Linked Life Data

16855387

Source:http://linkedlifedata.com/resource/pubmed/id/16855387

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
13
pubmed:dateCreated
2006-7-24
pubmed:abstractText
The INK4/ARF locus encodes three tumor suppressors, p15(INK4b), p16(INK4a) and ARF, which together constitute one of the main anti-oncogenic defenses of mammalian organisms. The activity of these tumor suppressors depends mostly on the transcriptional status of the locus. Recently, we have identified a conserved DNA element with the capacity to regulate the locus in a global manner. Inactivation of this element, which we have named RD(INK4/ARF), results in the silencing of the entire INK4/ARF locus. Interestingly, RD(INK4/ARF) is both a transcriptional regulatory element and a replication origin. The replication protein Cdc6 binds to RD(INK4/ARF) and is able to recruit histone deacetylases that, in turn, result in the heterochromatinization and repression of the INK4/ARF locus. This model has striking parallelisms with the silencing of the yeast mating-type loci, and it is a novel oncogenic mechanism that connects the replication machinery with the inactivation of tumor suppressors.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
1551-4005
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
5
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1382-4
pubmed:meshHeading
pubmed:year
2006
pubmed:articleTitle
A new mechanism of inactivation of the INK4/ARF locus.
pubmed:affiliation
Tumor Suppression Group, Spanish National Cancer Center (CNIO), Madrid, Spain.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't