated gene transfer into human hematopoietic
    stem/progenitor cells (HSPCs), followed by differentiation of the
    transduced cells into B cells, the most potent antibody-producing
    cells. To do this, we have developed a highly efficient system for in
    vitro maturation of secreting B lymphocytes and plasma cells from
    CD34(+) HSPCs. It is a 3-stage, in vitro culture system that supports
    normal human B-lineage development from HSPCs to antibody-secreting
    plasmablasts (similar to 36%) and plasma cells (similar to 20%). By
    transducing human cord blood CD34(+) cells with lentiviral vectors
    encoding a secretory monoclonal anti-HIV antibody, b12 (IgG(1)), we
    were able to program human B cells to produce in vitro up to 1.5 mu
    g/mL of this broadly neutralizing antibody. Our results suggest that an
    HIV vaccine might be delivered by autologous transplantation of in
    vitro-programmed HSPCs, which would develop into antibody-secreting B
    cells in vivo and provide a continuous supply of anti-HIV neutralizing
    antibodies. ( Blood. 2009; 113: 1422-1431)
 C1 [Luo, Xin M.; Maarschalk, Emily; O'Connell, Ryan M.; Yang, Lili; Baltimore, David] CALTECH, Div Biol, Pasadena, CA 91125 USA.
    [Wang, Pin] Univ So Calif, Mork Family Dept Chem Engn & Mat Sci, Los Angeles, CA USA.
 RP Baltimore, D, CALTECH, Div Biol, M-C 147-75,1200 E Calif Blvd,
    Pasadena, CA 91125 USA.
 EM liyang@caltech.edu
    baltimo@caltech.edu
 FU Bill and Melinda Gates Foundation 
 FX This study was supported by the Bill and Melinda Gates Foundation (
    Seattle, WA) through the Grand Challenges in Global Health Initiative (
    D. B.).
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 TC 15
 PU AMER SOC HEMATOLOGY
 PI WASHINGTON
 PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
 SN 0006-4971
 J9 BLOOD
 JI Blood
 PD FEB 12
 PY 2009
 VL 113
 IS 7
 BP 1422
 EP 1431
 DI 10.1182/blood-2008-09-177139
 PG 10
 SC Hematology
 GA 406SY
 UT ISI:000263316400007
 ER
 
 PT J
 AU Hao, DC
    Yang, L
    Huang, BL
 AF Hao, Da Cheng
    Yang, Ling
    Huang, Beili
 TI Molecular evolution of paclitaxel biosynthetic genes TS and DBAT of
    Taxus species
 SO GENETICA
 LA English
 DT Article
 DE Adaptive evolution; 10-Deacetylbaccatin III-10
    beta-O-acetyltransferase; Paclitaxel; Positive selection; Taxadiene
    synthase; Taxus
 ID AMINO-ACID SITES; TAXOL BIOSYNTHESIS; TAXADIENE SYNTHASE; SELECTION
    PRESSURE; ESCHERICHIA-COLI; COMMITTED STEP; NUCLEOTIDE; MODELS;
    SUBSTITUTIONS; CYCLIZATION
 AB Evolutionary patterns of sequence divergence were analyzed in genes
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    beta-O-acetyltransferase (DBAT). N-terminal fragments of TS,
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    significantly elevated rates of amino acid substitution using a genetic
    algorithm. These findings demonstrate that the pattern of adaptive
    paclitaxel biosynthetic enzyme evolution can be documented between
    closely related Taxus species, where species-specific taxane metabolism
    has evolved recently.
 C1 [Yang, Ling] Chinese Acad Sci, Dalian Inst Chem Phys, Lab Pharmaceut Resource Discovery, Dalian, Peoples R China.
 RP Yang, L, Chinese Acad Sci, Dalian Inst Chem Phys, Lab Pharmaceut
    Resource Discovery, Dalian, Peoples R China.
 EM haodc@126.com
    yling@dicp.ac.cn
 FU Ministry of Science & Technology of China [2007CB707802]
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    Geng (YunNan Academy of Forestry, KunMing, China), YinKe Zhang
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    British Columbia Botanical Garden, Canada), and James Stevenson
    (University of Oxford Botanic Garden, UK). We are grateful to Sergei L.
    Kosakovsky Pond and Leslie M. Turner (University of California, San
    Diego, USA) for suggestions in genetic algorithm and parallel amino
    acid substitutions, respectively, and to two anonymous reviewers for
    their critical comments. This study is supported by the National 973
    Project (2007CB707802) of the Ministry of Science & Technology of China.
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 NR 36
 TC 5
 PU SPRINGER
 PI DORDRECHT
 PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
 SN 0016-6707
 J9 GENETICA
 JI Genetica
 PD MAR
 PY 2009
 VL 135
 IS 2
 BP 123
 EP 135
 DI 10.1007/s10709-008-9257-7
 PG 13
 SC Genetics & Heredity
 GA 403CE
 UT ISI:000263058600001
 ER
 
 PT J
 AU Sun, BL
    Zheng, CB
    Yang, MF
    Yuan, H
    Zhang, SM
    Wang, LX
 AF Sun, Bao-Liang
    Zheng, Cheng-Bi
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    Yuan, Hui
    Zhang, Su-Ming
    Wang, Le-Xin
 TI Dynamic Alterations of Cerebral Pial Microcirculation During
    Experimental Subarachnoid Hemorrhage
 SO CELLULAR AND MOLECULAR NEUROBIOLOGY
 LA English
 DT Article
 DE Subarachnoid hemorrhage; Secondary cerebral ischemia; Microcirculation;
    Rat
 ID NITRIC-OXIDE DONOR; BLOOD-FLOW; VASOSPASM; RATS; DYSFUNCTION;
    ENDOTHELIN; NIMODIPINE; ISCHEMIA; ARTERIES; RABBITS
 AB The study aimed to investigate the involvement of cerebral
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    rats were divided into non-SAH and SAH groups. Autologous arterial
    hemolysate was injected into rat's cisterna magna to induce SAH.
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    that there were no obvious changes of the diameters, flow velocity, and
    fluid state of microvessels in non-SAH group. With the exception of
    rare linear-granular flow in A4 arteriole, linear flow was observed in
    most of the arterioles. There was no blood agglutination in any of the
    arterioles. After SAH, abnormal cerebral pial microcirculation was
    found. Spasm of microvessels, decreased blood flow, and agglutination
    of red blood cells occurred. Five minutes following the induction of
    SAH, the diameters of the arterioles and venules significantly
    decreased. The decreased diameters persisted for 2 h after cisternal
    injection. Decreased flow velocity of venules was found from 5 to 90
    min after induction of SAH. Spasm of the basilar artery and increased
    brain malondialdehyde were also found after SAH. We concluded that
    cerebral microcirculation turbulence plays an important role in the
    development of secondary cerebral ischemia following SAH.
 C1 [Sun, Bao-Liang; Yuan, Hui] Taishan Med Coll, Affiliated Hosp, Dept Neurol, Tai An 271000, Shandong, Peoples R China.
    [Sun, Bao-Liang; Yuan, Hui] Taishan Med Coll, Affiliated Hosp, Inst Microcirculat, Tai An 271000, Shandong, Peoples R China.
    [Zhang, Su-Ming] Huazhong Univ Sci & Technol, Tongji Hosp, Dept Neurol, Tongji Med Coll, Wuhan 430030, Peoples R China.
    [Wang, Le-Xin] Charles Sturt Univ, Sch Biomed Sci, Wagga Wagga, NSW 2650, Australia.
 RP Sun, BL, Taishan Med Coll, Affiliated Hosp, Dept Neurol, 706 Taishan
    Ave, Tai An 271000, Shandong, Peoples R China.
 EM blsun@tsmc.edu.cn
    lwang@csu.edu.au
 FU National Natural Science Foundation of China [30570651, 30670724];
    Natural Medicine Research Foundation of Shandong, China [2005-231]
 FX This work was supported by the National Natural Science Foundation of
    China ( No. 30570651, 30670724) and the Natural Medicine Research
    Foundation of Shandong, China (2005-231).
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 NR 26
 TC 2
 PU SPRINGER/PLENUM PUBLISHERS
 PI NEW YORK
 PA 233 SPRING ST, NEW YORK, NY 10013 USA
 SN 0272-4340
 J9 CELL MOL NEUROBIOL
 JI Cell. Mol. Neurobiol.
 PD MAR
 PY 2009
 VL 29
 IS 2
 BP 235
 EP 241
 DI 10.1007/s10571-008-9316-8
 PG 7
 SC Cell Biology; Neurosciences
 GA 403XB
 UT ISI:000263114200010
 ER
 
 PT J
 AU Wiederschain, D
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 AF Wiederschain, Dmitri
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    Yang, Guizhi
    Huang, Alan
    Chen, Yan
    Caponigro, Giordano
    Yao, Yung-mae
    Lengauer, Christoph
    Sellers, William R.
    Benson, John D.
 TI Single-vector inducible lentiviral RNAi system for oncology target
    validation
 SO CELL CYCLE
 LA English
 DT Article
 DE inducible; single-vector; shRNA; xenograft; cancer; Bmi-1; Mel-18
 ID SHRNA EXPRESSION; INTERFERENCE; PROMOTER; CANCER; GENES
 AB The use of RNA interference (RNAi) has enabled loss-of-function studies
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    and validating cancer drug targets. Current transient siRNA and stable
    shRNA systems, however, have limited utility in accurately assessing
    the cancer dependency due to their short-lived effects and limited in
    vivo utility, respectively. In this study, a single-vector lentiviral,
    Tet-inducible shRNA system (pLKO-Tet-On) was generated to allow for the
    rapid generation of multiple stable cell lines with regulatable shRNA
    expression. We demonstrate the advantages and versatility of this
    system by targeting two polycomb group proteins, Bmi-1 and Mel-18, in a
    number of cancer cell lines. Our data show that pLKO-Tet-On-mediated
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    derivative, doxycycline, in a concentration-and time-dependent manner.
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    of the inducing agent. An additional, 17 distinct gene products have
    been targeted by inducible shRNAs with robust regulation in all cases.
    Importantly, we functionally validate the ability of the pLKO-Tet-On
    vector to reversibly silence targeted transcripts in vivo. The
    versatile and robust inducible lentiviral RNAi system reported herein
    can therefore serve as a powerful tool to rapidly reveal tumor cell
    dependence.
 C1 [Wiederschain, Dmitri; Wee, Susan; Chen, Lin; Loo, Alice; Yang, Guizhi; Huang, Alan; Chen, Yan; Caponigro, Giordano; Yao, Yung-mae; Lengauer, Christoph; Sellers, William R.; Benson, John D.] Novartis Inst Biomed Res, Cambridge, MA 02139 USA.
 RP Wiederschain, D, Novartis Inst Biomed Res, 250 Massachusetts Ave,
    Cambridge, MA 02139 USA.
 EM dmitri.wiederschain@novartis.com
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 NR 16
 TC 3
 PU LANDES BIOSCIENCE
 PI AUSTIN
 PA 1002 WEST AVENUE, 2ND FLOOR, AUSTIN, TX 78701 USA
 SN 1538-4101
 J9 CELL CYCLE
 JI Cell Cycle
 PD FEB 1
 PY 2009
 VL 8
 IS 3
 BP 498
 EP 504
 PG 7
 SC Cell Biology
 GA 402GS
 UT ISI:000263002800026
 ER
 
 PT J
 AU Yan, Y
    Zhang, J
    Guo, JL
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    Yang, YZ
 AF Yan, Yuan
    Zhang, Jie
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    Huang, Wei
    Yang, Yu-Zhen
 TI Multiple shRNA-mediated knockdown of TACE reduces the malignancy of
    HeLa cells
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 LA English
 DT Article
 DE shRNA; TACE; HeLa cell; Malignancy
 ID NECROSIS-FACTOR-ALPHA; CONVERTING-ENZYME; BREAST-CANCER; EXPRESSION;
    ADAM17; DISINTEGRIN; RECEPTOR; EGFR; RNA; INTERFERENCE
 AB Tumor necrosis factor-alpha (TNF-alpha) converting enzyme (TACE) is a
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    any single shRNA vector containing only one TACE shRNA. Silencing TACE
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    proliferation, adhesion and migration, as well as inducing apoptosis in
    these cells. Furthermore, our data suggest that the effects of TACE on
    the malignancy of HeLa cells may be mediated via activation of the EGFR
    (epidermal growth factor receptor) signaling pathway. Our findings
    suggest that using a combination of shRNAs within one vector to silence
    the expression of TACE might be a potential therapeutic strategy for
    tumors. (C) 2008 Published by Elsevier Ltd on behalf of International
    Federation for Cell Biology.
 C1 [Yan, Yuan; Zhang, Jie; Guo, Jian-Li; Yang, Yu-Zhen] Huazhong Univ Sci & Technol, Dept Biochem & Mol Biol, Tongji Med Coll, Wuhan 430030, Peoples R China.
    [Huang, Wei] Inst Med Sci, Wuhan 430014, Peoples R China.
 RP Yang, YZ, Huazhong Univ Sci & Technol, Dept Biochem & Mol Biol, Tongji
    Med Coll, Wuhan 430030, Peoples R China.
 EM yangyz@mails.tjmu.edu.cn
 FU The Natural Science Foundation of China [30500085]
 FX We sincerely thank Dr. Xiao-ou Li, Dr. Guishen Zhao and Dr. Wenfang
    Feng for their excellent technical assistance. This work was supported
    by a grant from The Natural Science Foundation of China (No. 30500085).
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 NR 30
 TC 2
 PU ACADEMIC PRESS LTD ELSEVIER SCIENCE LTD
 PI LONDON
 PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
 SN 1065-6995
 J9 CELL BIOL INT
 JI Cell Biol. Int.
 PD FEB
 PY 2009
 VL 33
 IS 2
 BP 158
 EP 164
 DI 10.1016/j.cellbi.2008.10.008
 PG 7
 SC Cell Biology
 GA 401YO
 UT ISI:000262980300004
 ER
 
