| pubmed-article:15166087 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:15166087 | lifeskim:mentions | umls-concept:C1522449 | lld:lifeskim |
| pubmed-article:15166087 | lifeskim:mentions | umls-concept:C0162638 | lld:lifeskim |
| pubmed-article:15166087 | lifeskim:mentions | umls-concept:C0033684 | lld:lifeskim |
| pubmed-article:15166087 | lifeskim:mentions | umls-concept:C1326912 | lld:lifeskim |
| pubmed-article:15166087 | lifeskim:mentions | umls-concept:C1704632 | lld:lifeskim |
| pubmed-article:15166087 | lifeskim:mentions | umls-concept:C0033414 | lld:lifeskim |
| pubmed-article:15166087 | lifeskim:mentions | umls-concept:C0871261 | lld:lifeskim |
| pubmed-article:15166087 | lifeskim:mentions | umls-concept:C1155661 | lld:lifeskim |
| pubmed-article:15166087 | lifeskim:mentions | umls-concept:C2911692 | lld:lifeskim |
| pubmed-article:15166087 | lifeskim:mentions | umls-concept:C1706817 | lld:lifeskim |
| pubmed-article:15166087 | lifeskim:mentions | umls-concept:C1519755 | lld:lifeskim |
| pubmed-article:15166087 | lifeskim:mentions | umls-concept:C0681829 | lld:lifeskim |
| pubmed-article:15166087 | pubmed:issue | 10 | lld:pubmed |
| pubmed-article:15166087 | pubmed:dateCreated | 2004-9-23 | lld:pubmed |
| pubmed-article:15166087 | pubmed:abstractText | DNA mismatch repair (MMR) proteins are integral to the maintenance of genomic stability and suppression of tumorigenesis due to their role in repair of post-replicative DNA errors. Recent data also support a role for MMR proteins in cellular responses to exogenous DNA damage that does not involve removal of DNA adducts. We have demonstrated previously that both Msh2- and Msh6-null primary mouse embryonic fibroblasts are significantly less sensitive to UVB (ultraviolet B)-induced cytotoxicity and apoptosis than wild-type control cells. In order to ascertain the physiological relevance of the data we have exposed MMR-deficient mice to acute and chronic UVB radiation. We found that MMR-deficiency was associated with reduced levels of apoptosis and increased residual UVB-induced DNA adducts in the epidermis 24-h following acute UVB exposure. Moreover, Msh2-null mice developed UVB-induced skin tumors at a lower level of cumulative UVB exposure and with a greater severity of onset than wild-type mice. The Msh2-null skin tumors did not display microsatellite instability, suggesting that these tumors develop via a different tumorigenic pathway than tumors that develop spontaneously. Therefore, we propose that dysfunctional MMR promotes UVB-induced tumorigenesis through reduced apoptotic elimination of damaged epidermal cells. | lld:pubmed |
| pubmed-article:15166087 | pubmed:language | eng | lld:pubmed |
| pubmed-article:15166087 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15166087 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:15166087 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15166087 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:15166087 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15166087 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:15166087 | pubmed:month | Oct | lld:pubmed |
| pubmed-article:15166087 | pubmed:issn | 0143-3334 | lld:pubmed |
| pubmed-article:15166087 | pubmed:author | pubmed-author:AndrewSusan... | lld:pubmed |
| pubmed-article:15166087 | pubmed:author | pubmed-author:TronVictor... | lld:pubmed |
| pubmed-article:15166087 | pubmed:author | pubmed-author:CampbellMarci... | lld:pubmed |
| pubmed-article:15166087 | pubmed:author | pubmed-author:YoungLeah CLC | lld:pubmed |
| pubmed-article:15166087 | pubmed:author | pubmed-author:ThulienKyle... | lld:pubmed |
| pubmed-article:15166087 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:15166087 | pubmed:volume | 25 | lld:pubmed |
| pubmed-article:15166087 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:15166087 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:15166087 | pubmed:pagination | 1821-7 | lld:pubmed |
| pubmed-article:15166087 | pubmed:dateRevised | 2006-11-15 | lld:pubmed |
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| pubmed-article:15166087 | pubmed:year | 2004 | lld:pubmed |
| pubmed-article:15166087 | pubmed:articleTitle | DNA mismatch repair proteins promote apoptosis and suppress tumorigenesis in response to UVB irradiation: an in vivo study. | lld:pubmed |
| pubmed-article:15166087 | pubmed:affiliation | Department of Medical Genetics, University of Alberta, Edmonton, Alberta, Canada. | lld:pubmed |
| pubmed-article:15166087 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:15166087 | pubmed:publicationType | Comparative Study | lld:pubmed |
| pubmed-article:15166087 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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