pubmed-article:9563521 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:9563521 | lifeskim:mentions | umls-concept:C0596508 | lld:lifeskim |
pubmed-article:9563521 | lifeskim:mentions | umls-concept:C0012899 | lld:lifeskim |
pubmed-article:9563521 | lifeskim:mentions | umls-concept:C1155873 | lld:lifeskim |
pubmed-article:9563521 | pubmed:issue | 3 | lld:pubmed |
pubmed-article:9563521 | pubmed:dateCreated | 1998-5-13 | lld:pubmed |
pubmed-article:9563521 | 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. | lld:pubmed |
pubmed-article:9563521 | pubmed:language | eng | lld:pubmed |
pubmed-article:9563521 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:9563521 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:9563521 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:9563521 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:9563521 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:9563521 | pubmed:month | Apr | lld:pubmed |
pubmed-article:9563521 | pubmed:issn | 0014-5793 | lld:pubmed |
pubmed-article:9563521 | pubmed:author | pubmed-author:WyllieA HAH | lld:pubmed |
pubmed-article:9563521 | pubmed:author | pubmed-author:ProtaGG | lld:pubmed |
pubmed-article:9563521 | pubmed:author | pubmed-author:HarrisonD JDJ | lld:pubmed |
pubmed-article:9563521 | pubmed:author | pubmed-author:ClarkeA RAR | lld:pubmed |
pubmed-article:9563521 | pubmed:author | pubmed-author:BellamyC OCO | lld:pubmed |
pubmed-article:9563521 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:9563521 | pubmed:day | 3 | lld:pubmed |
pubmed-article:9563521 | pubmed:volume | 425 | lld:pubmed |
pubmed-article:9563521 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:9563521 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:9563521 | pubmed:pagination | 499-504 | lld:pubmed |
pubmed-article:9563521 | pubmed:dateRevised | 2008-11-21 | lld:pubmed |
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pubmed-article:9563521 | pubmed:meshHeading | pubmed-meshheading:9563521-... | lld:pubmed |
pubmed-article:9563521 | pubmed:year | 1998 | lld:pubmed |
pubmed-article:9563521 | pubmed:articleTitle | p53-independent DNA repair and cell cycle arrest in embryonic stem cells. | lld:pubmed |
pubmed-article:9563521 | pubmed:affiliation | Cancer Research Campaign Laboratories, University Department of Pathology, Medical School, Edinburgh, Scotland, UK. | lld:pubmed |
pubmed-article:9563521 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:9563521 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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