Eukaryotic mismatch repair: an update

被引:116
作者
Jiricny, J
机构
[1] Univ Zurich, Inst Med Radiobiol, CH-8008 Zurich, Switzerland
[2] Paul Scherrer Inst, CH-8008 Zurich, Switzerland
来源
MUTATION RESEARCH-DNA REPAIR | 1998年 / 409卷 / 03期
关键词
mismatch repair; mutator phenotype; hereditary nonpolyposis colon cancer; drug resistance; replication error;
D O I
10.1016/S0921-8777(98)00056-1
中图分类号
Q81 [生物工程学(生物技术)]; Q93 [微生物学];
学科分类号
071005 ; 0836 ; 090102 ; 100705 ;
摘要
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 conservation among functional homologues of bacteria, yeast and mammals. The phenotypes of mismatch repair deficient mutants are also similar in many ways. In humans, mismatch repair malfunction demonstrates itself in the form of a mutator phenotype of the affected cells, an instability of microsatellite sequences and increased levels of somatic recombination. Moreover, mismatch repair deficient cells display also varying levels of tolerance to DNA damaging agents and are thought to be involved in the cell killing mediated by these agents. This article discusses some recent developments in this fast-moving field. (C) 1998 Elsevier Science B.V. AU rights reserved.
引用
收藏
页码:107 / 121
页数:15
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