Results 221 to 230 of about 97,339 (261)
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Discrimination and versatility in mismatch repair

DNA Repair, 2005
Evolutionarily-conserved mismatch-repair (MMR) systems correct all or almost all base-mismatch errors from DNA replication via excision-resynthesis pathways, and respond to many different DNA lesions. Consideration of DNA polymerase error rates and possible consequences of excess gratuitous excision of perfectly paired (homoduplex) DNA in vivo suggests
John B, Hays   +2 more
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DNA mismatch repair and cancer

Frontiers in Bioscience, 2003
DNA mismatch repair (MMR) is an important genome caretaker system. It ensures genomic stability by correcting mismatches generated during DNA replication and recombination and by triggering apoptosis of cells with large amounts of DNA damage. Protein components responsible for these reactions are highly conserved through evolution, and homologs of ...
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Mismatch repair and cancer susceptibility

Current Opinion in Biotechnology, 1994
Mismatch-repair systems have been identified in organisms ranging from Escherichia coli to humans. They can repair almost all DNA base pair mismatches as well as small insertion/deletion mismatches. Molecular and biochemical analyses have shown that the core components of eukaryotic mismatch-repair systems are highly homologous to their bacterial ...
R D, Kolodner, E, Alani
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Eukaryotic DNA mismatch repair

Current Opinion in Genetics & Development, 1999
Eukaryotic mismatch repair (MMR) has been shown to require two different heterodimeric complexes of MutS-related proteins: MSH2-MSH3 and MSH2-MSH6. These two complexes have different mispair recognition properties and different abilities to support MMR. Alternative models have been proposed for how these MSH complexes function in MMR.
R D, Kolodner, G T, Marsischky
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Mismatch repair defects in cancer

Current Opinion in Genetics & Development, 2000
Post-replicative mismatch repair in humans utilises the hMSH2, hMSH6, hMSH3, hMLH1 and hPMS2 genes and possibly the newly identified hMLH3 gene. Recently, a link has been established between hMSH6 mutations and 'atypical' hereditary non-polyposis colon cancer (HNPCC) with an increased incidence of endometrial cancers.
Jiricny, J, Nyström-Lahti, M
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Mismatch repair prefers exons

Nature Genetics, 2017
A new analysis of cancer genomes identifies a decrease in the mutation burden of exons, but not introns, as compared to expectation. This difference can be explained by preferential recruitment of the DNA mismatch repair machinery to a protein modification that marks exons.
Dashiell J, Massey, Amnon, Koren
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The multifaceted mismatch-repair system

Nature Reviews Molecular Cell Biology, 2006
By removing biosynthetic errors from newly synthesized DNA, mismatch repair (MMR) improves the fidelity of DNA replication by several orders of magnitude. Loss of MMR brings about a mutator phenotype, which causes a predisposition to cancer. But MMR status also affects meiotic and mitotic recombination, DNA-damage signalling, apoptosis and cell-type ...
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Mismatch repair and homeologous recombination

DNA Repair, 2016
DNA mismatch repair influences the outcome of recombination events between diverging DNA sequences. Here we discuss how mismatch repair proteins are active in different homologous recombination subpathways and specific reaction steps, resulting in differential modulation of these recombination events, with a focus on the mechanism of heteroduplex ...
Khek-Chian Tham   +2 more
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DNA mismatch repair in cancer

Pharmacology & Therapeutics, 2018
Microsatellite instability (MSI) refers to the hypermutator phenotype secondary to frequent polymorphism in short repetitive DNA sequences and single nucleotide substitution, as consequence of DNA mismatch repair (MMR) deficiency. MSI secondary to germline mutation in DNA MMR proteins is the molecular fingerprint of Lynch syndrome (LS), while ...
Marina, Baretti, Dung T, Le
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Eukaryotic mismatch repair: an update

Mutation Research/DNA Repair, 1998
The discovery that mutations in mismatch repair genes segregate with hereditary nonpolyposis colon cancer has awakened a great deal of interest in the study of the process of postreplicative mismatch repair. The characterisation of the principal players involved in this important metabolic pathway has been greatly facilitated by the amino acid sequence
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