Cofactor dynamics and sufficiency in estrogen receptor-regulated transcription.
Many cofactors bind the hormone-activated estrogen receptor ( ER), yet the specific regulators of endogenous ER-mediated gene transcription are unknown. Using chromatin immunoprecipitation (ChIP), we find that ER and a number of coactivators rapidly associate with estrogen responsive promoters following estrogen treatment in a cyclic fashion that is not predicted by current models of hormone activation. Cycles of ER complex assembly are followed by transcription. In contrast, the anti-estrogen tamoxifen (TAM) recruits corepressors but not coactivators. Using a genetic approach, we show that recruitment of the p160 class of coactivators is sufficient for gene activation and for the growth stimulatory actions of estrogen in breast cancer supporting a model in which ER cofactors play unique roles in estrogen signaling.[1]References
- Cofactor dynamics and sufficiency in estrogen receptor-regulated transcription. Shang, Y., Hu, X., DiRenzo, J., Lazar, M.A., Brown, M. Cell (2000) [Pubmed]
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