ReviewDNA repair2015
Oxidant and environmental toxicant-induced effects compromise DNA ligation during base excision DNA repair.
Review in DNA repair, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
26 citing papers in PubMed, 1 synthesis or guideline pooled it, 51 citations in OpenAlex.
- XRCC1 Arg194Trp polymorphism and thyroid cancer.Journal of endocrinological investigation · 2020Pooled it
- The relationship between DNA damage and repair and the occurrence and development of disease.Frontiers in genetics · 2026Review
- Processing of DNA single-strand breaks with oxidatively damaged ends by LIG1.Nucleic acids research · 2025Article
- Repair pathway coordination from gap filling by polβ and subsequent nick sealing by LIG1 or LIG3α governs BER efficiency at the downstream steps.DNA repair · 2025Article
- Impact of DNA ligase inhibition on the nick sealing of polβ nucleotide insertion products at the downstream steps of base excision repair pathway.Mutagenesis · 2024Article
- Impact of polβ/XRCC1 Interaction Variants on the Efficiency of Nick Sealing by DNA Ligase IIIα in the Base Excision Repair Pathway.Journal of molecular biology · 2024Article
- The Role of Genetic Polymorphisms in Differentiated Thyroid Cancer: A 2023 Update.Biomedicines · 2023Review
- Structures of LIG1 that engage with mutagenic mismatches inserted by polβ in base excision repair.Nature communications · 2022Article
- A Novel Ex Vivo Approach Based on Proteomics and Biomarkers to Evaluate the Effects of Chrysene, MEHP, and PBDE-47 on Loggerhead Sea Turtles (International journal of environmental research and public health · 2022Article
- AOP report: Development of an adverse outcome pathway for oxidative DNA damage leading to mutations and chromosomal aberrations.Environmental and molecular mutagenesis · 2022Article
- Dynamic Modelling of DNA Repair Pathway at the Molecular Level: A New Perspective.Frontiers in molecular biosciences · 2022Article
- The base excision repair process: comparison between higher and lower eukaryotes.Cellular and molecular life sciences : CMLS · 2021Review
- DNA ligase I variants fail in the ligation of mutagenic repair intermediates with mismatches and oxidative DNA damage.Mutagenesis · 2020Article
- Pol β gap filling, DNA ligation and substrate-product channeling during base excision repair opposite oxidized 5-methylcytosine modifications.DNA repair · 2020Article
- The ligation of pol β mismatch insertion products governs the formation of promutagenic base excision DNA repair intermediates.Nucleic acids research · 2020Article
- Pol μ ribonucleotide insertion opposite 8-oxodG facilitates the ligation of premutagenic DNA repair intermediate.Scientific reports · 2020Article
- Interplay between DNA Polymerases and DNA Ligases: Influence on Substrate Channeling and the Fidelity of DNA Ligation.Journal of molecular biology · 2019Review
- Pol μ dGTP mismatch insertion opposite T coupled with ligation reveals promutagenic DNA repair intermediate.Nature communications · 2018Article
- Complementation of aprataxin deficiency by base excision repair enzymes in mitochondrial extracts.Nucleic acids research · 2017Article
- Role of DNA polymerase β oxidized nucleotide insertion in DNA ligation failure.Journal of radiation research · 2017Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
DNA lesions arise from many endogenous and environmental agents, and such lesions can promote deleterious events leading to genomic instability and cell death. Base excision repair (BER) is the main DNA repair pathway responsible for repairing single strand breaks, base lesions and abasic sites in mammalian cells. During BER, DNA substrates and repair intermediates are channeled from one step to the next in a sequential fashion so that release of toxic repair intermediates is minimized. This includes handoff of the product of gap-filling DNA synthesis to the DNA ligation step. The conformational differences in DNA polymerase β (pol β) associated with incorrect or oxidized nucleotide (8-oxodGMP) insertion could impact channeling of the repair intermediate to the final step of BER, i.e., DNA ligation by DNA ligase I or the DNA Ligase III/XRCC1 complex. Thus, modified DNA ligase substrates produced by faulty pol β gap-filling could impair coordination between pol β and DNA ligase. Ligation failure is associated with 5'-AMP addition to the repair intermediate and accumulation of strand breaks that could be more toxic than the initial DNA lesions. Here, we provide an overview of the consequences of ligation failure in the last step of BER. We also discuss DNA-end processing mechanisms that could play roles in reversal of impaired BER.
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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.