Journal
CELL
Volume 103, Issue 6, Pages 843-852Publisher
CELL PRESS
DOI: 10.1016/S0092-8674(00)00188-4
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Funding
- NCI NIH HHS [CA57374] Funding Source: Medline
- NIDDK NIH HHS [DK43806] Funding Source: Medline
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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.
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