Linked Life Data

20374706

Source:http://linkedlifedata.com/resource/pubmed/id/20374706

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
2010-4-8
pubmed:abstractText
The ability to associate with corepressors and to inhibit transcription is an intrinsic property of most members of the nuclear receptor (NR) superfamily. NRs induce transcriptional repression by recruiting multiprotein corepressor complexes. Nuclear receptor corepressor (NCoR) and silencing mediator of retinoic and thyroid receptors (SMRT) are the most well characterized corepressor complexes and mediate repression for virtually all NRs. In turn, corepressor complexes repress transcription because they either contain or associate with chromatin modifying enzymes. These include histone deacetylases, histone H3K4 demethylases, histone H3K9 or H3K27 methyltransferases, and ATP-dependent chromatin remodeling factors. Two types of NR-interacting corepressors exist. Ligand-independent corepressors, like NCoR/SMRT, bind to unliganded or antagonist-bound NRs, whereas ligand-dependent corepressors (LCoRs) associate with NRs in the presence of agonist. Therefore, LCoRs may serve to attenuate NR-mediated transcriptional activation. Somewhat unexpectedly, classical coactivators may also function as "corepressors" to mediate repression by agonist-bound NRs. In this chapter, we will discuss the various modes and mechanisms of repression by NRs as well as discuss the known physiological functions of NR-mediated repression.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
1878-0814
pubmed:author
pubmed:copyrightInfo
Copyright © 2009 Elsevier Inc. All rights reserved.
pubmed:issnType
Electronic
pubmed:volume
87
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
235-59
pubmed:meshHeading
pubmed:year
2009
pubmed:articleTitle
Nuclear receptor repression: regulatory mechanisms and physiological implications.
pubmed:affiliation
Department of Genetics, University of Texas M.D. Anderson Cancer Center, Houston, Texas 77030, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, Non-P.H.S., Review, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural