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Base Excision Repair
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DOI：10.1101/cshperspect.a012583.png)
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Abstract
En 中文
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.
Keywords:
3-METHYLADENINE DNA GLYCOSYLASE
STRAND BREAK REPAIR
HAIRPIN-HELIX SUPERFAMILY
POLYMERASE-BETA
ESCHERICHIA-COLI
CRYSTAL-STRUCTURE
STRUCTURAL BASIS
DAMAGED DNA
CELL-CYCLE
SOMATIC HYPERMUTATION
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