 PT J
 AU Li, Y
    Song, JL
    Yang, P
    Zou, R
    Fan, XF
    Zhao, ZH
 AF Li, Yu
    Song, Jinlin
    Yang, Pu
    Zou, Rui
    Fan, Xiaofeng
    Zhao, Zhihe
 TI Establishment of a three-dimensional culture and mechanical loading
    system for skeletal myoblasts
 SO CELL BIOLOGY INTERNATIONAL
 LA English
 DT Article
 DE PLGA; Scaffolds; Myoblast; 3-D culture; Mechanical loading; Device;
    Cytomechanics
 ID PERIODONTAL-LIGAMENT CELLS; SMOOTH-MUSCLE-CELLS; SCAFFOLDS; STRETCH;
    STRESS; STRAIN; GROWTH; EXPRESSION; DIFFERENTIATION; PROLIFERATION
 AB Establishment of a three-dimensional (3-D) culture and mechanical
    loading system which simulates the in vivo environment is critical in
    cytomechanical studies. The present article attempts to do this by
    integrating porous PLGA scaffolds with a four-point bending strain
    unit. Three types of PLGA scaffolds with three average pore sizes were
    synthesized, i.e., type I (60-88 mm), type II (88-100 mm) and type III
    (100-125 mm). To establish the 3-D mechanical loading system, PLGA
    membrane was integrated with conventional force-loading plates and the
    third passage skeletal myoblasts from neonatal Sprague-Dawley (SD) rats
    were seeded. Small PLGA membranes were put in 24-well plates followed
    by cell implantation and MTT assay was performed on days 1, 2, 4, 6 and
    8 to compare biocompatibility of the three types of scaffolds. After 3
    days' culture, many more cells had grown in type II than in type I or
    type III under fluorescence microscopy. In the MTT assay, OD of type II
    was significantly higher (P < 0.05) than the other two, especially at
    the early stage. As type II proved to be the best among the three, it
    was used as the scaffold in the preliminary mechanical loading study
    and 4000 mu strain cyclic uniaxial strain was imposed. The system
    worked well and it was found that short to median time of stretching
    enhances while prolonged time of stretching inhibits cell proliferative
    activity of the 3-D cultured skeletal myoblasts(P < 0.05). It is
    concluded that the combination of PLGA scaffolds with a four-point
    bending strain unit provides a satisfactory 3-D mechanical loading
    system. (C) 2008 International Federation for Cell Biology. Published
    by Elsevier Ltd. All rights reserved.
 C1 [Li, Yu; Yang, Pu; Zou, Rui; Fan, Xiaofeng; Zhao, Zhihe] Sichuan Univ, W China Stomatol Hosp, Dept Orthodont, State Key Lab Oral Dis, Chengdu 610041, Sichuan, Peoples R China.
    [Song, Jinlin] Chongqing Med Univ, Dept Orthodont, Coll Stomatol, Chongqing 400015, Peoples R China.
    [Zou, Rui] Xi An Jiao Tong Univ, Dept Orthodont, Stomatol Hosp, Xian 710004, Shanxi, Peoples R China.
 RP Zhao, ZH, Sichuan Univ, W China Stomatol Hosp, Dept Orthodont, State
    Key Lab Oral Dis, Chengdu 610041, Sichuan, Peoples R China.
 EM zhaozhihe1963@yahoo.com.cn
 FU National Nature Science Foundation of China [10472138]
 FX We owe our thanks to Chengdu Institute of Organic Chemistry, the
    Chinese Academy of Sciences, for the synthesis of PLGA membrane. This
    work was supported by the National Nature Science Foundation of China
    (No. 10472138).
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 TC 4
 PU ACADEMIC PRESS LTD ELSEVIER SCIENCE LTD
 PI LONDON
 PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
 SN 1065-6995
 J9 CELL BIOL INT
 JI Cell Biol. Int.
 PD FEB
 PY 2009
 VL 33
 IS 2
 BP 192
 EP 198
 DI 10.1016/j.cellbi.2008.11.002
 PG 7
 SC Cell Biology
 GA 401YO
 UT ISI:000262980300009
 ER
 
 PT J
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    Bergman, P
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    Triantafellow, E
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 AF Nicklin, Paul
    Bergman, Philip
    Zhang, Bailin
    Triantafellow, Ellen
    Wang, Henry
    Nyfeler, Beat
    Yang, Haidi
    Hild, Marc
    Kung, Charles
    Wilson, Christopher
    Myer, Vic E.
    MacKeigan, Jeffrey P.
    Porter, Jeffrey A.
    Wang, Y. Karen
    Cantley, Lewis C.
    Finan, Peter M.
    Murphy, Leon O.
 TI Bidirectional Transport of Amino Acids Regulates mTOR and Autophagy
 SO CELL
 LA English
 DT Article
 ID P70 S6 KINASE; CELL-GROWTH; FUNCTIONAL-CHARACTERIZATION;
    GLUTAMINE-METABOLISM; MAMMALIAN-CELLS; GENE-EXPRESSION; RAG GTPASES;
    SYSTEM L; TOR; PROTEIN
 AB Amino acids are required for activation of the mammalian target of
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 C1 Novartis Inst BioMed Res, Dev & Mol Pathways, Cambridge, MA 02139 USA.
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    [Cantley, Lewis C.] Beth Israel Deaconess Med Ctr, Div Signal Transduct, Boston, MA 02115 USA.
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 RP Murphy, LO, Novartis Inst BioMed Res, Dev & Mol Pathways, 250
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 EM leon.murphy@novartis.com
 FU Novartis Pharmaceuticals 
 FX We would like to thank Stephen Helliwell, Dan Garza, Dmitri
    Wiederschain, Greg Michaud, Alex Huang, Leslie Pond, and John Westwick
    for support, comments, and advice; and to Alan Abrams for help with
    graphics; and Akos Szilvasi for help with confocal imaging. All authors
    ( except L. C. C.) are employees of Novartis Pharmaceuticals.
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 NR 59
 TC 85
 PU CELL PRESS
 PI CAMBRIDGE
 PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
 SN 0092-8674
 J9 CELL
 JI Cell
 PD FEB 6
 PY 2009
 VL 136
 IS 3
 BP 521
 EP 534
 DI 10.1016/j.cell.2008.11.044
 PG 14
 SC Biochemistry & Molecular Biology; Cell Biology
 GA 403ZN
 UT ISI:000263120600021
 ER
 
 PT J
 AU Chauhan, SC
    Vannatta, K
    Ebeling, MC
    Vinayek, N
    Watanabe, A
    Pandey, KK
    Bell, MC
    Koch, MD
    Aburatani, H
    Lio, YL
    Jaggi, M
 AF Chauhan, Subhash C.
    Vannatta, Kelley
    Ebeling, Mara C.
    Vinayek, Namita
    Watanabe, Akira
    Pandey, Krishan K.
    Bell, Maria C.
    Koch, Michael D.
    Aburatani, Hiroyuki
    Lio, Yuhlong
    Jaggi, Meena
 TI Expression and Functions of Transmembrane Mucin MUC13 in Ovarian Cancer
 SO CANCER RESEARCH
 LA English
 DT Article
 ID CELL-SURFACE MUCIN; GENE-EXPRESSION; PANCREATIC ADENOCARCINOMA;
    DIAGNOSTIC-SIGNIFICANCE; EPISIALIN MUC1; OVEREXPRESSION; ADHESION;
    P21-ACTIVATED-KINASE-1; MOTILITY; KINASE
 AB MUC13, a transmembrane mucin, is normally expressed in gastrointestinal
    and airway epithelium. Its aberrant expression has been correlated with
    gastric colon and cancer. However, the expression and functions of
    MUC13 in ovarian cancer are unknown. In the present study, the
    expression profile and functions of MUC13 were analyzed to elucidate
    its potential role in ovarian cancer diagnosis and pathogenesis. A
    recently generated monoclonal antibody (clone PPZ0020) was used to
    determine the expression profile of MUC13 by immunohistochemistry using
    ovarian cancer tissue micro-arrays and 56 additional epithelial ovarian
    cancer (EOC) samples. The expression of MUC13 was significantly (P <
    0.005) higher in cancer samples compared with the normal ovary/benign
    tissues. Among all ovarian cancer types, MUC13 expression was
    specifically present in EOC. For the functional analyses, a full-length
    MUC13 gene cloned in pcDNA3.1 was expressed in a MUC13 null ovarian
    cancer cell line, SKOV-3. Here, we show that the exogenous MUC13
    expression induced morphologic changes, including scattering of cells.
    These changes were abrogated through c-Jun NH2 kinase (JNK) chemical
    inhibitor (SP600125) or JNK2 siRNA. Additionally, a marked reduction in
    cell-cell adhesion and significant (P < 0.05) increases in cell
    motility, proliferation, and tumorigenesis in a xenograft mouse model
    system were observed upon exogenous MUC13 expression. These cellular
    characteristics were correlated with up-regulation of HER2,
    p21-activated kinase 1, and p38 protein expression. Our findings show
    the aberrant expression of MUC13 in ovarian cancer and that its
    expression alters the cellular characteristics of SKOV-3 cells. This
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    2009;69(3):765-74]
 C1 [Chauhan, Subhash C.] Univ S Dakota, Sanford Res Univ S Dakota, Canc Biol Res Ctr, Sanford Sch Med,Dept Obstet & Gynecol, Sioux Falls, SD 57105 USA.
    [Koch, Michael D.] Sanford Sch Med, Lab Med & Pathol, Sioux Falls, SD USA.
    [Watanabe, Akira; Aburatani, Hiroyuki] Univ Tokyo, Tokyo, Japan.
    [Lio, Yuhlong] Univ S Dakota, Dept Math Sci, Vermillion, SD 57069 USA.
    [Pandey, Krishan K.] St Louis Univ, Inst Mol Virol, St Louis, MO 63103 USA.
 RP Chauhan, SC, Univ S Dakota, Sanford Res Univ S Dakota, Canc Biol Res
    Ctr, Sanford Sch Med,Dept Obstet & Gynecol, 1400 W 22nd St, Sioux
    Falls, SD 57105 USA.
 EM subhash.chauhan@usd.edu
 FU Sanford Research/University of South Dakota ; Sanford School of
    Medicine research ; NFAT ; NEDO, Japan ; NIH NCRR [P20 RR17662]
 FX Grant support: Sanford Research/University of South Dakota grant,
    Sanford School of Medicine research grant. (S.C. Chauhan). and NFAT
    project (H. Aburatani) from NEDO, Japan. Confocal microscopy studies
    were conducted at the Sanford Research/University of South Dakota
    Imaging Core. This core facility is supported by NIH NCRR grant P20
    RR17662 to A. Martin Gerdes.
    The costs of publication of this article were defrayed in part by the
    payment of page charges. This article must therefore be hereby marked
    advertisement in accordance with 18 U.S.C. Section 1734 solely to
    indicate this fact.
    We thank Cathy Christopherson for editorial assistance and Dr. Keith
    Miskimins (director of Cancer Biology Research Center) for his
    constructive suggestions.
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 NR 37
 TC 8
 PU AMER ASSOC CANCER RESEARCH
 PI PHILADELPHIA
 PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
 SN 0008-5472
 J9 CANCER RES
 JI Cancer Res.
 PD FEB 1
 PY 2009
 VL 69
 IS 3
 BP 765
 EP 774
 DI 10.1158/0008-5472.CAN-08-0587
 PG 10
 SC Oncology
 GA 402YJ
 UT ISI:000263048700009
 ER
 
