pubmed-article:8875987 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:8875987 | lifeskim:mentions | umls-concept:C0012655 | lld:lifeskim |
pubmed-article:8875987 | lifeskim:mentions | umls-concept:C0162638 | lld:lifeskim |
pubmed-article:8875987 | lifeskim:mentions | umls-concept:C0033414 | lld:lifeskim |
pubmed-article:8875987 | lifeskim:mentions | umls-concept:C0376515 | lld:lifeskim |
pubmed-article:8875987 | lifeskim:mentions | umls-concept:C0079866 | lld:lifeskim |
pubmed-article:8875987 | lifeskim:mentions | umls-concept:C1332397 | lld:lifeskim |
pubmed-article:8875987 | lifeskim:mentions | umls-concept:C0301625 | lld:lifeskim |
pubmed-article:8875987 | pubmed:issue | 7 | lld:pubmed |
pubmed-article:8875987 | pubmed:dateCreated | 1996-12-9 | lld:pubmed |
pubmed-article:8875987 | pubmed:abstractText | Bcl-2 appears to contribute to neoplasia primarily by promoting cell survival, rather than by stimulating cellular proliferation. Bcl-2, and the related protein Bcl-xL, each suppress apoptosis induced by a wide variety of stimuli in many different cell types. Here we report that suppression of apoptosis by Bcl-2 or Bcl-xL markedly elevates the levels of radiation-induced mutations. This enhanced mutagenesis is the result of an increase in mutation frequency (mutations per survivor) together with a moderate increase in viability. Ectopic expression of either Bcl-2 or Bcl-xL enhances radiation mutagenesis in cells with wtp53. Surprisingly, we found that ectopic expression of Bcl-xL also promotes mutagenesis in p53- cells. These results support the hypothesis that apoptosis plays a crucial role in maintaining genomic integrity by selectively eliminating highly mutated cells from the population. | lld:pubmed |
pubmed-article:8875987 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:8875987 | pubmed:keyword | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:8875987 | pubmed:language | eng | lld:pubmed |
pubmed-article:8875987 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:8875987 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:8875987 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:8875987 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:8875987 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:8875987 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:8875987 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:8875987 | pubmed:month | Oct | lld:pubmed |
pubmed-article:8875987 | pubmed:issn | 0950-9232 | lld:pubmed |
pubmed-article:8875987 | pubmed:author | pubmed-author:KronenbergAA | lld:pubmed |
pubmed-article:8875987 | pubmed:author | pubmed-author:GauntTT | lld:pubmed |
pubmed-article:8875987 | pubmed:author | pubmed-author:Cherbonnel-La... | lld:pubmed |
pubmed-article:8875987 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:8875987 | pubmed:day | 3 | lld:pubmed |
pubmed-article:8875987 | pubmed:volume | 13 | lld:pubmed |
pubmed-article:8875987 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:8875987 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:8875987 | pubmed:pagination | 1489-97 | lld:pubmed |
pubmed-article:8875987 | pubmed:dateRevised | 2007-11-14 | lld:pubmed |
pubmed-article:8875987 | pubmed:meshHeading | pubmed-meshheading:8875987-... | lld:pubmed |
pubmed-article:8875987 | pubmed:meshHeading | pubmed-meshheading:8875987-... | lld:pubmed |
pubmed-article:8875987 | pubmed:meshHeading | pubmed-meshheading:8875987-... | lld:pubmed |
pubmed-article:8875987 | pubmed:meshHeading | pubmed-meshheading:8875987-... | lld:pubmed |
pubmed-article:8875987 | pubmed:meshHeading | pubmed-meshheading:8875987-... | lld:pubmed |
pubmed-article:8875987 | pubmed:meshHeading | pubmed-meshheading:8875987-... | lld:pubmed |
pubmed-article:8875987 | pubmed:meshHeading | pubmed-meshheading:8875987-... | lld:pubmed |
pubmed-article:8875987 | pubmed:meshHeading | pubmed-meshheading:8875987-... | lld:pubmed |
pubmed-article:8875987 | pubmed:meshHeading | pubmed-meshheading:8875987-... | lld:pubmed |
pubmed-article:8875987 | pubmed:meshHeading | pubmed-meshheading:8875987-... | lld:pubmed |
pubmed-article:8875987 | pubmed:meshHeading | pubmed-meshheading:8875987-... | lld:pubmed |
pubmed-article:8875987 | pubmed:meshHeading | pubmed-meshheading:8875987-... | lld:pubmed |
pubmed-article:8875987 | pubmed:meshHeading | pubmed-meshheading:8875987-... | lld:pubmed |
pubmed-article:8875987 | pubmed:year | 1996 | lld:pubmed |
pubmed-article:8875987 | pubmed:articleTitle | Suppression of apoptosis by Bcl-2 or Bcl-xL promotes susceptibility to mutagenesis. | lld:pubmed |
pubmed-article:8875987 | pubmed:affiliation | Life Sciences Division, Lawrence Berkeley National Laboratory, University of California, Berkeley 94720, USA. | lld:pubmed |
pubmed-article:8875987 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:8875987 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
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