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[错配修复]

[Mismatch repair].

作者信息

Goliasnaia N V, Tsvetkova N A

出版信息

Mol Biol (Mosk). 2006 Mar-Apr;40(2):211-23.

Abstract

Specific repair systems are activated in response to the DNA damage. Mismatch repair protects the genome of prokaryotic and eukaryotic cells from lesions that appear during process of DNA replication or are induced by mutagenic factors. The methyl directed mismatch repair distinguishes the new strand from the old strand by the hemi-methylated state of the DNA and controls the fidelity of genetic information after homologous recombination. The very short patch repair restores the mismatches at the sites with nucleotide sequence CC(W/T)GG. The "8-oxoG" pathway is independent of the hemi-methylated state of the DNA, and removes the oxidated nucleotides from the genome of prokaryotes and eukaryotes. Mutations in genes of mismatch repair enhance the process of mutagenesis in prokaryotic cell, and are the reason for the development of the colon cancer in humans. The mechanisms of mismatch repair and the role of defective repair proteins in mutagenesis and carcinogenesis are discussed in this review.

摘要

特定的修复系统会因DNA损伤而被激活。错配修复可保护原核和真核细胞的基因组免受DNA复制过程中出现的或由诱变因素诱导产生的损伤。甲基化导向的错配修复通过DNA的半甲基化状态区分新链和旧链,并在同源重组后控制遗传信息的保真度。极短补丁修复可修复核苷酸序列为CC(W/T)GG位点的错配。“8-氧代鸟嘌呤”途径独立于DNA的半甲基化状态,可从原核生物和真核生物的基因组中去除氧化核苷酸。错配修复基因的突变会增强原核细胞中的诱变过程,也是人类结肠癌发生的原因。本文综述了错配修复机制以及缺陷修复蛋白在诱变和致癌过程中的作用。

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