 PT J
 AU Watanabe, T
    Kobunai, T
    Sakamoto, E
    Yamamoto, Y
    Konishi, T
    Horiuchi, A
    Shimada, R
    Oka, T
    Nagawa, H
 AF Watanabe, Toshiaki
    Kobunai, Takashi
    Sakamoto, Etsuko
    Yamamoto, Yoko
    Konishi, Tsuyoshi
    Horiuchi, Atsushi
    Shimada, Ryu
    Oka, Toshinori
    Nagawa, Hirokazu
 TI Gene Expression Signature for Recurrence in Stage III Colorectal Cancers
 SO CANCER
 LA English
 DT Article
 DE colorectal cancer; recurrence; lymph node metastasis; stage III;
    microarray; prediction; copy number; CABIN1; Duke stage C; tailored
    therapy
 ID MICROARRAY ANALYSIS; DNA MICROARRAY; HYBRIDIZATION; POLYMORPHISM;
    PREDICTION; MUTATIONS; PROFILES; SURVIVAL
 AB BACKGROUND: Colorectal cancer patients with lymph node metastases
    (stage III) show poorer prognosis than those without. Predicting
    development of recurrence may guide the need for intensive follow-up
    and/or adjuvant chemotherapy in such patients. The authors' objective
    was to identify a set of discriminating genes that could predict
    recurrence in stage III colorectal cancer. METHODS: Thirty-six stage
    III colorectal cancer patients were studied. Tumor samples were
    obtained from surgically resected specimens. Thirteen patients
    developed recurrence, whereas 23 patients did not. Gene expression
    profiles were determined using human HG-U133 Plus 2.0 Gene Chip
    (Affymetrix, Santa Clara, Calif). RESULTS: The authors identified 45
    discriminating genes between patients with and without recurrence. By
    using this gene set, they established a new model to predict recurrence
    with an accuracy of 90.9%. The discriminating genes included
    calcineurin-binding protein 1 (CABIN1), whose expression differed
    remarkably between patients with and without recurrence (P = .0073).
    The authors further examined the DNA copy number of CABIN1 and were
    able to show a significant relation with recurrence (P < .012).
    Patients having CABIN1 gene loss demonstrated a higher risk of
    recurrence (odds ratio, 18.8). DNA copy number of CABIN1 alone could
    predict recurrence with an accuracy of 80.0%. CONCLUSIONS: The results
    of the current study demonstrated that gene expression profiling is
    useful in predicting recurrence in stage III colorectal cancer. The
    authors identified CABIN1 among discriminating genes that may play a
    key role in the development of recurrence. These results may help to
    establish an individualized therapy for stage III colorectal cancer.
    Cancer 2009;115:28392. (C) 2009 American Cancer Society.
 C1 [Watanabe, Toshiaki] Teikyo Univ, Sch Med, Dept Surg, Itabashi Ku, Tokyo 1738605, Japan.
    [Sakamoto, Etsuko; Oka, Toshinori] Taiho Pharmaceut Co Ltd, Tokushima Res Ctr, Personalized Med Res Lab, Tokushima, Japan.
    [Konishi, Tsuyoshi; Nagawa, Hirokazu] Univ Tokyo, Dept Surg Oncol, Tokyo, Japan.
 RP Watanabe, T, Teikyo Univ, Sch Med, Dept Surg, Itabashi Ku, 2-11-1 Kaga,
    Tokyo 1738605, Japan.
 EM toshwatanabe@yahoo.co.jp
 FU Ministry of Education, Culture, sports, Science, and Technology of
    Japan ; Ministry of Health, Labor and Welfare of Japan 
 FX This study was supported by a Grant-in-Aid for Scientific Research from
    the Ministry of Education, Culture, sports, Science, and Technology of
    Japan and a grant from the Ministry of Health, Labor and Welfare of
    Japan.
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 NR 20
 TC 5
 PU JOHN WILEY & SONS INC
 PI HOBOKEN
 PA 111 RIVER ST, HOBOKEN, NJ 07030 USA
 SN 0008-543X
 J9 CANCER
 JI Cancer
 PD JAN 15
 PY 2009
 VL 115
 IS 2
 BP 283
 EP 292
 DI 10.1002/cncr.24023
 PG 10
 SC Oncology
 GA 401LJ
 UT ISI:000262941900008
 ER
 
 PT J
 AU Patel, N
    Gonsalves, CS
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    Malik, P
    Kalra, VK
 AF Patel, Nitin
    Gonsalves, Caryn S.
    Yang, Minyang
    Malik, Punam
    Kalra, Vijay K.
 TI Placenta growth factor induces 5-lipoxygenase-activating protein to
    increase leukotriene formation in sickle cell disease
 SO BLOOD
 LA English
 DT Article
 ID HYPOXIA-INDUCIBLE FACTOR; ACUTE CHEST SYNDROME; PHOSPHOLIPASE A(2)
    LEVELS; VEIN ENDOTHELIAL-CELLS; LUNG-FUNCTION; SIGNAL-TRANSDUCTION;
    THP-1 CELLS; PULMONARY-HYPERTENSION; ADVERSE OUTCOMES; GENE-EXPRESSION
 AB Individuals with sickle cell disease (SCD) have increased inflammation,
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    peripheral blood mononuclear cells (MNCs) in patients with SCD,
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    hypoxia inducible factor-1 alpha (HIF-1 alpha). HIF-1 alpha small
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    immunoprecipitation (ChIP) analysis. PlGF also increased HIF-1 alpha
    binding to the HRE in the FLAP promoter. Therefore, it is likely that
    the intrinsically elevated levels of PlGF in SCD subjects contribute to
    increased LT, which in turn, mediate both inflammation and AH. Herein,
    we identify a mechanism of increased LT in SCD and show HIF-1 alpha as
    a hypoxia-independent target of PlGF. These studies provide new avenues
    to ameliorate these complications. (Blood. 2009;113:1129-1138)
 C1 [Patel, Nitin; Gonsalves, Caryn S.; Kalra, Vijay K.] Univ So Calif, Dept Biochem & Mol Biol, Keck Sch Med, Los Angeles, CA 90033 USA.
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 RP Kalra, VK, Univ So Calif, Dept Biochem & Mol Biol, Keck Sch Med, HMR
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 EM Punam.Malik@cchmc.org
    vkalra@usc.edu
 FU Institutional Core of USC Research Center for Liver Disease for the use
    of the spectrofluorometer and sequence detection instrument [NIH-P30-DK
    048522]; National Institutes of Health (NIH) [HL-070595, R01-HL-079916]
 FX We thank Dr Timothy Bigby (VA Hospital San Diego, La Jolla, CA) for
    kindly providing FLAP promoter constructs. We thank Institutional Core
    of USC Research Center for Liver Disease for the use of the
    spectrofluorometer and sequence detection instrument (NIH-P30-DK
    048522).
    This work was supported by National Institutes of Health (NIH) grant
    HL-070595 (CSCC) and R01-HL-079916.
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 NR 66
 TC 9
 PU AMER SOC HEMATOLOGY
 PI WASHINGTON
 PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
 SN 0006-4971
 J9 BLOOD
 JI Blood
 PD JAN 29
 PY 2009
 VL 113
 IS 5
 BP 1129
 EP 1138
 DI 10.1182/blood-2008-07-169821
 PG 10
 SC Hematology
 GA 400RD
 UT ISI:000262885300021
 ER
 
 PT J
 AU Be'er, A
    Zhang, HP
    Florin, EL
    Payne, SM
    Ben-Jacob, E
    Swinney, HL
 AF Be'er, Avraham
    Zhang, H. P.
    Florin, E. -L.
    Payne, Shelley M.
    Ben-Jacob, Eshel
    Swinney, Harry L.
 TI Deadly competition between sibling bacterial colonies
 SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
    AMERICA
 LA English
 DT Article
 DE bacterial competition; bacterial growth; growth inhibition;
    Paenibacillus dendritiformis
 ID COOPERATIVE ORGANIZATION; MULTICELLULAR ORGANISMS; SELF-ORGANIZATION;
    BACILLUS-SUBTILIS; ADAPTIVE MUTATION; ESCHERICHIA-COLI; GROWTH;
    COMMUNICATION; CANNIBALISM; PATTERNS
 AB Bacteria can secrete a wide array of antibacterial compounds when
    competing with other bacteria for the same resources. Some of these
    compounds, such as bacteriocins, can affect bacteria of similar or
    closely related strains. In some cases, these secretions have been
    found to kill sibling cells that belong to the same colony. Here, we
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    inhibition is observed. However, growth inhibition and cell death are
    observed if material extracted from the agar between 2 growing colonies
    is introduced outside a growing single colony. To interpret the
    observations, we devised a simple mathematical model for the secretion
    of an antibacterial compound. Simulations of this model illustrate how
    secretions from neighboring colonies can be deadly, whereas secretions
    from a single colony growing from a droplet are not.
 C1 [Be'er, Avraham; Zhang, H. P.; Florin, E. -L.; Swinney, Harry L.] Univ Texas Austin, Ctr Nonlinear Dynam, Austin, TX 78712 USA.
    [Be'er, Avraham; Zhang, H. P.; Florin, E. -L.; Swinney, Harry L.] Univ Texas Austin, Dept Phys, Austin, TX 78712 USA.
    [Payne, Shelley M.] Univ Texas Austin, Sect Mol Genet & Microbiol, Austin, TX 78712 USA.
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 RP Be'er, A, Univ Texas Austin, Ctr Nonlinear Dynam, Austin, TX 78712 USA.
 EM abeer@chaos.utexas.edu
    eshelbj@gmail.com
    swinney@chaos.utexas.edu
 FU Robert A. Welch Foundation ; Tauber Funds ; Maguy-Glass chair in
    Physics of Complex Systems ; Sid W. Richardson Foundation 
 FX We thank Inna Brainis for providing the bacterial strain and the growth
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    boundary conditions; and Efrat Hagai, Dalit Roth, and Oren Kalisman for
    their help. E.-L. F. acknowledges support by the Robert A. Welch
    Foundation, E. B.-J. acknowledges support by the Tauber Funds and the
    Maguy-Glass chair in Physics of Complex Systems, and H. L. S.
    acknowledges support by the Sid W. Richardson Foundation.
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 TC 13
 PU NATL ACAD SCIENCES
 PI WASHINGTON
 PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA
 SN 0027-8424
 J9 PROC NAT ACAD SCI USA
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 PD JAN 13
 PY 2009
 VL 106
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 BP 428
 EP 433
 DI 10.1073/pnas.0811816106
 PG 6
 SC Multidisciplinary Sciences
 GA 399MM
 UT ISI:000262804000015
 ER
 
 PT J
 AU Kessler, JD
    Hasegawa, H
    Brun, SN
    Emmenegger, BA
    Yang, ZJ
    Dutton, JW
    Wang, F
    Wechsler-Reya, RJ
 AF Kessler, Jessica D.
    Hasegawa, Hiroshi
    Brun, Sonja N.
    Emmenegger, Brian A.
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    Wechsler-Reya, Robert J.
 TI N-myc alters the fate of preneoplastic cells in a mouse model of
    medulloblastoma
 SO GENES & DEVELOPMENT
 LA English
 DT Article
 DE Medulloblastoma; brain tumor; preneoplastic; hedgehog; patched
 ID GRANULE NEURON PRECURSORS; SONIC HEDGEHOG; STEM-CELLS; BRAIN-TUMORS;
    CEREBELLAR DEVELOPMENT; GENETIC ALTERATIONS; PANCREATIC-CANCER;
    NERVOUS-SYSTEM; IN-SITU; K-RAS
 AB Studying the early stages of cancer can provide important insight into
    the molecular basis of the disease. We identified a preneoplastic stage
    in the patched (ptc) mutant mouse, a model for the brain tumor
    medulloblastoma. Preneoplastic cells (PNCs) are found in most ptc
    mutants during early adulthood, but only 15% of these animals develop
    tumors. Although PNCs are found in mice that develop tumors, the
    ability of PNCs to give rise to tumors has never been demonstrated
    directly, and the fate of cells that do not form tumors remains
    unknown. Using genetic fate mapping and orthotopic transplantation, we
    provide definitive evidence that PNCs give rise to tumors, and show
    that the predominant fate of PNCs that do not form tumors is
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    amplified in medulloblastoma, can dramatically alter the fate of PNCs,
    preventing differentiation and driving progression to tumors.
    Importantly, N-myc allows PNCs to grow independently of hedgehog
    signaling, making the resulting tumors resistant to hedgehog
    antagonists. These studies provide the first direct evidence that PNCs
    can give rise to tumors, and demonstrate that identification of genetic
    changes that promote tumor progression is critical for designing
    effective therapies for cancer.
 C1 [Kessler, Jessica D.; Brun, Sonja N.; Emmenegger, Brian A.; Yang, Zeng-Jie; Dutton, John W.; Wechsler-Reya, Robert J.] Duke Univ, Med Ctr, Dept Pharmacol & Canc Biol, Durham, NC 27710 USA.
    [Hasegawa, Hiroshi; Wang, Fan] Duke Univ, Med Ctr, Dept Cell Biol, Durham, NC 27710 USA.
 RP Wechsler-Reya, RJ, Duke Univ, Med Ctr, Dept Pharmacol & Canc Biol,
    Durham, NC 27710 USA.
 EM rw.reya@duke.edu
 FU National Cancer Center ; NIDCR [DE016550]; Whitehall Foundation ;
    McKnight Endowment Fund for Neuroscience ; Japanese Society for the
    Promotion of Science ; Children's Brain Tumor Foundation ; McDonnell
    Foundation ; Pediatric Brain Tumor Foundation of the US ; NINDS
    [NS-052323-01]
 FX We thank Sam Johnson and the Duke Light Microscopy Core Facility for
    assistance with microscopy, Bob Weinberg for helpful advice and
    insight, Simon Gregory for use of the Laser Capture Microdissection
    system, and Tracy-Ann Read for assistance with transplantation. This
    work was supported by funding from the National Cancer Center (J.D.K.),
    NIDCR grant #DE016550 ( F. W), the Whitehall Foundation ( F. W), the
    McKnight Endowment Fund for Neuroscience ( F. W), the Japanese Society
    for the Promotion of Science ( H. H), the Children's Brain Tumor
    Foundation ( R. W. R.), the McDonnell Foundation ( R. W. R.), the
    Pediatric Brain Tumor Foundation of the US ( R. W. R.), and NINDS grant
    #NS-052323-01 ( R. W. R.).
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 NR 70
 TC 15
 PU COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT
 PI WOODBURY
 PA 500 SUNNYSIDE BLVD, WOODBURY, NY 11797-2924 USA
 SN 0890-9369
 J9 GENE DEVELOP
 JI Genes Dev.
 PD JAN 15
 PY 2009
 VL 23
 IS 2
 BP 157
 EP 170
 DI 10.1101/gad.1759909
 PG 14
 SC Cell Biology; Developmental Biology; Genetics & Heredity
 GA 399JR
 UT ISI:000262796700005
 ER
 
