Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
7
pubmed:dateCreated
1999-10-19
pubmed:abstractText
Interleukin-4 (IL-4) functions as a critical regulatory cytokine of the immune response. A major effect of IL-4 is the induction of specific gene expression mediated by activation of a latent transcription factor, Stat6. To understand the mechanism by which Stat6 induces gene transcription, the effects of two histone acetylase coactivators, CREB binding protein (CBP) and p300, were evaluated. Both CBP and p300 were found to cooperate with Stat6 for induction of Stat6-dependent transcription. This cooperation does not appear to be due to acetylation of Stat6. The adenoviral E1A oncoprotein, known to bind CBP and p300, can inhibit the ability of CBP and p300 to function as coactivators of Stat6. The cooperative effect of CBP and p300 depends on the presence of a carboxyl-terminal region of Stat6. Stat6 molecules lacking this region behave as negative interfering molecules for Stat6-dependent transcription. Point mutations within this region also affect transcription by Stat6 in response to IL-4, identifying a motif that appears to be required for transcription, possibly through functional cooperation with CBP/p300.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
1079-9907
pubmed:author
pubmed:issnType
Print
pubmed:volume
19
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
711-22
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1999
pubmed:articleTitle
Cooperation of the transcriptional coactivators CBP and p300 with Stat6.
pubmed:affiliation
Department of Pathology, University at Stony Brook, NY 11794, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.