作者: Jason L. Parsons , Irina I. Dianova , Sarah L. Allinson , Grigory L. Dianov
DOI: 10.1111/J.1742-4658.2005.04628.X
关键词:
摘要: Base excision repair (BER), a major pathway for the removal of simple lesions in DNA, requires co-ordinated action several and ancillary proteins, impairment which can lead to genetic instability. We here address role poly(ADP-ribose) polymerase-1 (PARP-1) BER. Using an vitro cross-linking assay, we reveal that PARP-1 is always involved uracil-containing oligonucleotide it binds damaged DNA during early stages repair. Inhibition poly(ADP-ribosyl)ation by 3-aminobenzamide blocks dissociation from prevents further find excessive occurs when intermediates containing single-strand breaks are excess capacity cell extract, suggesting repeated binding nicked occurs. also increased sensitivity nuclease cleavage PARP-deficient mouse fibroblasts after depletion HeLa whole extracts. Our data support model or plays protective limited.