 PT J
 AU Yang, XH
    Zou, L
 AF Yang, Xiaohong H.
    Zou, Lee
 TI Dual functions of DNA replication forks in checkpoint signaling and
    PCNA ubiquitination
 SO CELL CYCLE
 LA English
 DT Article
 DE DNA damage; checkpoint; replication fork; PCNA; ATR; Chk1;
    ubiquitination
 ID S-PHASE CHECKPOINT; SACCHAROMYCES-CEREVISIAE; MONOUBIQUITINATED PCNA;
    INTERACTING PROTEIN; MAMMALIAN-CELLS; STRANDED-DNA; MRC1; PROGRESSION;
    POLYMERASE; COMPLEX
 AB During cell proliferation, DNA damage inflicted by intrinsic or
    extrinsic genotoxic stresses impose a thereat to DNA replication. The
    stability of the DNA replication forks that encounter DNA damage is
    crucial for genomic integrity. Both the ATR-regulated checkpoint
    pathway and the translesion DNA synthesis mediated by the ubiquitinated
    PCNA are important for continuous replication of damaged DNA. We have
    recently shown that Chk1, a key effector kinase of ATR in checkpoint
    response, is required for efficient PCNA ubiquitination after DNA
    damage. Surprisingly, the ubiquitination of PCNA is independent of ATR,
    but regulated by Claspin, a replication protein that mediates the
    activation of Chk1 by ATR. Like Claspin, Timeless and Rad17, two other
    Chk1 regulators at stressed replication forks, are also implicated in
    PCNA ubiquitination. These findings suggest that while ATR signaling
    and PCNA ubiquitination are two independent processes, they are
    mediated by a common group of proteins including Chk1 and it regulators
    at replication forks. Furthermore, these data raise the possibility
    that Chk1 and its regulators may constitute a functional module at
    replication forks to enable multiple stress responses.
 C1 [Yang, Xiaohong H.; Zou, Lee] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Ctr Canc, Charlestown, MA 02129 USA.
    [Zou, Lee] Harvard Univ, Sch Med, Dept Pathol, Boston, MA 02115 USA.
 RP Zou, L, Harvard Univ, Massachusetts Gen Hosp, Sch Med, Ctr Canc, Bldg
    149-7404,13th St, Charlestown, MA 02129 USA.
 EM zou.lee@mgh.harvard.edu
 FU NIH [GM076388]; Ellison Medical Foundation ; Susan G. Komen for the
    Cure 
 FX The Zou laboratory is supported by grants from the NIH (GM076388),
    Susan G. Komen for the Cure, and the Ellison Medical Foundation.
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 NR 43
 TC 7
 PU LANDES BIOSCIENCE
 PI AUSTIN
 PA 1002 WEST AVENUE, 2ND FLOOR, AUSTIN, TX 78701 USA
 SN 1538-4101
 J9 CELL CYCLE
 JI Cell Cycle
 PD JAN 15
 PY 2009
 VL 8
 IS 2
 BP 191
 EP 194
 PG 4
 SC Cell Biology
 GA 396WT
 UT ISI:000262622800005
 ER
 
 PT J
 AU Zhang, YX
    Yan, LB
    Zhou, Z
    Yang, PG
    Tian, E
    Zhang, K
    Zhao, Y
    Li, ZP
    Song, B
    Han, JH
    Miao, L
    Zhang, H
 AF Zhang, Yuxia
    Yan, Libo
    Zhou, Zhi
    Yang, Peiguo
    Tian, E.
    Zhang, Kai
    Zhao, Yu
    Li, Zhipeng
    Song, Bing
    Han, Jinghua
    Miao, Long
    Zhang, Hong
 TI SEPA-1 Mediates the Specific Recognition and Degradation of P Granule
    Components by Autophagy in C. elegans
 SO CELL
 LA English
 DT Article
 ID CAENORHABDITIS-ELEGANS; GERM GRANULES; MOLECULAR MACHINERY;
    SELF-DIGESTION; MECHANISMS; MICE; NEURODEGENERATION; PROTEINS; DISEASE;
    P62
 AB How autophagy, an evolutionarily conserved intracellular catabolic
    system for bulk degradation, selectively degrades protein aggregates is
    poorly understood. Here, we show that several maternally derived germ P
    granule components are selectively eliminated by autophagy in somatic
    cells during C. elegans embryogenesis. The activity of sepa-1 is
    required for the degradation of these P granule components and for
    their accumulation into aggregates, termed PGL granules, in autophagy
    mutants. SEPA-1 forms protein aggregates and is also a preferential
    target of autophagy. SEPA-1 directly binds to the P granule component
    PGL-3 and also to the autophagy protein LGG-1/Atg8. SEPA-1 aggregates
    consistently colocalize with PGL granules and with LGG-1 puncta. Thus,
    SEPA-1 functions as a bridging molecule in mediating the specific
    recognition and degradation of P granule components by autophagy. Our
    study reveals a mechanism for preferential degradation of protein
    aggregates by autophagy and emphasizes the physiological significance
    of selective autophagy during animal development.
 C1 [Zhang, Yuxia; Yan, Libo; Zhou, Zhi; Yang, Peiguo; Tian, E.; Zhao, Yu; Li, Zhipeng; Song, Bing; Han, Jinghua; Zhang, Hong] Natl Inst Biol Sci, Beijing 102206, Peoples R China.
    [Yan, Libo] Chinese Acad Med Sci, Grad Program, Beijing 100730, Peoples R China.
    [Yan, Libo] Peking Union Med Coll, Beijing 100730, Peoples R China.
    [Zhang, Kai; Miao, Long] Chinese Acad Sci, Inst Biophys, Natl Lab Biomacromol, Beijing 100101, Peoples R China.
 RP Zhang, H, Natl Inst Biol Sci, Beijing 102206, Peoples R China.
 EM zhanghong@nibs.ac.cn
 FU National High Technology Projects 863 [2005AA210910]
 FX We thank Drs. Susan Strome and Xiaodong Wang for their helpful comments
    on the manuscript, Dr. David Hall for his advice on immuno EM, and Dr.
    Isabel Hanson for editing the manuscript. This work was supported by
    the National High Technology Projects 863 (2005AA210910).
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 NR 20
 TC 30
 PU CELL PRESS
 PI CAMBRIDGE
 PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
 SN 0092-8674
 J9 CELL
 JI Cell
 PD JAN 23
 PY 2009
 VL 136
 IS 2
 BP 308
 EP 321
 DI 10.1016/j.cell.2008.12.022
 PG 14
 SC Biochemistry & Molecular Biology; Cell Biology
 GA 397FR
 UT ISI:000262648800019
 ER
 
 PT J
 AU Das, J
    Ho, M
    Zikherman, J
    Govern, C
    Yang, M
    Weiss, A
    Chakraborty, AK
    Roose, JP
 AF Das, Jayajit
    Ho, Mary
    Zikherman, Julie
    Govern, Christopher
    Yang, Ming
    Weiss, Arthur
    Chakraborty, Arup K.
    Roose, Jeroen P.
 TI Digital Signaling and Hysteresis Characterize Ras Activation in
    Lymphoid Cells
 SO CELL
 LA English
 DT Article
 ID NUCLEOTIDE EXCHANGE FACTOR; T-CELLS; POSITIVE FEEDBACK; DENDRITIC
    CELLS; SOS; SEVENLESS; GENE; TRANSDUCTION; REQUIREMENT; LYMPHOCYTES
 AB Activation of Ras proteins underlies functional decisions in diverse
    cell types. Two molecules, RasGRP and SOS, catalyze Ras activation in
    lymphocytes. Binding of active Ras to SOS' allosteric pocket markedly
    increases SOS' activity establishing a positive feedback loop for
    SOS-mediated Ras activation. Integrating in silico and in vitro
    studies, we demonstrate that digital signaling in lymphocytes (cells
    are "on'' or "off'') is predicated upon feedback regulation of SOS.
    SOS' feedback loop leads to hysteresis in the dose-response curve,
    which can enable a capacity to sustain Ras activation as stimuli are
    withdrawn and exhibit "memory'' of past encounters with antigen. Ras
    activation via RasGRP alone is analog (graded increase in amplitude
    with stimulus). We describe how complementary analog (RasGRP) and
    digital (SOS) pathways act on Ras to efficiently convert analog input
    to digital output. Numerous predictions regarding the impact of our
    findings on lymphocyte function and development are noted.
 C1 [Zikherman, Julie; Weiss, Arthur] Univ Calif San Francisco, Dept Med, Div Rheumatol, San Francisco, CA 94143 USA.
    [Weiss, Arthur] Univ Calif San Francisco, Howard Hughes Med Inst, San Francisco, CA 94143 USA.
    [Ho, Mary; Roose, Jeroen P.] Univ Calif San Francisco, Dept Anat, San Francisco, CA 94143 USA.
    [Das, Jayajit; Govern, Christopher; Yang, Ming; Chakraborty, Arup K.] MIT, Dept Chem Engn, Cambridge, MA 02139 USA.
    [Chakraborty, Arup K.] MIT, Dept Chem, Cambridge, MA 02139 USA.
    [Chakraborty, Arup K.] MIT, Dept Biol Engn, Cambridge, MA 02139 USA.
 RP Weiss, A, Univ Calif San Francisco, Dept Med, Div Rheumatol, 513
    Parnassus Ave, San Francisco, CA 94143 USA.
 EM aweiss@medicine.ucsf.edu
    arupc@mit.edu
    jeroen.roose@ucsf.edu
 FU NIH Director's Pioneer [1PO1/AI071195/01]; Rosalind Russell Medical
    Research Center for Arthritis ; NCI [K01CA113367]; Arthritis Foundation
    ; Sandler Foundation 
 FX We thank Dr. Kurosaki for DT40 lines and Dr. Dafna Bar-sagi for the
    H-RasG59E38 plasmid. We are grateful to Dr. DeFranco and members of the
    Weiss, Chakraborty, and Roose labs for critical reading of the
    manuscript. We apologize to colleagues we could not cite due to space
    constraints. Financial support: NIH Director's Pioneer Award and
    1PO1/AI071195/01 (A. K. C.), the Howard Hughes Medical Institute as
    well as the Rosalind Russell Medical Research Center for Arthritis (A.
    W.), and the NCI (K01CA113367), Arthritis Foundation, and Sandler
    Foundation (J.P.R.).
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 NR 39
 TC 44
 PU CELL PRESS
 PI CAMBRIDGE
 PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
 SN 0092-8674
 J9 CELL
 JI Cell
 PD JAN 23
 PY 2009
 VL 136
 IS 2
 BP 337
 EP 351
 DI 10.1016/j.cell.2008.11.051
 PG 15
 SC Biochemistry & Molecular Biology; Cell Biology
 GA 397FR
 UT ISI:000262648800021
 ER
 
 PT J
 AU Aihara, T
    Takatsuka, Y
    Osumi, S
    Aogi, K
    Hozumi, Y
    Imoto, S
    Mukai, H
    Iwata, H
    Watanabe, T
    Shimizu, C
    Nakagami, K
    Tamura, M
    Ito, T
    Masuda, N
    Ogino, N
    Hisamatsu, K
    Mitsuyama, S
    Abe, H
    Yamaguchi, T
    Ohashi, Y
 AF Aihara, T.
    Takatsuka, Y.
    Osumi, S.
    Aogi, K.
    Hozumi, Y.
    Imoto, S.
    Mukai, H.
    Iwata, H.
    Watanabe, T.
    Shimizu, C.
    Nakagami, K.
    Tamura, M.
    Ito, T.
    Masuda, N.
    Ogino, N.
    Hisamatsu, K.
    Mitsuyama, S.
    Abe, H.
    Yamaguchi, T.
    Ohashi, Y.
 TI Phase III randomized adjuvant study of tamoxifen alone versus
    sequential tamoxifen and anastrozole in postmenopausal women with
    hormone-responsive breast cancer: N-SAS BC03 study
 SO CANCER RESEARCH
 LA English
 DT Meeting Abstract
 CT 31st Annual San Antonio Breast Cancer Symposium
 CY DEC 10-14, 2008
 CL San Antonio, TX
 C1 Aihara Hosp, Osaka, Japan.
    Kansai Rosai Hosp, Hyogo, Japan.
    Shikoku Canc Hosp, Ehime, Japan.
    Jichi Med Univ, Tochigi, Japan.
    Natl Canc Ctr Hosp E, Chiba, Japan.
    Aichi Canc Ctr Hosp, Aichi, Japan.
    Natl Canc Ctr, Tokyo, Japan.
    Shizuoka Prefectural Gen Hosp, Shizuoka, Japan.
    Hokkaido Canc Ctr, Sapporo, Hokkaido, Japan.
    Rinku Gen Med Ctr, Osaka, Japan.
    Osaka Natl Hosp, Osaka, Japan.
    Tondabayashi Hosp, Osaka, Japan.
    Hiroshima City Asa Hosp, Hiroshima, Japan.
    Kitakyushu Municipal Med Ctr, Fukuoka, Japan.
    Shiga Univ Med Sci, Shiga, Japan.
    Univ Tokyo, Tokyo, Japan.
 NR 0
 TC 0
 PU AMER ASSOC CANCER RESEARCH
 PI PHILADELPHIA
 PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
 SN 0008-5472
 J9 CANCER RES
 JI Cancer Res.
 PD JAN 15
 PY 2009
 VL 69
 IS 2
 SU Suppl. S
 BP 148S
 EP 148S
 PG 1
 SC Oncology
 GA 396HQ
 UT ISI:000262583200268
 ER
 
