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Processing of 3′-End Modified DNA Strand Breaks Induced by Oxidative Damage

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Oxidative Damage to Nucleic Acids

Abstract

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

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Parsons, J.L., Boswell, E., Dianov, G.L. (2007). Processing of 3′-End Modified DNA Strand Breaks Induced by Oxidative Damage. In: Evans, M.D., Cooke, M.S. (eds) Oxidative Damage to Nucleic Acids. Molecular Biology Intelligence Unit. Springer, New York, NY. https://doi.org/10.1007/978-0-387-72974-9_6

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