Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
2005-11-2
pubmed:abstractText
Eukaryotic chromosome replication is mediated by multiple replicons and is coordinated with sister chromatid cohesion, DNA recombination, transcription and cell cycle progression. Replication forks stall or collapse at DNA lesions or problematic genomic regions, and these events have often been associated with recombination and chromosomal rearrangements. Stalled forks generate single-stranded DNA that activates the replication checkpoint, which in turn functions to protect the stability of the fork until the replication can resume. Recombination-mediated and damage-bypass processes are the main mechanisms responsible for replication restart. New findings have helped to unmask the molecular mechanisms that sense replication stress, control the stability of replication forks, and regulate the mechanisms that promote replication restart, thereby giving us a better understanding of how genome integrity is preserved during replication.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0955-0674
pubmed:author
pubmed:issnType
Print
pubmed:volume
17
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
568-75
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
2005
pubmed:articleTitle
The DNA damage response during DNA replication.
pubmed:affiliation
FIRC Institute of Molecular Oncology Foundation and DSBB-University of Milan, Via Adamello 16, 20139, Milan, Italy.
pubmed:publicationType
Journal Article, Review, Research Support, Non-U.S. Gov't