Linked Life Data

16258284

Source:http://linkedlifedata.com/resource/pubmed/id/16258284

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
12
pubmed:dateCreated
2005-12-16
pubmed:abstractText
The p53 tumor suppressor functions as a sequence-specific DNA-binding transcription factor that promotes antiproliferative responses, including cell cycle checkpoints, cellular senescence and apoptosis. The precise nature of the p53 transcriptional programs and the complex mechanisms that govern whether or not a cell dies in response to p53 activation remain elusive. We have recently reported the identification of a new direct p53 target, Ptprv, encoding a transmembrane tyrosine phosphatase. Ptprv expression is dramatically and preferentially increased in cells undergoing p53-dependent cell cycle exit, but not in cells undergoing p53-mediated apoptosis. Importantly, while p53-induced apoptosis is intact in mice lacking Ptprv, Ptprv-null cells are defective in G1 checkpoint control. In addition, we report herein that Ptprv is induced at high cell density and mediates contact inhibition of cell growth. Together, the data suggest that Ptprv is a potent inhibitor of cell proliferation and a critical mediator of p53-induced cell cycle exit.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
1551-4005
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
4
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1703-5
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed:year
2005
pubmed:articleTitle
PTPRV is a key mediator of p53-induced cell cycle exit.
pubmed:affiliation
Laboratory For Molecular Cancer Biology, Flanders Interuniversity Institute for Biotechnology (VIB), Ghent University, Ghent, Belgium.
pubmed:publicationType
Journal Article