Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
1998-5-13
pubmed:abstractText
The role of p53 in DNA repair and cell cycle checkpoint after ultraviolet irradiation was investigated in an embryonic stem cell line homozygous for a targeted deletion of p53. Results indicate that loss of p53 does not alter the capacity of ES cells to respond to DNA damage. Wild-type and p53-deficient cells showed similar cessation of DNA synthesis after UV damage and similar ultimate capacity to repair a transiently transfected reporter plasmid. Interestingly, in the absence of DNA damaging treatment, the transit of p53-deficient cells through S phase was slower than wild-type cells. We suggest that this may result from the absence of a p53-dependent response to endogenous DNA damage: without p53 sensing endogenous damage leading to immediate repair, such damage may persist and thus delay DNA synthesis.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0014-5793
pubmed:author
pubmed:issnType
Print
pubmed:day
3
pubmed:volume
425
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
499-504
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed:year
1998
pubmed:articleTitle
p53-independent DNA repair and cell cycle arrest in embryonic stem cells.
pubmed:affiliation
Cancer Research Campaign Laboratories, University Department of Pathology, Medical School, Edinburgh, Scotland, UK.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't