kbibtex-testset/isi/estrogen.isi

0001 FN ISI Export Format
0002 VR 1.0
0003 PT J
0004 AU Eertmans, F
0005    Dhooge, W
0006    De Wever, O
0007    Bracke, M
0008    Comhaire, F
0009    Kaufman, JM
0010 AF Eertmans, Frank
0011    Dhooge, Willem
0012    De Wever, Olivier
0013    Bracke, Marc
0014    Comhaire, Frank
0015    Kaufman, Jean-Marc
0016 TI Estrogen receptor alpha (ER alpha) and insulin-like growth factor I
0017    receptor (IGF-IR) cross-talk in the gonadotropic alpha T3-1 cell line
0018 SO JOURNAL OF CELLULAR PHYSIOLOGY
0019 LA English
0020 DT Article
0021 ID ACTIVATED PROTEIN-KINASE; BREAST-CANCER; PHOSPHORYLATION; HORMONE;
0022    ESTRADIOL; PATHWAY; VITRO; MEMBRANE; NEURONS; BRAIN
0023 AB In reproductive tissues such as the breast and the uterus, cell
0024    proliferation and differentiation is strongly regulated by complex
0025    interactions between estrogen receptor a (ER alpha) and growth factor
0026    receptors. In the present study, we investigated the potential
0027    occurrence of such cross-talk in the murine, gonadotropic alpha T3-I
0028    cell line, which expresses ER alpha and the IGF-I receptor (IGF-IR).
0029    Under estrogen-free conditions, basal cell proliferation and
0030    ER-mediated gene transcription was strongly inhibited by the selective
0031    estrogen receptor modulator (SERM) 4-hydroxy-tamoxifen (4-OH-Tam) and
0032    by the pure anti-estrogen ICI 182,780 (ICI). These effects can be
0033    reversed by either 17-beta-estradiol (E-2) or insulin-like growth
0034    factor I (IGF-1), both exerting modest mitogenic effects in the alpha
0035    T3-1 cell line. Furthermore, IGF-I enhanced both basal and E-2-induced
0036    ER-driven gene transcription. This may be explained, at least in part,
0037    by enhanced phosphorylation of ER alpha atserine 118, a prerequisite
0038    for the transactivation capacity of the receptor. Finally, the
0039    IGF-l-induced response on cell growth and ER-mediated transactivation
0040    can be inhibited with either ICI or 4-CH-Tam. In conclusion, our data
0041    indicate IGF-IR and ER interactions in the aT3-1 cell line, an in vitro
0042    model for the pituitary gonadotrophs, hereby suggesting a role of IGF-I
0043    in the regulation of gonaclotropin synthesis and secretion.
0044 C1 State Univ Ghent Hosp, Dept Endocrinol, B-9000 Ghent, Belgium.
0045    State Univ Ghent Hosp, Expt Cancerol Lab, B-9000 Ghent, Belgium.
0046 RP Eertmans, F, State Univ Ghent Hosp, Dept Endocrinol, 6K 121E,De
0047    Pintelaan 185, B-9000 Ghent, Belgium.
0048 EM Frank.Eertmans@ugent.be
0049 NR 50
0050 TC 1
0051 PU WILEY-LISS
0052 PI HOBOKEN
0053 PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA
0054 SN 0021-9541
0055 J9 J CELL PHYSIOL
0056 JI J. Cell. Physiol.
0057 PD SEP
0058 PY 2007
0059 VL 212
0060 IS 3
0061 BP 583
0062 EP 590
0063 PG 8
0064 SC Cell Biology; Physiology
0065 GA 200NQ
0066 UT ISI:000248770500005
0067 ER
0068
0069 EF