A possible mechanism for exonuclease 1-independent eukaryotic mismatch repair

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A possible mechanism for exonuclease 1-independent eukaryotic mismatch repair.

Mismatch repair contributes to genetic stability, and inactivation of the mammalian pathway leads to tumor development. Mismatch correction occurs by an excision-repair mechanism and has been shown to depend on the 5' to 3' hydrolytic activity exonuclease 1 (Exo1) in eukaryotic cells. However, genetic and biochemical studies have indicated that one or more Exo1-independent modes of mismatch rep...

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Biochemistry and genetics of eukaryotic mismatch repair.

The process of mismatch repair was first postulated to explain the results of experiments on genetic recombination and bacterial mutagenesis. Mismatch repair has long been known to play a major role in two cellular processes: (1) the repair of errors made during DNA replication or as the result of some types of chemical damage to DNA and DNA precursors; and (2) the processing of recombination i...

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Human exonuclease I interacts with the mismatch repair protein hMSH2.

DNA mismatch repair (MMR) plays a vital role in the faithful replication of DNA, and its inactivation leads to a mutator phenotype that has been associated with the common cancer susceptibility syndrome Hereditary Non-Polyposis Colorectal Cancer (HNPCC). Here, we report on a novel human exonuclease (hExoI) that is related to the yeast exonuclease 1. The hExoI cDNA comprises 2541 bp, which code ...

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Human Exonuclease I Interacts with the Mismatch Repair Protein HMSH21

DNA mismatch repair (MMR) plays a vital role in the faithful replica tion of DNA, and its inactivation leads to a mutator phenotype that has been associated with the common cancer susceptibility syndrome Hered itary Non-Polyposis Colorectal Cancer (HNPCC). Here, we report on a novel human exonuclease (hExol) that is related to the yeast exonuclease 1. The hl'AnI cDNA comprises 2541 bp, which co...

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Evidence Suggesting a Mismatch Repair Mechanism

In standard crosses, some rIIB mutants of T4 phage were found to be susceptible to an extra recombination mechanism to which the other mutants were much less susceptible. The following observations were interpreted as evidence for the mismatch-repair nature of the phenomenon: (1) Marker-dependent recombination generates exclusively double exchanges at both sides of the marker. (2) Marker-depend...

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ژورنال

عنوان ژورنال: Proceedings of the National Academy of Sciences

سال: 2009

ISSN: 0027-8424,1091-6490

DOI: 10.1073/pnas.0903654106