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pubmed-article:9563521pubmed:abstractTextThe 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.lld:pubmed
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pubmed-article:9563521pubmed:articleTitlep53-independent DNA repair and cell cycle arrest in embryonic stem cells.lld:pubmed
pubmed-article:9563521pubmed:affiliationCancer Research Campaign Laboratories, University Department of Pathology, Medical School, Edinburgh, Scotland, UK.lld:pubmed
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