ArticleNucleic acids research2003
Repair of single-strand DNA interruptions by redundant pathways and its implication in cellular sensitivity to DNA-damaging agents.
Article in Nucleic acids research, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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.
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Who cites it
8 citing papers in PubMed, 26 citations in OpenAlex.
- Programming of Cell Resistance to Genotoxic and Oxidative Stress.Biomedicines · 2018Review
- Partial complementation of a DNA ligase I deficiency by DNA ligase III and its impact on cell survival and telomere stability in mammalian cells.Cellular and molecular life sciences : CMLS · 2012Article
- Repair of the major lesion resulting from C5'-oxidation of DNA.Biochemistry · 2011Article
- Excision of a lyase-resistant oxidized abasic lesion from DNA.Chemical research in toxicology · 2010Article
- DNA tandem lesion repair by strand displacement synthesis and nucleotide excision repair.Biochemistry · 2008Article
- Methylating agents and DNA repair responses: Methylated bases and sources of strand breaks.Chemical research in toxicology · 2006Review
- Excision of formamidopyrimidine lesions by endonucleases III and VIII is not a major DNA repair pathway in Escherichia coli.Nucleic acids research · 2005Article
- Prediction of toxicant-specific gene expression signatures after chemotherapeutic treatment of breast cell lines.Environmental health perspectives · 2004Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Single-strand DNA interruptions (SSIs) are produced during the process of base excision repair (BER). Through biochemical studies, two SSI repair subpathways have been identified: a pathway mediated by DNA polymerase beta (Pol beta) and DNA ligase III (Lig III), and a pathway mediated by DNA polymerase delta/epsilon (Pol delta/epsilon) and DNA ligase I (Lig I). In addition, the existence of another pathway, mediated by Pol beta and DNA Lig I, has been suggested. Although each pathway may play a unique role in cellular DNA damage response, the functional implications of SSI repair by these three pathways are not clearly understood. To obtain a better understanding of the functional relevance of SSI repair by these pathways, we investigated the involvement of each pathway by monitoring the utilization of DNA ligases in cell-free extracts. Our results suggest that the majority of SSIs produced during the repair of alkylated DNA bases are repaired by the pathway mediated by Pol beta and either Lig I or Lig III, although some SSIs are repaired by Pol delta/epsilon and Lig I. At a cellular level, we found that Lig III over-expression increased the resistance of cells to DNA-damaging agents, while Lig I over-expression had little effect. Thus, repair pathways mediated by Lig III may have a role in the regulation of cellular sensitivity to DNA-damaging agents.
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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.