ArticleChemical research in toxicology2010
Excision of a lyase-resistant oxidized abasic lesion from DNA.
Article in Chemical research in toxicology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Structural snapshots of the mechanism of ATP-dependent DNA damage recognition by UvrA.Nature communications · 2025Article
- Dirty Ends: Formation, Repair, and Biological Relevance of Non-Canonical DNA Terminal Structures.Genes · 2025Review
- Abasic site-peptide cross-links are blocking lesions repaired by AP endonucleases.Nucleic acids research · 2023Article
- Recognition and repair of chemically heterogeneous structures at DNA ends.Environmental and molecular mutagenesis · 2015Review
- Abasic and oxidized abasic site reactivity in DNA: enzyme inhibition, cross-linking, and nucleosome catalyzed reactions.Accounts of chemical research · 2014Article
- Repair of the major lesion resulting from C5'-oxidation of DNA.Biochemistry · 2011Article
- Base excision repair and lesion-dependent subpathways for repair of oxidative DNA damage.Antioxidants & redox signaling · 2011Review
- Long patch base excision repair compensates for DNA polymerase β inactivation by the C4'-oxidized abasic site.Biochemistry · 2011Article
- Inhibition of short patch and long patch base excision repair by an oxidized abasic site.Biochemistry · 2010Article
Corrections and comments
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Authors and funding
3 authors.
Funding
Abstract
The C2'-oxidized abasic lesion (C2-AP) is produced in DNA that is subjected to oxidative stress. The lesion disrupts replication and gives rise to mutations that are dependent upon the identity of the upstream nucleotide. Ape1 incises C2-AP, but the 5'-phosphorylated fragment is not a substrate for the lyase activity of DNA polymerase beta. Excision of the lesion is achieved by strand displacement synthesis in the presence of flap endonuclease during which C2-AP and the 3'-adjacent nucleotide are replaced. The oxidized abasic lesion is also a substrate for the bacterial UvrABC nucleotide excision repair system. These data suggest that the redundant nature of DNA repair systems provides a means for removing a lesion that resists excision by short patch base excision repair.
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