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• W2116372783 startingPage "3742" @default.
• W2116372783 abstract "Approximately 50% of mutations that inactivate the p53 tumor suppressor gene in the germline and in colon tumors are C to T transitions at methylation sites (CpG sites). These mutations are believed to be caused by an endogenous mechanism and spontaneous deamination of 5-methyl-cytosine to T is likely to contribute significantly to this high mutation rate. The resulting T:G mismatches created by this process have been hypothesized to be less efficiently repaired than U:G mismatches formed by deamination of C. We have, therefore, performed the first study to directly compare rates of T:G versus U:G base excision repair at identical sites observed to be mutated in the p53 gene using extracts of human normal colon mucosa and colon carcinoma tissue. Mismatched U was excised up to 6000-fold more efficiently than T, suggesting that differences in repair efficiencies are the major source of C to T transition mutations at CpG sites in human tissues. The data also suggests that T:G mismatches are repaired by additional mechanisms in human cells." @default.
• W2116372783 created "2016-06-24" @default.
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• W2116372783 creator A5088347458 @default.
• W2116372783 date "1995-09-01" @default.
• W2116372783 modified "2023-10-03" @default.
• W2116372783 title "Base excision repair of U:G mismatches at a mutational hotspot in the p53 gene is more efficient than base excision repair of T:G mismatches in extracts of human colon tumors." @default.
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• W2116372783 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/7641186" @default.
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