| pubmed-article:18348985 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:18348985 | lifeskim:mentions | umls-concept:C0812258 | lld:lifeskim |
| pubmed-article:18348985 | lifeskim:mentions | umls-concept:C0017337 | lld:lifeskim |
| pubmed-article:18348985 | lifeskim:mentions | umls-concept:C0033414 | lld:lifeskim |
| pubmed-article:18348985 | lifeskim:mentions | umls-concept:C1366475 | lld:lifeskim |
| pubmed-article:18348985 | lifeskim:mentions | umls-concept:C0012899 | lld:lifeskim |
| pubmed-article:18348985 | lifeskim:mentions | umls-concept:C1158530 | lld:lifeskim |
| pubmed-article:18348985 | lifeskim:mentions | umls-concept:C0851285 | lld:lifeskim |
| pubmed-article:18348985 | pubmed:issue | 22 | lld:pubmed |
| pubmed-article:18348985 | pubmed:dateCreated | 2008-5-26 | lld:pubmed |
| pubmed-article:18348985 | pubmed:abstractText | The E2F1 transcription factor activates S-phase-promoting genes, mediates apoptosis, and stimulates DNA repair through incompletely understood mechanisms. XRCC1 (x-ray repair cross-complementing group 1) protein is important for efficient single strand break/base excision repair. Although both damage and proliferative signals increase XRCC1 levels, the mechanisms regulating XRCC1 transcription remain unclear. To study these upstream mechanisms, the XRCC1 promoter was cloned into a luciferase reporter. Ectopic expression of wild-type E2F1, but not an inactive mutant E2F1(132E), activated the XRCC1 promoter-luciferase reporter, and deletion of predicted E2F1 binding sites in the promoter attenuated E2F1-induced activation. Endogenous XRCC1 expression increased in cells conditionally expressing wild-type, but not mutant E2F1, and methyl methanesulfonate-induced DNA damage stimulated XRCC1 expression in E2F1(+/+) but not E2F1(-/-) mouse embryo fibroblasts (MEFs). Additionally, E2F1(-/-) MEFs displayed attenuated DNA repair after methyl methanesulfonate-induced damage compared with E2F1(+/+) MEFs. Moreover, Chinese hamster ovary cells with mutant XRCC1 (EM9) were more sensitive to E2F1-induced apoptosis compared with Chinese hamster ovary cells with wild-type XRCC1 (AA8). These results provide new mechanistic insight into the role of the E2F pathway in maintaining genomic stability. | lld:pubmed |
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| pubmed-article:18348985 | pubmed:language | eng | lld:pubmed |
| pubmed-article:18348985 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:18348985 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:18348985 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:18348985 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:18348985 | pubmed:month | May | lld:pubmed |
| pubmed-article:18348985 | pubmed:issn | 0021-9258 | lld:pubmed |
| pubmed-article:18348985 | pubmed:author | pubmed-author:VanS LSL | lld:pubmed |
| pubmed-article:18348985 | pubmed:author | pubmed-author:LopezCharles... | lld:pubmed |
| pubmed-article:18348985 | pubmed:author | pubmed-author:ZhuZhiyiZ | lld:pubmed |
| pubmed-article:18348985 | pubmed:author | pubmed-author:YuZhiyongZ | lld:pubmed |
| pubmed-article:18348985 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:18348985 | pubmed:day | 30 | lld:pubmed |
