Lancaster EPrints

Repair of abasic sites in DNA.

Dianov, Grigory L. and Sleeth, Kate M. and Dianova, Irina I. and Allinson, Sarah L. (2003) Repair of abasic sites in DNA. Mutation Research, 531 (1-2). pp. 157-163. ISSN 0027-5107

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Abstract

Repair of both normal and reduced AP sites is activated by AP endonuclease, which recognizes and cleaves a phosphodiester bond 5′ to the AP site. For a short period of time an incised AP site is occupied by poly(ADP-ribose) polymerase and then DNA polymerase β adds one nucleotide into the repair gap and simultaneously removes the 5′-sugar phosphate. Finally, the DNA ligase III/XRCC1 complex accomplishes repair by sealing disrupted DNA ends. However, long-patch BER pathway, which is involved in the removal of reduced abasic sites, requires further DNA synthesis resulting in strand displacement and the generation of a damage-containing flap that is later removed by the flap endonuclease. Strand-displacement DNA synthesis is accomplished by DNA polymerase δ/ and DNA ligase I restores DNA integrity. DNA synthesis by DNA polymerase δ/ is dependent on proliferating cell nuclear antigen, which also stimulates the DNA ligase I and flap endonuclease. These repair events are supported by multiple protein–protein interactions.

Item Type: Article
Journal or Publication Title: Mutation Research
Uncontrolled Keywords: Abasic sites ; DNA ; Alkylating agents
Subjects: Q Science > QH Natural history > QH301 Biology
Departments: Faculty of Health and Medicine > Biomedical & Life Sciences
ID Code: 10161
Deposited By: Dr Sarah Allinson
Deposited On: 08 Jul 2008 13:05
Refereed?: Yes
Published?: Published
Last Modified: 17 Sep 2013 10:47
Identification Number:
URI: http://eprints.lancs.ac.uk/id/eprint/10161

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