 PT J
 AU Duchnowska, R
    Jassem, J
    Shen, C
    Thorat, M
    Li, L
    Morimiya, A
    Zhao, Q
    Biernat, W
    Mandat, T
    Staszkiewicz, R
    Och, W
    Szostak, W
    Gugala, K
    Trojanowski, T
    Czartoryska-Arlukowicz, B
    Szczylik, C
    Nakshatri, H
    Steeg, P
    Sledge, G
    Badve, S
 AF Duchnowska, R.
    Jassem, J.
    Shen, C.
    Thorat, M.
    Li, L.
    Morimiya, A.
    Zhao, Q.
    Biernat, W.
    Mandat, T.
    Staszkiewicz, R.
    Och, W.
    Szostak, W.
    Gugala, K.
    Trojanowski, T.
    Czartoryska-Arlukowicz, B.
    Szczylik, C.
    Nakshatri, H.
    Steeg, P.
    Sledge, G.
    Badve, S.
 TI Molecular characteristics of matched brain metastasis (BM) versus the
    primary breast cancer (PBC).
 SO CANCER RESEARCH
 LA English
 DT Meeting Abstract
 CT 31st Annual San Antonio Breast Cancer Symposium
 CY DEC 10-14, 2008
 CL San Antonio, TX
 C1 Mil Inst Med, Warsaw, Poland.
    Med Univ, Gdansk, Poland.
    Indiana Univ, Indianapolis, IN 46204 USA.
    Gen Hosp, Olsztyn, Poland.
    Med Univ, Lublin, Poland.
    Reg Canc Ctr, Bialystok, Poland.
    NCI, Bethesda, MD 20892 USA.
 NR 0
 TC 0
 PU AMER ASSOC CANCER RESEARCH
 PI PHILADELPHIA
 PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
 SN 0008-5472
 J9 CANCER RES
 JI Cancer Res.
 PD JAN 15
 PY 2009
 VL 69
 IS 2
 SU Suppl. S
 BP 164S
 EP 164S
 PG 1
 SC Oncology
 GA 396HQ
 UT ISI:000262583200319
 ER
 
 PT J
 AU Ando, N
    Iwamitsu, Y
    Kuranami, M
    Okazaki, S
    Wada, M
    Yamamoto, K
    Watanabe, M
    Miyaoka, H
 AF Ando, N.
    Iwamitsu, Y.
    Kuranami, M.
    Okazaki, S.
    Wada, M.
    Yamamoto, K.
    Watanabe, M.
    Miyaoka, H.
 TI Analysis of factors associated with increased psychological distress in
    new outpatients at the breast clinic
 SO CANCER RESEARCH
 LA English
 DT Meeting Abstract
 CT 31st Annual San Antonio Breast Cancer Symposium
 CY DEC 10-14, 2008
 CL San Antonio, TX
 C1 Kitasato Univ, Grad Sch Med Sci, Kanagawa, Japan.
    Kitasato Univ, Sch Med, Kanagawa, Japan.
 NR 0
 TC 0
 PU AMER ASSOC CANCER RESEARCH
 PI PHILADELPHIA
 PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
 SN 0008-5472
 J9 CANCER RES
 JI Cancer Res.
 PD JAN 15
 PY 2009
 VL 69
 IS 2
 SU Suppl. S
 BP 235S
 EP 235S
 PG 1
 SC Oncology
 GA 396HQ
 UT ISI:000262583201129
 ER
 
 PT J
 AU Watanabe, T
    Kuranami, M
    Inoue, K
    Masuda, N
    Aogi, K
    Oono, S
    Iwata, H
    Mukai, H
    Tanaka, S
    Yamaguchi, T
    Ohashi, Y
 AF Watanabe, T.
    Kuranami, M.
    Inoue, K.
    Masuda, N.
    Aogi, K.
    Oono, S.
    Iwata, H.
    Mukai, H.
    Tanaka, S.
    Yamaguchi, T.
    Ohashi, Y.
 TI Phase III two by two factorial comparison of doxorubicin and
    cyclophosphamide followed by a taxan vs. a taxan alone, and paclitaxel
    vs. docetaxel in operable node positive breast cancer-results of the
    first interim analysis of NSASBC02 trial.
 SO CANCER RESEARCH
 LA English
 DT Meeting Abstract
 CT 31st Annual San Antonio Breast Cancer Symposium
 CY DEC 10-14, 2008
 CL San Antonio, TX
 C1 Hamamatsu Oncol Ctr, Hamamatsu, Shizuoka, Japan.
    Kitasato Univ Hosp, Sagamihara, Kanagawa, Japan.
    Saitama Canc Ctr, Ina, Saitama, Japan.
    Osaaka Med Ctr, Osaka, Japan.
    Shikoku Canc Ctr, Matsuyama, Ehime, Japan.
    Kyushu Canc Ctr, Fukuoka, Japan.
    Aichi Canc Ctr, Nagoya, Aichi 464, Japan.
    Natl Canc Ctr E, Kashiwa, Chiba, Japan.
    Kyoto Univ, Kyoto, Japan.
    Univ Tokyo, Tokyo, Japan.
 NR 0
 TC 0
 PU AMER ASSOC CANCER RESEARCH
 PI PHILADELPHIA
 PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
 SN 0008-5472
 J9 CANCER RES
 JI Cancer Res.
 PD JAN 15
 PY 2009
 VL 69
 IS 2
 SU Suppl. S
 BP 281S
 EP 281S
 PG 1
 SC Oncology
 GA 396HQ
 UT ISI:000262583201271
 ER
 
 PT J
 AU Liu, J
    Hong, DF
    Lu, W
    Liu, PW
    He, QB
    Yang, GS
 AF Liu, Jun
    Hong, Dengfeng
    Lu, Wei
    Liu, Pingwu
    He, Qingbiao
    Yang, Guangsheng
 TI Genetic Analysis and Molecular Mapping of Gene Associated with Dominant
    Genic Male Sterility in Rapeseed (Brassica napus L.)
 SO GENES & GENOMICS
 LA English
 DT Article
 DE Brassica napus (rapeseed); dominant genic male sterility (DGMS);
    inheritance model; molecular mapping; marker-assisted selection (MAS)
 ID SCAR MARKERS; IDENTIFICATION; AFLP; MS
 AB Rs1046AB is a dominant genic male sterility (DGMS) line derived from a
    spontaneous mutant in Brassica napus. The sterility of this mutant was
    previously regarded as to be conditioned by the interaction of a
    dominant male sterility gene Ms and its non-allelic dominant restorer
    gene Mf (or Rf in previous reports). Recent genetic analyses, however,
    indicated that Ms and Mf may be allelic. In this research, we confirmed
    that a multiple allele model should be more appropriate to elucidate
    the heredity of DGMS line Rs1046AB. Based on this result, the present
    study emphasized on identifying DNA markers linked to Ms/Mf an F-2
    population constructed by crossing Rs1046A with a double haploid (DH)
    restorer line (19514A). Twenty amplified fragment length polymorphism
    (AFLP) markers linked to the Ms/Mf locus were identified by combination
    of bulked segregant analysis (BSA) with AFLP technique. The target
    locus was detected to be co-segregating with the marker S05T05 and
    bracketed by two nearest markers, E14M01 and E01M02, with a genetic
    distance of 0.1 cM and 1.2 cM respectively. Furthermore, we
    successfully converted two AFLP markers into sequence characterized
    amplified region (SCAR) markers. These findings provided direct
    molecular marker proofs on the inheritance model of this DGMS line, and
    the high density molecular markers linkage map around the Ms/Mf locus
    will be more informative for both marker-assisted selection MAS) of
    elite male sterile lines and isolation of the Ms/Mf genes by positional
    cloning in future.
 C1 [Liu, Jun; Hong, Dengfeng; Lu, Wei; Liu, Pingwu; He, Qingbiao; Yang, Guangsheng] Huazhong Agr Univ, Natl Ctr Rapeseed Improvement Wuhan, Coll Plant Sci & Technol, Natl Key Lab Crop Genet Improvement, Wuhan 430070, Peoples R China.
 RP Yang, GS, Huazhong Agr Univ, Natl Ctr Rapeseed Improvement Wuhan, Coll
    Plant Sci & Technol, Natl Key Lab Crop Genet Improvement, Wuhan 430070,
    Peoples R China.
 EM gsyang@mail.hzau.edu.cn
 FU National Natural Science Foundation of China [30570999]; Doctoral
    Educational Program of the Minstry Education [20050504008]; National
    "973" project [2007CB109006]
 FX The authors thank Dr Fan ZX and Dr Wu JY for critically reading this
    manuscript. This research was supported by National Natural Science
    Foundation of China (No. 30570999), Doctoral Educational Program of the
    Minstry Education (No. 20050504008) and National "973" project (No.
    2007CB109006).
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 NR 33
 TC 0
 PU KOREAN SOC GENETICS
 PI SEOUL
 PA KOREAN SCIENCE & TECHNOLOGY CENTER, RM 1002, 635-4 YEOKSAM-DONG,
    KANGNAM, SEOUL, 135-703, SOUTH KOREA
 SN 1976-9571
 J9 GENES GENOM
 JI Genes Genom.
 PD DEC
 PY 2008
 VL 30
 IS 6
 BP 523
 EP 532
 PG 10
 SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology;
    Genetics & Heredity
 GA 396JK
 UT ISI:000262587800004
 ER
 
 PT J
 AU Yamashita, K
    Watanabe, M
 AF Yamashita, Keishi
    Watanabe, Masahiko
 TI Clinical significance of tumor markers and an emerging perspective on
    colorectal cancer
 SO CANCER SCIENCE
 LA English
 DT Review
 ID FECAL-OCCULT-BLOOD; KIRSTEN RAS MUTATIONS; COLON-CANCER; DNA-PLOIDY;
    PROGNOSTIC INDICATOR; PREDICT RECURRENCE; EARLY-STAGE; CEA; EXPRESSION;
    LEVEL
 AB Serum carcinoembryonic antigen (CEA) and CA19-9, a carbohydrate antigen
    recognized by the monoclonal antibody NS19-9, are commonly used as
    classical tumor markers in colorectal cancer (CRC) clinics. The roles
    of tumor markers include: (1) diagnostic screening (diagnostic
    markers); (2) prediction of prognosis after treatment (prognostic
    markers); and (3) judgment tools for treatment effect (surveillance
    markers). Tumor markers can be evaluated in serum, stools, or even in
    tissues depending on the clinical purpose. The American Society for
    Clinical Oncology recommends that CEA is the only marker of choice for
    monitoring the response of metastatic disease to systemic therapy at
    present. In the present paper, we are the first to review the clinical
    significance of the classical tumor markers CEA and CA19-9 in serum,
    allowing for our original data, and present our view on the newly
    emerging biomarkers in CRC. Novel promising biomarkers for diagnostic,
    prognostic, and surveillance purposes are reviewed and considered, some
    of which are anticipated for further validation. For diagnostic
    markers, urine or serum might replace fecal samples in the near future.
    On the other hand, prognostic or predictive markers for treatment
    sensitivity may be identified from the molecular profiles of primary
    cancer tissues. Selection of patients who are sensitive to chemotherapy
    will reduce the number of patients who undergo harmful chemotherapy
    with no effectiveness. The optimal tumor markers would be generalized,
    easy to assess, and accurate, and such markers are eagerly anticipated
    to enable personalized tailored therapy for CRC patients. (Cancer Sci
    2009; 100: 195-199).
 C1 [Yamashita, Keishi; Watanabe, Masahiko] Kitasato Univ Hosp, Dept Surg, Kanagawa 2288555, Japan.
 RP Yamashita, K, Kitasato Univ Hosp, Dept Surg, Kitasato 1-15-1, Kanagawa
    2288555, Japan.
 EM gekaw@med.kitasato-u.ac.jp
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 NR 41
 TC 7
 PU WILEY-BLACKWELL PUBLISHING, INC
 PI MALDEN
 PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
 SN 1347-9032
 J9 CANCER SCI
 JI Cancer Sci.
 PD FEB
 PY 2009
 VL 100
 IS 2
 BP 195
 EP 199
 DI 10.1111/j.1349-7006.2008.01022.x
 PG 5
 SC Oncology
 GA 395FG
 UT ISI:000262509400001
 ER
 
