ArticleBiochemistry2010
Inhibition of short patch and long patch base excision repair by an oxidized abasic site.
Article in Biochemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
24 citing papers in PubMed, 30 citations in OpenAlex.
- Abasic site-peptide cross-links are blocking lesions repaired by AP endonucleases.Nucleic acids research · 2023Article
- Bypass of Abasic Site-Peptide Cross-Links by Human Repair and Translesion DNA Polymerases.International journal of molecular sciences · 2023Article
- Translesion activity of PrimPol on DNA with cisplatin and DNA-protein cross-links.Scientific reports · 2021Article
- Selective Inhibition of DNA Polymerase β by a Covalent Inhibitor.Journal of the American Chemical Society · 2021Article
- Mitochondrial transcription factor A promotes DNA strand cleavage at abasic sites.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Reactivity of the Major Product of C5'-Oxidative DNA Damage in Nucleosome Core Particles.Chembiochem : a European journal of chemical biology · 2019Article
- Mitochondrial DNA degradation: A quality control measure for mitochondrial genome maintenance and stress response.The Enzymes · 2019Review
- Expanded Substrate Scope of DNA Polymerase θ and DNA Polymerase β: Lyase Activity on 5'-Overhangs and Clustered Lesions.Biochemistry · 2018Article
- An oxidized abasic lesion inhibits base excision repair leading to DNA strand breaks in a trinucleotide repeat tract.PloS one · 2018Article
- Synergistic Effects of an Irreversible DNA Polymerase Inhibitor and DNA Damaging Agents on HeLa Cells.ACS chemical biology · 2017Article
- Reactivity of Nucleic Acid Radicals.Advances in physical organic chemistry · 2016Article
- Mutagenic Bypass of an Oxidized Abasic Lesion-Induced DNA Interstrand Cross-Link Analogue by Human Translesion Synthesis DNA Polymerases.Biochemistry · 2015Article
- Rapid Histone-Catalyzed DNA Lesion Excision and Accompanying Protein Modification in Nucleosomes and Nucleosome Core Particles.Journal of the American Chemical Society · 2015Article
- Looking beneath the surface to determine what makes DNA damage deleterious.Current opinion in chemical biology · 2014Review
- Synthesis of cross-linked DNA containing oxidized abasic site analogues.The Journal of organic chemistry · 2014Article
- Irreversible inhibition of DNA polymerase β by small-molecule mimics of a DNA lesion.Journal of the American Chemical Society · 2014Article
- Abasic and oxidized abasic site reactivity in DNA: enzyme inhibition, cross-linking, and nucleosome catalyzed reactions.Accounts of chemical research · 2014Article
- DNA polymerase λ inactivation by oxidized abasic sites.Biochemistry · 2013Article
- DNA damage by C1027 involves hydrogen atom abstraction and addition to nucleobases.Bioorganic & medicinal chemistry · 2012Article
- Telomere proteins POT1, TRF1 and TRF2 augment long-patch base excision repair in vitro.Cell cycle (Georgetown, Tex.) · 2012Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
5'-(2-Phosphoryl-1,4-dioxobutane) (DOB) is an oxidized abasic lesion that is produced by a variety of DNA damaging agents, including several antitumor antibiotics. DOB efficiently and irreversibly inhibits DNA polymerase β, an essential base excision repair enzyme in mammalian cells. The generality of this mode of inhibition by DOB is supported by the inactivation of DNA polymerase λ, which may serve as a possible backup for DNA polymerase β during abasic site repair. Protein digests suggest that Lys72 and Lys84, which are present in the lyase active site of DNA polymerase β, are modified by DOB. Monoaldehyde analogues of DOB substantiate the importance of the 1,4-dicarbonyl component of DOB for efficient inactivation of Pol β and the contribution of a freely diffusible electrophile liberated from the inhibitor by the enzyme. Inhibition of DNA polymerase β's lyase function is accompanied by inactivation of its DNA polymerase activity as well, which prevents long patch base excision repair of DOB. Overall, DOB is highly refractory to short patch and long patch base excision repair. Its recalcitrance to succumb to repair suggests that DOB is a significant source of the cytotoxicity of DNA damaging agents that produce it.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.