| pubmed-article:1495996 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:1495996 | lifeskim:mentions | umls-concept:C0012854 | lld:lifeskim |
| pubmed-article:1495996 | lifeskim:mentions | umls-concept:C0026882 | lld:lifeskim |
| pubmed-article:1495996 | lifeskim:mentions | umls-concept:C0018321 | lld:lifeskim |
| pubmed-article:1495996 | lifeskim:mentions | umls-concept:C0376315 | lld:lifeskim |
| pubmed-article:1495996 | lifeskim:mentions | umls-concept:C0332120 | lld:lifeskim |
| pubmed-article:1495996 | lifeskim:mentions | umls-concept:C1883709 | lld:lifeskim |
| pubmed-article:1495996 | pubmed:issue | 15 | lld:pubmed |
| pubmed-article:1495996 | pubmed:dateCreated | 1992-9-4 | lld:pubmed |
| pubmed-article:1495996 | pubmed:abstractText | It has been previously shown both in vivo and in vitro that DNA synthesis past an oxidatively damaged form of guanine, 7,8-dihydro-8-oxoguanine (8-oxoG), can result in the misincorporation of adenine (A) opposite the 8-oxodG. In this study we show that MutY glycosylase is active on a site-specific, oxidatively damaged A/8-oxoG mispair and that it removes the undamaged adenine from this mispair. Strains that lack active MutY protein have elevated rates of G.C----T.A transversions. We find that the mutator phenotype of a mutY strain can be fully complemented by overexpressing MutM protein (Fpg protein) from a plasmid clone. The MutM protein removes 8-oxoG lesions from DNA. In addition, we have isolated a strain with a chromosomal mutation that suppresses the mutY phenotype and found that this suppressor also overexpresses MutM. Finally, a mutY mutM double mutant has a 25- to 75-fold higher mutation rate than either mutator alone. The data strongly suggest that MutY is part of an intricate repair system directed against 8-oxoG lesions in nucleic acids and that the primary function of MutY in vivo is the removal of adenines that are misincorporated opposite 8-oxoG lesions during DNA synthesis. | lld:pubmed |
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| pubmed-article:1495996 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:1495996 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:1495996 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:1495996 | pubmed:month | Aug | lld:pubmed |
| pubmed-article:1495996 | pubmed:issn | 0027-8424 | lld:pubmed |
| pubmed-article:1495996 | pubmed:author | pubmed-author:MillerJ HJH | lld:pubmed |
| pubmed-article:1495996 | pubmed:author | pubmed-author:GrollmanA PAP | lld:pubmed |
| pubmed-article:1495996 | pubmed:author | pubmed-author:CruzCC | lld:pubmed |
| pubmed-article:1495996 | pubmed:author | pubmed-author:MichaelsM LML | lld:pubmed |
| pubmed-article:1495996 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:1495996 | pubmed:day | 1 | lld:pubmed |
| pubmed-article:1495996 | pubmed:volume | 89 | lld:pubmed |
| pubmed-article:1495996 | pubmed:geneSymbol | mutY | lld:pubmed |
| pubmed-article:1495996 | pubmed:geneSymbol | mutM | lld:pubmed |
| pubmed-article:1495996 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:1495996 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:1495996 | pubmed:pagination | 7022-5 | lld:pubmed |
| pubmed-article:1495996 | pubmed:dateRevised | 2010-9-7 | lld:pubmed |
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| pubmed-article:1495996 | pubmed:year | 1992 | lld:pubmed |
| pubmed-article:1495996 | pubmed:articleTitle | Evidence that MutY and MutM combine to prevent mutations by an oxidatively damaged form of guanine in DNA. | lld:pubmed |
| pubmed-article:1495996 | pubmed:affiliation | Department of Microbiology and Molecular Genetics, University of California, Los Angeles 90024. | lld:pubmed |
| pubmed-article:1495996 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:1495996 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:1495996 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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