 PT J
 AU Kanda, J
    Matsuo, K
    Suzuki, T
    Kawase, T
    Hiraki, A
    Watanabe, M
    Mizuno, N
    Sawaki, A
    Yamao, K
    Tajima, K
    Tanaka, H
 AF Kanda, Junya
    Matsuo, Keitaro
    Suzuki, Takeshi
    Kawase, Takakazu
    Hiraki, Akio
    Watanabe, Miki
    Mizuno, Nobumasa
    Sawaki, Akira
    Yamao, Kenji
    Tajima, Kazuo
    Tanaka, Hideo
 TI Impact of alcohol consumption with polymorphisms in
    alcohol-metabolizing enzymes on pancreatic cancer risk in Japanese
 SO CANCER SCIENCE
 LA English
 DT Article
 ID GENETIC-POLYMORPHISM; POPULATION; DEHYDROGENASE; ALLELE; COFFEE;
    EPIDEMIOLOGY; TOBACCO; CARCINOGENESIS; GENOTYPES; SMOKING
 AB The putative impact of alcohol on pancreatic cancer (PC) risk remains
    controversial. Here, we conducted a case-control study in Japanese to
    assess the impact of alcohol in conjunction with polymorphisms in
    alcohol-metabolizing enzymes. Cases were 160 patients with pancreatic
    cancer at Aichi Cancer Center, Nagoya, Japan. Two control groups of 800
    age- and sex-matched non-cancer subjects each were independently
    selected. The impact of alcohol and polymorphisms in aldehyde
    dehydrogenase 2 (ALDH2) Glu504Lys, alcohol dehydrogenase (ADH) 1B
    His48Arg, and ADH1C Arg272Gln on PC risk was examined with multivariate
    analysis adjusted for potential confounders to estimate odds ratios
    (ORs) and 95% confidence intervals (CIs). Results showed no independent
    impact of alcohol or genotype on PC risk except former drinking. To
    avoid reverse causation, former drinkers were excluded in further
    analyses. In the analysis of the combined effects of alcohol
    consumption and genotype, significant impact of alcohol was seen for
    those subjects with ALDH2 Lys+ allele, ADH1B His/His, or ADH1C Arg/Arg
    (trend P = 0.077, 0.003, or 0.020, respectively), each of which is
    associated with a high concentration or rapid production of
    acetaldehyde. Analysis of genotype combinations showed that 'ever
    drinking' with both ADH1B His/His and ALDH2 Lys + was the most potent
    risk factor for PC relative to 'never drinkers' with both ADH1B His/His
    and ALDH2 Glu/Glu [OR (95% CI); 4.09 (1.30-12.85)]. These results
    indicate that alcohol has an impact on PC risk when the effects of
    alcohol consumption and metabolism are combined. Acetaldehyde may be
    involved in the mechanisms underlying PC development. (Cancer Sci 2009;
    100: 296-302).
 C1 [Kanda, Junya; Matsuo, Keitaro; Suzuki, Takeshi; Kawase, Takakazu; Hiraki, Akio; Watanabe, Miki; Tajima, Kazuo; Tanaka, Hideo] Aichi Canc Ctr, Res Inst, Div Epidemiol & Prevent, Chikusa Ku, Nagoya, Aichi 4648681, Japan.
    [Mizuno, Nobumasa; Sawaki, Akira; Yamao, Kenji] Aichi Canc Ctr, Cent Hosp, Dept Gastroenterol, Chikusa Ku, Nagoya, Aichi 4648681, Japan.
    [Matsuo, Keitaro; Tajima, Kazuo] Nagoya Univ, Grad Sch Med, Dept Epidemiol, Showa Ku, Nagoya, Aichi 4668550, Japan.
    [Kanda, Junya] Kyoto Univ, Grad Sch Med, Dept Hematol Oncol, Sakyo Ku, Kyoto 6068507, Japan.
 RP Matsuo, K, Aichi Canc Ctr, Res Inst, Div Epidemiol & Prevent, Chikusa
    Ku, 1-1 Kanokoden, Nagoya, Aichi 4648681, Japan.
 EM kmatsuo@aichi-cc.jp
 FU Ministry of Education, Science, Sports, Culture and Technology of Japan
    ; Ministry of Health, Labour and Welfare of Japan ; Uehara Memorial
    Foundation 
 FX This study was supported by a Grant-in-Aid for Scientific Research from
    the Ministry of Education, Science, Sports, Culture and Technology of
    Japan, by a Grant-in-Aid for Cancer Research from the Ministry of
    Health, Labour and Welfare of Japan, by a Grant-in-Aid for the Third
    Term Comprehensive 10-Year Strategy for Cancer Control from the
    Ministry of Health, Labour and Welfare of Japan and by a research grant
    from the Uehara Memorial Foundation.
    The authors are grateful to the doctors, nurses, technical staff, and
    hospital administration staff at Aichi Cancer Center Hospital for the
    daily administration of the HERPACC study.
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 NR 36
 TC 3
 PU WILEY-BLACKWELL PUBLISHING, INC
 PI MALDEN
 PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
 SN 1347-9032
 J9 CANCER SCI
 JI Cancer Sci.
 PD FEB
 PY 2009
 VL 100
 IS 2
 BP 296
 EP 302
 DI 10.1111/j.1349-7006.2008.01044.x
 PG 7
 SC Oncology
 GA 395FG
 UT ISI:000262509400015
 ER
 
 PT J
 AU Matsuo, J
    Tsukumo, Y
    Sakurai, J
    Tsukahara, S
    Park, HR
    Shin-ya, K
    Watanabe, T
    Tsuruo, T
    Tomida, A
 AF Matsuo, Junichi
    Tsukumo, Yoshinori
    Sakurai, Junko
    Tsukahara, Satomi
    Park, Hae-Ryong
    Shin-ya, Kazuo
    Watanabe, Toshiki
    Tsuruo, Takashi
    Tomida, Akihiro
 TI Preventing the unfolded protein response via aberrant activation of
    4E-binding protein 1 by versipelostatin
 SO CANCER SCIENCE
 LA English
 DT Article
 ID ENDOPLASMIC-RETICULUM STRESS; INDUCED GENE-EXPRESSION; RENAL-CELL
    CARCINOMA; TRANSLATION INITIATION; TUMOR-DEVELOPMENT; CANCER-THERAPY;
    ER STRESS; SURVIVAL; HYPOXIA; GROWTH
 AB We recently isolated a macrocyclic compound, versipelostatin (VST),
    that exerts in vivo antitumor activity. VST shows unique, selective
    cytotoxicity to glucose-deprived tumor cells by preventing the unfolded
    protein response (UPR). Here we show that eukaryotic initiation factor
    4E-binding protein 1 (4E-BP1), a negative regulator of eukaryotic
    initiation factor 4E-mediated protein translation, plays a role in the
    UPR-inhibitory action of VST. Indeed, 4E-BP1 is aberrantly activated by
    VST. This activation occurs specifically during glucose deprivation and
    results in profound translation repression and prevents induction of
    the typical UPR markers glucose-regulated protein (GRP) 78 and
    activating transcription factor (ATF) 4. Our overexpression and
    knockdown experiments showed that 4E-BP1 can regulate GRP78 and ATF4
    expression. These mechanisms appear to be specific for VST. By
    contrast, rapamycin, which activates 4E-BP1 regardless of cellular
    glucose availability, has only marginal effects on the expression of
    GRP78 and ATF4. Our present findings demonstrate that aberrant 4E-BP1
    activation can contribute to UPR preventing by VST, possibly through a
    mechanism that does not operate in rapamycin-treated cells. (Cancer Sci
    2009; 100: 327-333).
 C1 [Matsuo, Junichi; Tsukumo, Yoshinori; Sakurai, Junko; Tsukahara, Satomi; Tsuruo, Takashi; Tomida, Akihiro] Japanese Fdn Canc Res, Ctr Canc Chemotherapy, Koto Ku, Tokyo 1358550, Japan.
    [Matsuo, Junichi; Watanabe, Toshiki] Univ Tokyo, Grad Sch Frontier Sci, Dept Med Genome Sci, Tumor Cell Biol Lab,Minato Ku, Tokyo 1088639, Japan.
    [Park, Hae-Ryong] Kyungnam Univ, Dept Food Sci & Biotechnol, Masan 631701, South Korea.
    [Shin-ya, Kazuo] Natl Inst Adv Ind Sci & Technol, Biomed Informat Res Ctr, Koto Ku, Tokyo 1350064, Japan.
 RP Tomida, A, Japanese Fdn Canc Res, Ctr Canc Chemotherapy, Koto Ku,
    3-10-6 Ariake, Tokyo 1358550, Japan.
 EM akihiro.tomida@jfcr.or.jp
 FU Ministry of Health, Labor, and Welfare ; Ministry of Education,
    Culture, Sport, Science, and Technology of Japan 
 FX This work was supported in part by a Grant-in-Aid for Cancer Research
    (15-2) from the Ministry of Health, Labor, and Welfare (to A.T.), and a
    Grant-in-Aid for scientific research on priority areas for cancer from
    the Ministry of Education, Culture, Sport, Science, and Technology of
    Japan (to T.T.).
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 NR 35
 TC 2
 PU WILEY-BLACKWELL PUBLISHING, INC
 PI MALDEN
 PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
 SN 1347-9032
 J9 CANCER SCI
 JI Cancer Sci.
 PD FEB
 PY 2009
 VL 100
 IS 2
 BP 327
 EP 333
 DI 10.1111/j.1349-7006.2008.01036.x
 PG 7
 SC Oncology
 GA 395FG
 UT ISI:000262509400020
 ER
 
 PT J
 AU Iwasaki, R
    Ito, K
    Ishida, T
    Hamanoue, M
    Adachi, S
    Watanabe, T
    Sato, Y
 AF Iwasaki, Reo
    Ito, Kinji
    Ishida, Takaomi
    Hamanoue, Makoto
    Adachi, Souichi
    Watanabe, Toshiki
    Sato, Yuko
 TI Catechin, green tea component, causes caspase-independent necrosis-like
    cell death in chronic myelogenous leukemia
 SO CANCER SCIENCE
 LA English
 DT Article
 ID SERINE-PROTEASE ACTIVITY; NECROTIC TUMOR-CELLS; EPIGALLOCATECHIN
    GALLATE; CANCER-CELLS; IN-VITRO; POLYPHENOL
    (-)-EPIGALLOCATECHIN-3-GALLATE; MEDIATED APOPTOSIS; SIGNALING PATHWAYS;
    CARCINOMA-CELLS; CYCLE ARREST
 AB Management strategies of chronic phase chronic myelogenous leukemia
    (CML) have been revolutionized due to the discovery of a selective
    tyrosine kinase inhibitor, imatinib (Gleevec, STI571), which is
    substantially improving median survival. However, emergence of
    imatinib-resistance has put up a serious problem that requires novel
    treatment methods. Catechins, polyphenolic compounds in green tea, are
    gathering much attention due to their potential antitumor effects. So
    far (-)-epigallocatechin-3-gallate (EGCG), the most abundant component
    of catechin, has been shown to cause typical apoptosis in several tumor
    cell lines in most cases through activation of caspases. In this study,
    we showed that EGCG predominantly caused necrosis-like cell death via a
    caspase-independent mechanism in CML cells, K562 and C2F8, whereas
    imatinib induced the typical apoptotic cell death. Moreover, this
    caspase-independent cell death partially mediated the release of
    apoptosis-inducing factor, AIF, and serine protease, HtrA2/Omi, from
    the mitochondria to cytosol. In addition, EGCG enhanced the
    imatinib-induced cell death (P < 0.01) resulting in additive cell death
    in K562 cells and EGCG alone, effectively reduced the viability of
    imatinib-resistant K562 cells (P < 0.01). Catechin is a possible
    candidate for an antitumor agent that causes cell death in CML cells
    via a caspase-independent mechanism. (Cancer Sci 2009; 100: 349-356).
 C1 [Iwasaki, Reo; Sato, Yuko] Int Med Ctr Japan, Dept Pathol, Div Ultrafine Struct, Shinjuku Ku, Tokyo 1628655, Japan.
    [Iwasaki, Reo; Ishida, Takaomi; Watanabe, Toshiki] Univ Tokyo, Grad Sch Frontier Sci, Dept Med Genome Sci, Tumor Cell Biol Lab,Minato Ku, Tokyo 1088649, Japan.
    [Hamanoue, Makoto] Toho Univ, Sch Med, Dept Pathol, Ohta Ku, Tokyo 1430015, Japan.
    [Hamanoue, Makoto] Toho Univ, Sch Med, Dept Physiol, Ohta Ku, Tokyo 1430015, Japan.
    [Adachi, Souichi] Kyoto Univ, Grad Sch Med, Dept Pediat, Sakyo Ku, Kyoto 6068507, Japan.
 RP Sato, Y, Int Med Ctr Japan, Dept Pathol, Div Ultrafine Struct, Shinjuku
    Ku, 1-21-1 Toyama, Tokyo 1628655, Japan.
 EM ysato@ri.imcj.go.jp
 FU Japan Foundation for Promotion of International Medical Research
    Co-operation (JF-PIMRC) 
 FX This work was supported by the Japan Foundation for Promotion of
    International Medical Research Co-operation (JF-PIMRC).
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 NR 50
 TC 6
 PU WILEY-BLACKWELL PUBLISHING, INC
 PI MALDEN
 PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
 SN 1347-9032
 J9 CANCER SCI
 JI Cancer Sci.
 PD FEB
 PY 2009
 VL 100
 IS 2
 BP 349
 EP 356
 DI 10.1111/j.1349-7006.2008.01046.x
 PG 8
 SC Oncology
 GA 395FG
 UT ISI:000262509400023
 ER
 
 PT J
 AU Lin, M
    Wu, JR
    Yang, LY
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 SO BLOOD CELLS MOLECULES AND DISEASES
 LA English
 DT Letter
 ID HEMOGLOBIN-G-WAIMANALO; JAPANESE; ASP->ASN; FAMILY
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 NR 10
 TC 2
 PU ACADEMIC PRESS INC ELSEVIER SCIENCE
 PI SAN DIEGO
 PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
 SN 1079-9796
 J9 BLOOD CELLS MOLECULES DIS
 JI Blood Cells Mol. Dis.
 PD JAN-FEB
 PY 2009
 VL 42
 IS 1
 BP 36
 EP 37
 DI 10.1016/j.bcmd.2008.09.005
 PG 2
 SC Hematology
 GA 393CG
 UT ISI:000262347900007
 ER
 
