Linked Life Data

20628365

Source:http://linkedlifedata.com/resource/pubmed/id/20628365

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
10
pubmed:dateCreated
2010-10-4
pubmed:abstractText
Dishevelled (Dvl) is a highly conserved protein family that plays an important role in mediating Wnt signaling from membrane to cytoplasm. Recently we reported that Dvl also functions in the nucleus by stabilizing the ?-catenin/TCFs transcriptional complex. Here we describe that Dvl may function as a repressor of NF-?B. Our data show that Dvl directly binds to p65 and their interaction occurs in the nucleus. Dvl expression inhibits p65-mediated or TNF-?-stimulated activation of the NF-?B dependent reporter. This action of Dvl, however, is not dependent on Wnt or its downstream effector ?-catenin. Chromatin immunoprecipitation assay shows that recruitment of p65 to the promoters of NF-?B target genes is significantly enhanced when expression of Dvl is knocked down. Consistently, the expression level of a subset of NF-?B target genes is also increased after knock-down of Dvl. Moreover, our data suggest that Dvl may relieve the anti-apoptotic effect of NF-?B, thus play a role in promoting apoptosis. Therefore, this work demonstrates a novel function of Dvl in modulating NF-?B-regulated gene transcription.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
1748-7838
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
20
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1117-27
pubmed:meshHeading
pubmed:year
2010
pubmed:articleTitle
Dishevelled interacts with p65 and acts as a repressor of NF-?B-mediated transcription.
pubmed:affiliation
State Key Laboratory of Molecular Biology, Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200031, China.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't