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- W2100091975 abstract "‘Normal’ genomic DNA contains hundreds of mismatches that are generated daily by the spontaneous deamination of C (U/G) and methyl-C (T/G). Thus, a mutagenic effect of their repair could constitute a serious genetic burden. We show here that while mismatches introduced into human cells on an SV40-based episome were invariably repaired, this process induced mutations in flanking DNA at a significantly higher rate than no mismatch controls. Most mutations involved the C of TpC, the substrate of some single strand-specific APOBEC cytidine deaminases, similar to the mutations that can typify the ‘mutator phenotype’ of numerous tumors. siRNA knockdowns and chromatin immunoprecipitation showed that TpC preferring APOBECs mediate the mutagenesis, and siRNA knockdowns showed that both the base excision and mismatch repair pathways are involved. That naturally occurring mispairs can be converted to mutators, represents an heretofore unsuspected source of genetic changes that could underlie disease, aging, and evolutionary change." @default.
- W2100091975 created "2016-06-24" @default.
- W2100091975 creator A5034086813 @default.
- W2100091975 creator A5061130250 @default.
- W2100091975 creator A5090615800 @default.
- W2100091975 date "2014-04-29" @default.
- W2100091975 modified "2023-09-26" @default.
- W2100091975 title "Repair of naturally occurring mismatches can induce mutations in flanking DNA" @default.
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- W2100091975 doi "https://doi.org/10.7554/elife.02001" @default.
- W2100091975 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3999860" @default.
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