 PT J
 AU Payne, JL
    Boyer, AG
    Brown, JH
    Finnegan, S
    Kowalewski, M
    Krause, RA
    Lyons, SK
    McClain, CR
    McShea, DW
    Novack-Gottshall, PM
    Smith, FA
    Stempien, JA
    Wang, SC
 AF Payne, Jonathan L.
    Boyer, Alison G.
    Brown, James H.
    Finnegan, Seth
    Kowalewski, Michal
    Krause, Richard A., Jr.
    Lyons, S. Kathleen
    McClain, Craig R.
    McShea, Daniel W.
    Novack-Gottshall, Philip M.
    Smith, Felisa A.
    Stempien, Jennifer A.
    Wang, Steve C.
 TI Two-phase increase in the maximum size of life over 3.5 billion years
    reflects biological innovation and environmental opportunity
 SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
    AMERICA
 LA English
 DT Article
 DE body size; Cambrian; oxygen; Precambrian; trend
 ID BODY-SIZE; COPES RULE; ATMOSPHERIC OXYGEN; EVOLUTION; EUKARYOTES;
    OXIDATION; ANIMALS; FOSSILS; TRENDS; OCEANS
 AB The maximum size of organisms has increased enormously since the
    initial appearance of life > 3.5 billion years ago (Gya), but the
    pattern and timing of this size increase is poorly known. Consequently,
    controls underlying the size spectrum of the global biota have been
    difficult to evaluate. Our period-level compilation of the largest
    known fossil organisms demonstrates that maximum size increased by 16
    orders of magnitude since life first appeared in the fossil record. The
    great majority of the increase is accounted for by 2 discrete steps of
    approximately equal magnitude: the first in the middle of the
    Paleoproterozoic Era (approximate to 1.9 Gya) and the second during the
    late Neoproterozoic and early Paleozoic eras (0.6-0.45 Gya). Each size
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    eukaryotic cell and later eukaryotic multicellularity. These size steps
    coincide with, or slightly postdate, increases in the concentration of
    atmospheric oxygen, suggesting latent evolutionary potential was
    realized soon after environmental limitations were removed.
 C1 [Payne, Jonathan L.; Finnegan, Seth] Stanford Univ, Dept Geol & Environm Sci, Stanford, CA 94305 USA.
    [Boyer, Alison G.; Brown, James H.; Smith, Felisa A.] Univ New Mexico, Dept Biol, Albuquerque, NM 87131 USA.
    [Kowalewski, Michal] Virginia Polytech Inst & State Univ, Dept Geosci, Blacksburg, VA 24061 USA.
    [Krause, Richard A., Jr.] Humboldt Univ, Museum Naturkunde, D-10115 Berlin, Germany.
    [Lyons, S. Kathleen] Smithsonian Inst, Natl Museum Nat Hist, Dept Paleobiol, Washington, DC 20560 USA.
    [McClain, Craig R.] Monterey Bay Aquarium Res Inst, Moss Landing, CA 95039 USA.
    [McShea, Daniel W.] Duke Univ, Dept Biol, Durham, NC 27708 USA.
    [Novack-Gottshall, Philip M.] Univ W Georgia, Dept Geosci, Carrollton, GA 30118 USA.
    [Stempien, Jennifer A.] Univ Colorado, Dept Geol Sci, Boulder, CO 80309 USA.
    [Wang, Steve C.] Swarthmore Coll, Dept Math & Stat, Swarthmore, PA 19081 USA.
 RP Payne, JL, Stanford Univ, Dept Geol & Environm Sci, 450 Serra Mall,Bldg
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 EM jlpayne@stanford.edu
 FU National Evolutionary Synthesis Center (NESCent) ; National Science
    Foundation [EF-0423641]
 FX This study is a product of the working group on body size evolution (
    principal investigators: J.L.P., J.A.S., and M. K.) funded by the
    National Evolutionary Synthesis Center (NESCent), National Science
    Foundation Grant EF-0423641. We thank N. Butterfield, M, Carrano, W.
    DiMichele, L. Dong, R. Feldmann, P. Gensel, J. Huntley, P. Janvier, A.
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    Denton and especially S. Porter for comments on previous drafts of the
    manuscript; and G. Hunt and 2 anonymous reviewers for constructive and
    thoughtful suggestions.
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 PT J
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    Cheng, PH
    Sullivan, RT
    Thomas, JW
    Chan, AWS
 AF Yang, Shang-Hsun
    Cheng, Pei-Hsun
    Sullivan, Robert T.
    Thomas, James W.
    Chan, Anthony W. S.
 TI Lentiviral Integration Preferences in Transgenic Mice
 SO GENESIS
 LA English
 DT Article
 DE lentiviral vector; transgenesis; integration; preference genome; mouse
    zygote
 ID IMMUNODEFICIENCY-VIRUS TYPE-1; OVINE PULMONARY ADENOCARCINOMA;
    PSEUDOTYPED RETROVIRAL VECTORS; GENE-TRANSFER; HUMAN GENOME;
    CHROMOSOMAL POSITION; SITE SELECTION; HIGH-TITER; GERM LINE; IN-VITRO
 AB Lentiviral gene transfer has a significant impact on the development of
    biomedical research. One of the most important features of lentiviruses
    is the capability to infect both dividing and nondividing cells.
    However, little is known whether integration preference exists,
    specifically in early embryos. An in-depth genome analysis on 112
    independent lentiviral integration sites from 43 transgenic founder
    mice was performed to determine if there are preferable sites for
    lentiviral integration in early embryonic genome. Our results
    demonstrated that lentiviruses were biased in integrating within
    intragenic regions, especially in the introns. However, no integration
    preference was found associated with specific chromosomes, repetitive
    elements, or CpG islands, nor was there any preference for integrating
    at close proximity to transcription start sites. Our findings suggested
    that lentiviruses were biased to integrate into the intragenic regions
    of early embryonic genome of mouse. genesis 46:711-718, 2008. (C) 2008
    Wiley-Liss, Inc.
 C1 [Yang, Shang-Hsun; Cheng, Pei-Hsun; Chan, Anthony W. S.] Emory Univ, Yerkes Natl Primate Res Ctr, Div Neurosci, Atlanta, GA 30329 USA.
    [Yang, Shang-Hsun; Thomas, James W.; Chan, Anthony W. S.] Emory Univ, Genet & Mol Biol Program, Atlanta, GA 30329 USA.
    [Yang, Shang-Hsun; Cheng, Pei-Hsun; Sullivan, Robert T.; Thomas, James W.; Chan, Anthony W. S.] Emory Univ, Sch Med, Dept Human Genet, Atlanta, GA 30329 USA.
 RP Chan, AWS, Emory Univ, Yerkes Natl Primate Res Ctr, Div Neurosci, Rm
    2212,Neurosci Res Bldg,954 Gatewood Rd,NE, Atlanta, GA 30329 USA.
 EM achan@genetics.emory.eclu
 FU NIH (Yerkes National Primate Research Center) [RR-00165]; NCRR/NIH
    [RR018827-04]
 FX Contract grant sponsor: NIH (Yerkes National Primate Research Center),
    Contract grant number: RR-00165. Contract grant sponsor: NCRR/NIH,
    Contract grant number: RR018827-04.
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 NR 40
 TC 4
 PU WILEY-LISS
 PI HOBOKEN
 PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA
 SN 1526-954X
 J9 GENESIS
 JI Genesis
 PD DEC
 PY 2008
 VL 46
 IS 12
 BP 711
 EP 718
 DI 10.1002/dvg.20435
 PG 8
 SC Developmental Biology; Genetics & Heredity
 GA 390HW
 UT ISI:000262155900001
 ER
 
 PT J
 AU Sun, WJ
    Yu, Y
    Dotti, G
    Shen, T
    Tan, XJ
    Savoldo, B
    Pass, AK
    Chu, MJ
    Zhang, DK
    Lu, XB
    Fu, SB
    Lin, X
    Yang, JH
 AF Sun, Wenjing
    Yu, Yang
    Dotti, Gianpietro
    Shen, Tao
    Tan, Xiaojie
    Savoldo, Barbara
    Pass, Amy K.
    Chu, Meijin
    Zhang, Dekai
    Lu, Xiongbin
    Fu, Songbin
    Lin, Xia
    Yang, Jianhua
 TI PPM1A and PPM1B act as IKK beta phosphatases to terminate TNF
    alpha-induced IKK beta-NF-kappa B activation
 SO CELLULAR SIGNALLING
 LA English
 DT Article
 DE Tumor necrosis factor; Kinase; Phosphatase; I kappa B kinase; NF-kappa
    B; Signal transduction
 ID KINASE COMPLEX; SIGNALING PATHWAY; PROTEIN-KINASE; PHOSPHORYLATION;
    SUBUNIT; 2C; ASSOCIATION; MECHANISM; CLONING; MAPK
 AB IKK beta serves as a central intermediate signaling molecule in the
    activation of the NF-kappa B pathway. However, the precise mechanism
    for the termination of IKK beta activity is still not fully understood.
    Using a functional genomic approach, we have identified two protein
    serine/threonine phosphatases, PPM1A and PPM1B, as IKK beta
    phosphatases. Overexpression of PPM1A or PPM1B results in
    dephosphorylation of IKK beta at Ser177 and Ser181 and termination of
    IKK beta-induced NF-kappa B activation. PPM1A and PPM1B associate with
    the phosphorylated form of IKK beta, and the interaction between
    PPM1A/PPM1B and IKK beta is induced by TNF alpha in a transient fashion
    in the cells. Furthermore, knockdown of PPM1A and PPM1B expression
    enhances TNF alpha-induced IKK beta phosphorylation, NF-kappa B nuclear
    translocation and NF-kappa B-dependent gene expression. These data
    suggest that PPM1A and PPM1B play an important role in the termination
    of TNF alpha-mediated NF-kappa B activation through dephosphorylating
    and inactivating IKK beta. (C) 2008 Elsevier Inc. All rights reserved.
 C1 [Sun, Wenjing; Yu, Yang; Tan, Xiaojie; Pass, Amy K.; Yang, Jianhua] Baylor Coll Med, Dept Pediat, Texas Childrens Canc Ctr, Dan L Duncan Canc Ctr, Houston, TX 77030 USA.
    [Dotti, Gianpietro; Savoldo, Barbara] Baylor Coll Med, Ctr Cell & Gene Therapy, Houston, TX 77030 USA.
    [Shen, Tao; Chu, Meijin; Lin, Xia] Baylor Coll Med, Michael E DeBakey Dept Surg, Houston, TX 77030 USA.
    [Zhang, Dekai] Texas A&M Univ, Inst Biosci & Technol, Ctr Extracellular Matrix Biol, Houston, TX 77030 USA.
    [Lu, Xiongbin] Univ S Carolina, Dept Biol Sci, Columbia, SC 29208 USA.
    [Fu, Songbin] Harbin Med Coll, Med Genet Lab, Harbin 150081, Peoples R China.
 RP Yang, JH, Baylor Coll Med, Dept Pediat, Texas Childrens Canc Ctr, Dan L
    Duncan Canc Ctr, Houston, TX 77030 USA.
 EM jianhuay@bcm.tmc.edu
 FU National Institutes of Health [1R21CA106513-01A2]; American Cancer
    Society [RSG-06-070-01-TBE]; NIH/NCI T32 [1T32CA115303-01A1]
 FX We thank Susan Burlingame for technical assistance. We are very
    grateful to Dr. Paul Chiao, Dr. Sergei Nekhai, Dr. Larry Donehower and
    Dr. Xiaofan Wang for providing IKK beta, PPP1, PPM1D and PPP5C
    expression plasmids, respectively. This work was supported by National
    Institutes of Health Grant 1R21CA106513-01A2 and American Cancer
    Society grant RSG-06-070-01-TBE (to J. Y.). A.K.P. was supported by the
    NIH/NCI T32 training grant 1T32CA115303-01A1.
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 NR 34
 TC 12
 PU ELSEVIER SCIENCE INC
 PI NEW YORK
 PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
 SN 0898-6568
 J9 CELL SIGNAL
 JI Cell. Signal.
 PD JAN
 PY 2009
 VL 21
 IS 1
 BP 95
 EP 102
 DI 10.1016/j.cellsig.2008.09.012
 PG 8
 SC Cell Biology
 GA 389AB
 UT ISI:000262060900012
 ER
 
