Linked Life Data

18076574

Source:http://linkedlifedata.com/resource/pubmed/id/18076574

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
12
pubmed:dateCreated
2007-12-13
pubmed:abstractText
Cellular senescence is a program in normal cells triggered in response to various types of stress that cells experience when they are explanted into culture. In this study, functional analyses on the role of the class II polycomb complex in cellular senescence were performed using mouse embryo fibroblasts (MEFs) with a genetically deleted member of the complex, Mel18. Mel18-null MEFs undergo typical premature senescence accompanied by the up-regulation of ARF/p53/p16(INK4a) and decrease of Ring1b/Bmi1. Our results demonstrated that ARF or p53 deletion cancels the senescence in Mel18-null MEFs, and the fact that p16(INK4a) is up-regulated in double-null MEFs suggests that the ARF/p53 pathway plays a central role in stress-induced senescence. The in vivo binding of Ring1b and E2F3b to the ARF promoter decreased progressively in senescence, and Mel18 inactivation accelerated the exfoliation of Ring1b/E2F3b from the promoter sequence, indicating the cooperation of polycombs/E2F3b on ARF expression and cellular senescence. Taken together, it seems that class II polycomb proteins and E2F3b dually control cellular senescence via the ARF/p53 pathway.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
1356-9597
pubmed:author
pubmed:issnType
Print
pubmed:volume
12
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1371-82
pubmed:meshHeading
pubmed:year
2007
pubmed:articleTitle
Polycomb complexes regulate cellular senescence by repression of ARF in cooperation with E2F3.
pubmed:affiliation
Department of Pediatrics, Shinshu University School of Medicine, Matsumoto, Nagano 390-8621, Japan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't