Results 221 to 230 of about 97,151 (260)
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Cellular Physiology of Mismatch Repair
Current Pharmaceutical Design, 2004The DNA mismatch repair system maintains genomic stability by correcting DNA sequence errors generated during DNA replication, during genetic exchanges between chromosomes i.e., recombination, and by correcting DNA lesions caused by mutagenic agents such as cis-platinum.
X, Wu, Z, Khalpey, M, Cascalho
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Discrimination and versatility in mismatch repair
DNA Repair, 2005Evolutionarily-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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Annual Review of Genetics, 1999
▪ Abstract DNA mismatch repair (MMR) is one of multiple replication, repair, and recombination processes that are required to maintain genomic stability in prokaryotes and eukaryotes. In the wake of the discoveries that hereditary nonpolyposis colorectal cancer (HNPCC) and other human cancers are associated with mutations in MMR genes, intensive ...
A B, Buermeyer +3 more
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▪ Abstract DNA mismatch repair (MMR) is one of multiple replication, repair, and recombination processes that are required to maintain genomic stability in prokaryotes and eukaryotes. In the wake of the discoveries that hereditary nonpolyposis colorectal cancer (HNPCC) and other human cancers are associated with mutations in MMR genes, intensive ...
A B, Buermeyer +3 more
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DNA mismatch repair and cancer
Gastroenterology, 1995The genetic basis of cancer involves certain classes of genes, particularly oncogenes, tumor-suppressor genes, and DNA mismatch repair genes. Originally identified in bacteria and yeast, the human homologues of DNA mismatch repair genes have been implicated in the pathogenesis of the hereditary nonpolyposis colorectal cancer syndromes, as well as a ...
D C, Chung, A K, Rustgi
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Mismatch repair and cancer susceptibility
Current Opinion in Biotechnology, 1994Mismatch-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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DNA mismatch repair and cancer
Frontiers in Bioscience, 2003DNA 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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Eukaryotic DNA mismatch repair
Current Opinion in Genetics & Development, 1999Eukaryotic 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, 2000Post-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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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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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, 2006By 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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