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• W2792896330 abstract "Significance Mismatch repair pathway (MMR)-mediated mismatch correction has largely been recapitulated in the test tube using mismatch-containing DNA substrates. However, a long-standing question remains: How does MMR respond to Me G/T mismatches caused by alkylation damage, and does this affect cellular replication forks? We demonstrate that MMR-mediated processing of Me G/T mismatches creates replication stress, perhaps due to iterative futile repair cycles that affects DNA replication. Activation of an ensuing ATR-Chk1–mediated replication stress response becomes important for mitigating DNA damage accumulation and prolonging cell survival. This study provides evidence that MMR processing may disturb replication forks encountering alkylation damage, which has important implications for sensitivity to DNA alkylating agents and for the MMR mechanism." @default.
• W2792896330 created "2018-03-29" @default.
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• W2792896330 date "2018-01-29" @default.
• W2792896330 modified "2023-10-16" @default.
• W2792896330 title "ATR-Chk1 activation mitigates replication stress caused by mismatch repair-dependent processing of DNA damage" @default.
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• W2792896330 doi "https://doi.org/10.1073/pnas.1720355115" @default.
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