The current evidence for defective repair of oxidatively damaged DNA in Cockayne syndrome

被引：16

作者：

Frosina, Guido ^{[1
]}

机构：

[1] Ist Nazl Ric Canc, Dept Translat Oncol, Expt Oncol Lab B, I-16132 Genoa, Italy

来源：

FREE RADICAL BIOLOGY AND MEDICINE | 2007年 / 43卷 / 02期

关键词：

Cockayne syndrome; DNA base excision repair; oxidative DNA damage; 8-oxo-7,8-dihydroguanine; glycosylase; mutation; neurological deterioration; aging; transcription-coupled repair; free radicals;

D O I：

10.1016/j.freeradbiomed.2007.04.001

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Cockayne syndrome (CS) is a rare recessive disorder characterized by a number of developmental abnormalities and premature aging. Two complementation groups (A and B) have been identified so far in CS cases. Defective transcription-coupled nucleotide excision repair is the hallmark of these patients, but in recent years evidence has been presented for a possible defect in the base excision repair pathway that removes oxidized bases. Recent results indicate that both A and B complementation groups are involved but the phenotypical consequences of this flaw remain undetermined. (C) 2007 Elsevier Inc. All rights reserved.

引用

页码：165 / 177

页数：13

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