 PT J
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 AF Han, Jinju
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    Kim, Young-Kook
    Yeom, Kyu-Hyeon
    Yang, Woo-Young
    Haussler, David
    Blelloch, Robert
    Kim, V. Narry
 TI Posttranscriptional Crossregulation between Drosha and DGCR8
 SO CELL
 LA English
 DT Article
 ID MICROPROCESSOR COMPLEX; MICRORNA BIOGENESIS; ALZHEIMERS-DISEASE; RNA
    INTERFERENCE; EXPRESSION; PROLIFERATION; DROSOPHILA; MIR-222; PATHWAY;
    CELLS
 AB The Drosha-DGCR8 complex, also known as Microprocessor, is essential
    for microRNA (miRNA) maturation. Drosha functions as the catalytic
    subunit, while DGCR8 (also known as Pasha) recognizes the RNA
    substrate. Although the action mechanism of this complex has been
    intensively studied, it remains unclear how Drosha and DGCR8 are
    regulated and if these proteins have any additional role(s) apart from
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    other posttranscriptionally. The Drosha-DGCR8 complex cleaves the
    hairpin structures embedded in the DGCR8 mRNA and thereby destabilizes
    the mRNA. We further find that DGCR8 stabilizes the Drosha protein via
    protein-protein interaction. This crossregulation between Drosha and
    DGCR8 may contribute to the homeostatic control of miRNA biogenesis.
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    downregulated in a Microprocessor-dependent, miRNA-independent manner.
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    in mRNA stability control.
 C1 [Han, Jinju; Kwon, S. Chul; Kim, Young-Kook; Yeom, Kyu-Hyeon; Yang, Woo-Young; Kim, V. Narry] Seoul Natl Univ, Sch Biol Sci, Seoul 151742, South Korea.
    [Pedersen, Jakob S.] Univ Copenhagen, Dept Biol, Bioinformat Ctr, DK-2200 Copenhagen, Denmark.
    [Belair, Cassandra D.; Blelloch, Robert] Univ Calif San Francisco, Inst Regenerat Med, Ctr Reprod Sci, San Francisco, CA 94143 USA.
    [Belair, Cassandra D.; Blelloch, Robert] Univ Calif San Francisco, Dept Urol, San Francisco, CA 94143 USA.
    [Haussler, David] Univ Calif Santa Cruz, Ctr Biomol Sci & Engn, Santa Cruz, CA 95064 USA.
 RP Kim, VN, Seoul Natl Univ, Sch Biol Sci, Seoul 151742, South Korea.
 EM narrykim@snu.ac.kr
 FU Creative Research Initiatives Program [R16-2007-073-01000-0]; BK21
    Research Fellowships ; Ministry of Education, Science, and Technology
    of Korea ; Danish Medical Research Council [271-06-0711]; University of
    California, San Francisco, Urology Developmental Award ; Prostate
    Cancer Foundation ; National Institutes of Health [K08 NS48118, RO1
    NS057221]; Stem Cell Research Foundation 
 FX We are grateful to Dr. Seogang Hyun for help with S2 transfection, to
    Dr. Chirlmin Joo for critical reading of this manuscript, and to
    members of our laboratory for helpful discussion. We also thank Dr.
    Young-Joon Kim for kindly providing S2 cell. This work was supported by
    the Creative Research Initiatives Program (R16-2007-073-01000-0)
    (V.N.K.) and the BK21 Research Fellowships (J.H. and S.C.K.) from the
    Ministry of Education, Science, and Technology of Korea. J.S.P. was
    supported by the Danish Medical Research Council (271-06-0711). C.B.
    was supported through a University of California, San Francisco,
    Urology Developmental Award and the Prostate Cancer Foundation. R.B. is
    a Pew Scholar and was supported by National Institutes of Health grants
    (K08 NS48118, RO1 NS057221), the Prostate Cancer Foundation, and Stem
    Cell Research Foundation. J.H., S.C.K., Y.K.K., K.H.Y., and W.Y.Y.
    performed the experiments and analyzed the data. C.B. and R.B. carried
    out experiments with Dgcr8 KO mES cells, generated Dgcr8 KO MEF, and
    helped with manuscript preparation. J.S.P. performed bioinformatics
    analyses with D.H. and helped with editing of paper. J.H. and V.N.K.
    designed the study and wrote the paper.
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 NR 41
 TC 47
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 PI CAMBRIDGE
 PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
 SN 0092-8674
 J9 CELL
 JI Cell
 PD JAN 9
 PY 2009
 VL 136
 IS 1
 BP 75
 EP 84
 DI 10.1016/j.cell.2008.10.053
 PG 10
 SC Biochemistry & Molecular Biology; Cell Biology
 GA 392QX
 UT ISI:000262318400016
 ER
 
 PT J
 AU Maeshima, AM
    Taniguchi, H
    Nomoto, J
    Maruyama, D
    Kim, SW
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 AF Maeshima, Akiko Miyagi
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    Maruyama, Dai
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 TI Histological and immunophenotypic changes in 59 cases of B-cell
    non-Hodgkin's lymphoma after rituximab therapy
 SO CANCER SCIENCE
 LA English
 DT Article
 ID ANTI-CD20 ANTIBODY RITUXIMAB; CHRONIC LYMPHOCYTIC-LEUKEMIA; FOLLICULAR
    LYMPHOMA; PLASMACYTIC DIFFERENTIATION; MONOCLONAL-ANTIBODY; CD20;
    EXPRESSION; TRANSFORMATION; DISEASE; LINES
 AB Rituximab is a chimeric monoclonal antibody that recognizes the CD20
    antigen. It has been used to treat B-cell non-Hodgkin lymphoma (B-NHL),
    but recently rituximab resistance has been a cause for concern. We
    examined histological and immunohistochemical changes in 59 patients
    with B-NHL after rituximab therapy. The patients comprised 32 men and
    27 women with a median age of 59 years. Pre-rituximab specimens
    comprised 34 follicular lymphomas (FL), 11 diffuse large B-cell
    lymphomas (DLBCL), 10 mantle cell lymphomas, two marginal zone B-cell
    lymphomas (MZBCL), and two chronic lymphocytic leukemias (CLL). CD20
    expression in lymphoma cells was evaluated by immunohistochemistry or
    flow cytometry. Post-rituximab materials were taken a median of 6
    months (4 days to 59 months) after rituximab therapy. Sixteen cases
    (27%) showed loss of CD20 expression with four histological patterns:
    pattern 1, no remarkable histological change (FL, 5; DLBCL, 3; and CLL,
    2); pattern 2, proliferation of plasmacytoid cells (FL, 2; DLBCL, 1;
    and MZBCL, 1); pattern 3, transformation to classical Hodgkin's
    lymphoma (FL, 1); and pattern 4, transformation to anaplastic large
    cell lymphoma-like undifferentiated lymphoma (FL, 1). Loss of CD20 was
    unrelated to the interval of biopsies, treatment regimen, clinical
    response, and frequency of rituximab administration. Loss of CD20
    within 1 month of rituximab therapy (3/14, 21%) and regain of CD20
    (2/7, 29%) were not frequent. CD20-positive relapse with transformation
    occurred most frequently in cases of early relapse. In conclusion,
    B-NHL showed various histological and immunophenotypic changes after
    rituximab therapy, including not only CD20 loss but also proliferation
    of plasmacytoid cells or transformation to special subtypes of
    lymphoma. (Cancer Sci 2009; 100: 54-61).
 C1 [Maeshima, Akiko Miyagi; Taniguchi, Hirokazu] Natl Canc Ctr, Clin Lab, Tokyo, Japan.
    [Nomoto, Junko; Maruyama, Dai; Kim, Sung-Won; Watanabe, Takashi; Kobayashi, Yukio; Tobinai, Kensei] Natl Canc Ctr, Div Hematol, Tokyo, Japan.
    [Nomoto, Junko; Maruyama, Dai; Kim, Sung-Won; Watanabe, Takashi; Kobayashi, Yukio; Tobinai, Kensei] Natl Canc Ctr, Stem Cell Transplantat Div, Tokyo, Japan.
    [Matsuno, Yoshihiro] Hokkaido Univ Hosp, Dept Surg Pathol, Sapporo, Hokkaido 060, Japan.
 RP Maeshima, AM, Natl Canc Ctr, Clin Lab, 1-1 Tsukiji 5 chome, Tokyo,
    Japan.
 EM akmaeshi@ncc.go.jp
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 NR 35
 TC 7
 PU WILEY-BLACKWELL PUBLISHING, INC
 PI MALDEN
 PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
 SN 1347-9032
 J9 CANCER SCI
 JI Cancer Sci.
 PD JAN
 PY 2009
 VL 100
 IS 1
 BP 54
 EP 61
 DI 10.1111/j.1349-7006.2008.01005.x
 PG 8
 SC Oncology
 GA 390FN
 UT ISI:000262149800009
 ER
 
 PT J
 AU Tobinai, K
    Watanabe, T
    Ogura, M
    Morishima, Y
    Hotta, T
    Ishizawa, K
    Itoh, K
    Okamoto, S
    Taniwaki, M
    Tsukamoto, N
    Okumura, H
    Terauchi, T
    Nawano, S
    Matsusako, M
    Matsuno, Y
    Nakamura, S
    Mori, S
    Ohashi, Y
    Hayashi, M
    Endo, K
 AF Tobinai, Kensei
    Watanabe, Takashi
    Ogura, Michinori
    Morishima, Yasuo
    Hotta, Tomomitsu
    Ishizawa, Kenichi
    Itoh, Kuniaki
    Okamoto, Shin-ichiro
    Taniwaki, Masafumi
    Tsukamoto, Norifumi
    Okumura, Hirokazu
    Terauchi, Takashi
    Nawano, Shigeru
    Matsusako, Masaki
    Matsuno, Yoshihiro
    Nakamura, Shigeo
    Mori, Shigeo
    Ohashi, Yasuo
    Hayashi, Masaki
    Endo, Keigo
 TI Japanese phase II study of Y-90-ibritumomab tiuxetan in patients with
    relapsed or refractory indolent B-cell lymphoma
 SO CANCER SCIENCE
 LA English
 DT Article
 ID NON-HODGKINS-LYMPHOMA; MONOCLONAL-ANTIBODY THERAPY; Y-90 IBRITUMOMAB
    TIUXETAN; FOLLICULAR LYMPHOMA; LOW-GRADE; CHOP CHEMOTHERAPY; FOLLOW-UP;
    RESPONSE CRITERIA; ONCOLOGY-GROUP; STAGE-I
 AB There is no data about the efficacy and safety of radioimmunotherapy
    with Y-90-ibritumomab tiuxetan in patients with relapsed or refractory
    indolent B-cell lymphoma pretreated with rituximab-containing
    chemotherapy. We focused on this in a Japanese phase II study.
    Radioimmunotherapy with Y-90-ibritumomab tiuxetan (11.1 and 14.8 MBq)
    was evaluated in patients with 100-149 x 10(9) and > 150 x 10(9)
    platelets/L, respectively. The primary endpoint was the overall
    response rate. Forty patients were treated with Y-90-ibritumomab
    tiuxetan (18 with 11.1 MBq/kg and 22 with 14.8 MBq/kg). Thirty-five
    patients (88%) had been pretreated with rituximab, including 27 (68%)
    pretreated with rituximab-containing chemotherapy. The overall response
    rate was 83% (33/40; 95% confidence interval, 67-93%), and the complete
    response rate was 68% (27/40; 95% confidence interval, 51-81%). The
    overall response rates in patients pretreated with rituximab-containing
    chemotherapy and rituximab plus cyclophosphamide, doxorubicin,
    vincristine, and prednisone (R-CHOP) were 83% (19/23) and 94% (17/18),
    respectively. The median progression-free survival time of the 40
    patients who received Y-90-ibritumomab tiuxetan was 9.6 months.
    Toxicity was primarily hematological and mostly transient. No grade 4
    non-hematological toxicity was observed. In conclusion,
    radioimmunotherapy with Y-90-ibritumomab tiuxetan is safe and highly
    effective in patients with relapsed or refractory indolent B-cell
    lymphoma, including those pretreated with rituximab-containing
    chemotherapy. (ClinicalTrials.gov number NCT00220285) (Cancer Sci 2009;
    100: 158-164).
 C1 [Tobinai, Kensei; Watanabe, Takashi] Natl Canc Ctr, Hematol & Stem Cell Transplantat Div, Chuo Ku, Tokyo 1040045, Japan.
    [Matsuno, Yoshihiro] Natl Canc Ctr, Clin Lab Div, Chuo Ku, Tokyo 1040045, Japan.
    [Ogura, Michinori; Morishima, Yasuo] Aichi Canc Ctr Hosp, Dept Hematol & Cell Therapy, Chikusa Ku, Nagoya, Aichi 4648681, Japan.
    [Hotta, Tomomitsu] Tokai Univ, Sch Med, Dept Hematol & Oncol, Kanagawa 2591193, Japan.
    [Ishizawa, Kenichi] Tohoku Univ Hosp, Dept Rheumatol & Hematol, Aoba Ku, Sendai, Miyagi 9808574, Japan.
    [Nawano, Shigeru] Natl Canc Ctr Hosp E, Diagnost Radiol Div, Chiba 2778577, Japan.
    [Itoh, Kuniaki] Natl Canc Ctr Hosp E, Div Hematol Oncol, Chiba 2778577, Japan.
    [Okamoto, Shin-ichiro] Keio Univ, Sch Med, Div Hematol Infect Dis Rheumatol, Shinjuku Ku, Tokyo 1608582, Japan.
    [Taniwaki, Masafumi] Kyoto Prefectural Univ Med, Dept Hematol & Oncol, Kamikyo Ku, Hirokoji Noboru, Japan.
    [Endo, Keigo] Gunma Univ, Grad Sch Med, Dept Diagnost Radiol & Nucl Med, Maebashi, Gumma 3718511, Japan.
    [Tsukamoto, Norifumi] Gunma Univ, Grad Sch Med, Dept Med & Clin Sci, Maebashi, Gumma 3718511, Japan.
    [Okumura, Hirokazu] Kanazawa Univ, Grad Sch Med Sci, Dept Cellular Transplantat Biol, Kanazawa, Ishikawa 9208641, Japan.
    [Terauchi, Takashi] Natl Canc Ctr, Canc Screening Div, Res Ctr Canc Prevent & Screening, Chuo Ku, Tokyo 1040045, Japan.
    [Matsusako, Masaki] St Lukes Int Hosp, Dept Radiol, Chuo Ku, Tokyo 1048560, Japan.
    [Nakamura, Shigeo] Nagoya Univ Hosp, Dept Pathol, Showa Ku, Nagoya, Aichi 4668560, Japan.
    [Mori, Shigeo] Teikyo Univ, Sch Med, Dept Pathol, Itabashi Ku, Tokyo 1738606, Japan.
    [Ohashi, Yasuo] Univ Tokyo, Sch Publ Hlth, Dept Biostat, Bunkyo Ku, Tokyo 1138655, Japan.
    [Hayashi, Masaki] Bayer HealthCare, Dept Clin Dev, Yodogawa Ku, Osaka 5328577, Japan.
 RP Tobinai, K, Natl Canc Ctr, Hematol & Stem Cell Transplantat Div, Chuo
    Ku, 5-1-1 Tsukiji, Tokyo 1040045, Japan.
 EM ktobinai@ncc.go.jp
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 NR 28
 TC 6
 PU WILEY-BLACKWELL PUBLISHING, INC
 PI MALDEN
 PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
 SN 1347-9032
 J9 CANCER SCI
 JI Cancer Sci.
 PD JAN
 PY 2009
 VL 100
 IS 1
 BP 158
 EP 164
 DI 10.1111/j.1349-7006.2008.00999.x
 PG 7
 SC Oncology
 GA 390FN
 UT ISI:000262149800023
 ER
 
 EF