Oestrogen receptor function at classical and alternative response elements

Peter J. Kushner, David Agard, Wei Jun Feng, Gabriela Lopez, Andrew Schiau, Rosalie Uht, Paul Webb, Geoffrey Greene

Research output: Chapter in Book/Report/Conference proceedingChapter

66 Scopus citations


The oestrogen receptor (ER), bound to classical response elements (EREs) in the promoter of target genes, activates transcription by recruiting coactivator proteins. We will describe structural studies that show that oestrogens allow the formation of a hydrophobic cleft on the surface of the ER that serves as a docking site for coactivators. Anti-oestrogens displace part of the receptor, which then occludes the site, blocking coactivator access. In addition to activating at classical EREs, the ER activates transcription at alternative elements such as AP-1 sites. These bind the Jun/Fos proteins but not ER. Interestingly both oestrogen and tamoxifen activate transcription at AP-1 sites. We propose a mechanism whereby oestrogen and anti-oestrogen allow ER to activate transcription from alternative response elements. ER binds to the coactivators, CBP and GRIP1, that have been recruited by Jun/Fos and through this contact 'triggers' these coactivators into full activity. In this circumstance the ER is part of the coactivator complex for Jun/Fos.

Original languageEnglish
Title of host publicationNovartis Foundation Symposium
Number of pages13
StatePublished - Dec 1 2000

Publication series

NameNovartis Foundation Symposium

ASJC Scopus subject areas

  • Medicine(all)


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