Base Excision Repair

被引：897

作者：

Krokan, Hans E. ^{[1
]}

Bjoras, Magnar ^{[2
]}

机构：

[1] Norwegian Univ Sci & Technol, Dept Canc Res & Mol Med, N-7489 Trondheim, Norway

[2] Oslo Univ Hosp, Dept Microbiol, N-0424 Oslo, Norway

来源：

COLD SPRING HARBOR PERSPECTIVES IN BIOLOGY | 2013年 / 5卷 / 04期

关键词：

3-METHYLADENINE DNA GLYCOSYLASE; STRAND BREAK REPAIR; HAIRPIN-HELIX SUPERFAMILY; POLYMERASE-BETA; ESCHERICHIA-COLI; CRYSTAL-STRUCTURE; STRUCTURAL BASIS; DAMAGED DNA; CELL-CYCLE; SOMATIC HYPERMUTATION;

D O I：

10.1101/cshperspect.a012583

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

Base excision repair (BER) corrects DNA damage from oxidation, deamination and alkylation. Such base lesions cause little distortion to the DNA helix structure. BER is initiated by a DNA glycosylase that recognizes and removes the damaged base, leaving an abasic site that is further processed by short-patch repair or long-patch repair that largely uses different proteins to complete BER. At least 11 distinct mammalian DNA glycosylases are known, each recognizing a few related lesions, frequently with some overlap in specificities. Impressively, the damaged bases are rapidly identified in a vast excess of normal bases, without a supply of energy. BER protects against cancer, aging, and neurodegeneration and takes place both in nuclei and mitochondria. More recently, an important role of uracil-DNA glycosylase UNG2 in adaptive immunity was revealed. Furthermore, other DNA glycosylases may have important roles in epigenetics, thus expanding the repertoire of BER proteins.

引用

页码：1 / 22

页数：22

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