Abstract
DNA mismatch repair (MMR) is a highly conserved biological pathway that plays a key role in maintaining genomic stability. The specificity of MMR is primarily for base-base mismatches and insertion/deletion mispairs generated during DNA replication and recombination. MMR also suppresses homeologous recombination and was recently shown to play a role in DNA damage signaling in eukaryotic cells. Escherichia coli MutS and MutL and their eukaryotic homologs, MutSα and MutLα, respectively, are key players in MMR-associated genome maintenance. Many other protein components that participate in various DNA metabolic pathways, such as PCNA and RPA, are also essential for MMR. Defects in MMR are associated with genome-wide instability, predisposition to certain types of cancer including hereditary non-polyposis colorectal cancer, resistance to certain chemotherapeutic agents, and abnormalities in meiosis and sterility in mammalian systems.
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Acknowledgements
The author acknowledges research support from the National Institutes of Health (GM072756 and CA115942) and the Kentucky Lung Cancer Research Program, USA. The author regrets the lack of citations for many important observations mentioned in the text, but their omission is made necessary by restrictions in the preparation of this review. The author holds the James-Gardner Endowed Chair in Cancer Research.
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Li, GM. Mechanisms and functions of DNA mismatch repair. Cell Res 18, 85ā98 (2008). https://doi.org/10.1038/cr.2007.115
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DOI: https://doi.org/10.1038/cr.2007.115


