作者: Jason L. Parsons , Emma Boswell , Grigory L. Dianov
DOI: 10.1007/978-0-387-72974-9_6
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摘要: In living cells, the DNA molecule is subject to attack from reactive oxygen species generated as result of endogenous oxidative metabolism and exogenous factors, such ionising radiation. Reactive can produce a variety lesions, including single strand breaks containing modified 3′-ends that are threat cellular genomic integrity. However, cell equipped with multiple repair mechanisms able efficiently remove lesion followed by subsequent break. The majority small base damages in repaired proteins excision pathway involves removal damaged glycosylase, incision AP site produced endonuclease gap filling ligation polymerase β ligase IIIα-XRCC1 complex, respectively. 3′-end modifications may require different subset enzymes due complexity damage. this review, we summarise currently identified playing major role lesions.