Linked Life Data

14512770

Source:http://linkedlifedata.com/resource/pubmed/id/14512770

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
2003-9-26
pubmed:abstractText
There is mounting evidence that replication defects are the major source of spontaneous genomic instability in the cell and that S phase checkpoints are the principle defense against such instability. In Saccharomyces cerevisiae, S phase checkpoints can be provoked by either depletion of dNTPs or DNA damage. In both cases the checkpoint kinases Mec1 and Rad53 act to suppress late origin firing, stabilize slowed or stalled replication forks and prevent S phase progression until conditions are appropriate for the resumption of DNA replication. The present review highlights recent work emphasizing the central importance of replication forks, not just as targets, but also as sensors and primary effectors of checkpoint responses, and identifies the roles played by specific fork-associated factors in these processes.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
1538-4101
pubmed:author
pubmed:issnType
Print
pubmed:volume
2
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
568-72
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:articleTitle
Multiple roles of replication forks in S phase checkpoints: sensors, effectors and targets.
pubmed:affiliation
Institute of Molecular Genetics, CNRS UMR 5535 and Université Montpellier II, 34293 Montpellier cedex 5, France.
pubmed:publicationType
Journal Article, Review, Research Support, Non-U.S. Gov't