Journal
CELL RESEARCH
Volume 18, Issue 1, Pages 85-98Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/cr.2007.115
Keywords
MutS; MutL; microsatellite instability; cancer
Categories
Funding
- NATIONAL CANCER INSTITUTE [R01CA115942] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCES [R01GM072756] Funding Source: NIH RePORTER
- NCI NIH HHS [CA115942] Funding Source: Medline
- NIGMS NIH HHS [GM072756] Funding Source: Medline
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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, MutS alpha and MutL alpha, 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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