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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Smad4 as a transcription corepressor for estrogen receptor alpha.

Antiestrogen compounds exhibit a variety of different effects in different tissues and are widely used for the treatment of osteoporosis, breast cancer, and other diseases. Upon examining the molecular mechanisms, we found that Smad4, a common signal transducer in the bone morphogenetic protein (BMP)/transforming growth factor-beta (TGF-beta) signaling pathway, functions as a transcription corepressor for human estrogen receptor alpha (ERalpha). Endogenous ERalpha was co-immunoprecipitated with Smad4, and the interaction was induced by antiestrogen ligands such as tamoxifen, raloxifene, and droloxifen, which was confirmed in chromatin immunoprecipitation assays. Smad4 and ERalpha form a complex when ERalpha binds to the estrogen-responsive element within the estrogen target gene promoter. Importantly, the expression of Smad4 inhibits both antiestrogen-induced luciferase activity and estrogen downstream target gene transcription in breast cancer cells. Mapping of the interaction domains indicates that the activation function 1 ( AF1) domain of ERalpha is essential for its interaction with Smad4, while the MH1 domain and linker region of Smad4 are essential for the interaction. Our findings represent a novel mechanism that TGF-beta may regulate cell fate through Smad4-mediated cross-talk with estrogen.[1]


  1. Smad4 as a transcription corepressor for estrogen receptor alpha. Wu, L., Wu, Y., Gathings, B., Wan, M., Li, X., Grizzle, W., Liu, Z., Lu, C., Mao, Z., Cao, X. J. Biol. Chem. (2003) [Pubmed]
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