Base excision repair fidelity in normal and cancer cells

被引：46

作者：

Chan, Katie K. L.

Zhang, Qiu-Mei

Dianov, Grigory L. ^{[1
]}

机构：

[1] MRC, Radiat & Genome Stabil Unit, Harwell OX11 0RD, Berks, England

[2] Kyoto Univ, Lab Radiat Biol, Grad Sch Sci, Sakyo Ku, Kyoto 6068502, Japan

来源：

MUTAGENESIS | 2006年 / 21卷 / 03期

基金：

英国医学研究理事会;

关键词：

D O I：

10.1093/mutage/gel020

中图分类号：

Q3 [遗传学];

学科分类号：

071007 ; 090102 ;

摘要：

In mammalian cells, base excision repair (BER) is the major repair pathway involved in the removal of non-bulky damaged nucleotides. The fidelity of BER is dependent on the polymerization step, where the major BER DNA polymerase (Pol beta) must incorporate the correct Watson-Crick base paired nucleotide into the one nucleotide repair gap. Recent studies have indicated that expression of some Pol beta variants or changes in expression of wild-type Pol beta protein, frequently found in cancer cells, can lead to DNA repair synthesis errors and confers to cells a mutator phenotype.

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收藏

页码：173 / 178

页数：6

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