Linked Life Data

18469861

Source:http://linkedlifedata.com/resource/pubmed/id/18469861

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
37
pubmed:dateCreated
2008-8-28
pubmed:abstractText
The transcription factor snail represses epithelial gene expression and thereby promotes epithelial-mesenchymal transitions (EMT) and tumor invasion. The Wnt/beta-catenin pathway is also involved in EMT and was shown to activate snail. Here, we demonstrate that snail increases Wnt reporter gene activity induced by beta-catenin, LRP6 or dishevelled, and also promotes transcription activated by GAL4-beta-catenin fusion proteins. Snail mutants lacking the transcriptional repressor domain also stimulate beta-catenin-dependent transcription indicating that downregulation of snail target genes is not required for this activity. Snail interacts with beta-catenin in immunoprecipitation experiments at its N-terminus, which is required for activation by snail. In colorectal cancer cell lines, overexpression of snail leads to increased expression of Wnt target genes, whereas downregulation of endogenous snail by siRNA reduces target gene expression. Our data indicate a positive feedback stimulation of the Wnt pathway by activation of snail.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
1476-5594
pubmed:author
pubmed:issnType
Electronic
pubmed:day
28
pubmed:volume
27
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
5075-80
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed:year
2008
pubmed:articleTitle
Snail promotes Wnt target gene expression and interacts with beta-catenin.
pubmed:affiliation
Nikolaus-Fiebiger-Center for Molecular Medicine, University Erlangen-Nürnberg, Erlangen, Germany.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't