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Publication : Coactivation of estrogen receptor beta by gonadotropin-induced cofactor GIOT-4.

First Author  Kouzu-Fujita M Year  2009
Journal  Mol Cell Biol Volume  29
Issue  1 Pages  83-92
PubMed ID  18981223 Mgi Jnum  J:143222
Mgi Id  MGI:3823183 Doi  10.1128/MCB.00884-08
Citation  Kouzu-Fujita M, et al. (2009) Coactivation of estrogen receptor beta by gonadotropin-induced cofactor GIOT-4. (Retracted 2014 34(5)919). Mol Cell Biol 29(1):83-92
abstractText  Estrogen exerts its diverse effects through two subtypes of estrogen receptors (ER), ERalpha and ERbeta. Each subtype has its own distinct function and expression pattern in its target tissues. Little, however, is known about the transcriptional regulatory mechanism of ERbeta in the major ERbeta-expressing tissues. Using biochemical methods, we identified and described a novel ERbeta coactivator. This protein, designated GIOT-4, was biochemically purified from 293F cells. It coactivated ERbeta in ovarian granulosa cells. GIOT-4 expression was induced by stimulation with follicle-stimulating hormone (FSH). GIOT-4 recruited an SWI/SNF-type complex in a ligand-independent manner to ERbeta as an ER subtype-specific physical bridging factor and induced subsequent histone modifications in the ERbeta target gene promoters in a human ovarian granulosa cell line (KGN). Indeed, two ERbeta-specific target genes were upregulated by FSH at a specific stage of a normal ovulatory cycle in intact mice. These findings imply the presence of a novel regulatory convergence between the gonadotropin signaling cascade and ERbeta-mediated transcription in the ovary.
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