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      Cofactor dynamics and sufficiency in estrogen receptor-regulated transcription.

      Cell

      Breast Neoplasms, Cathepsin D, genetics, metabolism, Chromatin, DNA-Binding Proteins, Estradiol, pharmacology, Estrogen Receptor alpha, Female, Gene Expression Regulation, drug effects, Histones, chemistry, Humans, Macromolecular Substances, Nuclear Receptor Coactivator 2, Nuclear Receptor Coactivator 3, Precipitin Tests, Promoter Regions, Genetic, Proteins, Receptors, Estrogen, Signal Transduction, Tamoxifen, Transcription Factors, Transcriptional Activation, Tumor Cells, Cultured, Tumor Suppressor Proteins

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          Abstract

          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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          11136970

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