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2013 ; 5
(4
): a012583
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Base excision repair
#MMPMID23545420
Krokan HE
; Bjørås M
Cold Spring Harb Perspect Biol
2013[Apr]; 5
(4
): a012583
PMID23545420
show ga
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.