Dianov, Grigory L. and Sleeth, Kate M. and Dianova, Irina I. and Allinson, Sarah L. (2003) Repair of abasic sites in DNA. Mutation Research - Fundamental and Molecular Mechanisms of Mutagenesis, 531 (1-2). pp. 157-163. ISSN 0027-5107
Full text not available from this repository.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.