Linked Life Data

10965500

Source:http://linkedlifedata.com/resource/pubmed/id/10965500

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
2000-12-4
pubmed:abstractText
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.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
1528-2511
pubmed:author
pubmed:issnType
Print
pubmed:volume
230
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
20-6; discussion 27-40
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed:year
2000
pubmed:articleTitle
Oestrogen receptor function at classical and alternative response elements.
pubmed:affiliation
Metabolic Research Unit, University of California, San Francisco 94143-0540, USA.
pubmed:publicationType
Journal Article, Review