ReviewInternational journal of molecular sciences2021
Excision of Oxidatively Generated Guanine Lesions by Competitive DNA Repair Pathways.
Review in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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Who cites it
10 citing papers in PubMed, 14 citations in OpenAlex.
- Unravelling the noncanonical extracellular DNA structures in biofilm and NETosis.Nucleic acids research · 2026Review
- Telomeric DNA damage landscapes distinguish oxidative from inflammatory cellular stress.Nucleic acids research · 2025Article
- Pathways and products of base excision DNA repair in Xenopus laevis eggs: contrast with human cell pathways.Nucleic acids research · 2025Article
- Oxidative damage within alternative DNA structures results in aberrant mutagenic processing.Nucleic acids research · 2025Article
- Base excision repair of the N-(2-deoxy-d-erythro-pentofuranosyl)-urea lesion by the hNEIL1 glycosylase.Nucleic acids research · 2023Article
- A combinatorial system to examine the enzymatic repair of multiply damaged DNA substrates.Nucleic acids research · 2022Article
- Chemical and enzymatic modifications of 5-methylcytosine at the intersection of DNA damage, repair, and epigenetic reprogramming.PloS one · 2022Article
- The Physical Chemistry and Chemical Physics (PCCP) Section of theInternational journal of molecular sciences · 2021Article
- Impact of Oxidative DNA Damage and the Role of DNA Glycosylases in Neurological Dysfunction.International journal of molecular sciences · 2021Review
- Potential of Telomerase in Age-Related Macular Degeneration-Involvement of Senescence, DNA Damage Response and Autophagy and a Key Role of PGC-1α.International journal of molecular sciences · 2021Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The base and nucleotide excision repair pathways (BER and NER, respectively) are two major mechanisms that remove DNA lesions formed by the reactions of genotoxic intermediates with cellular DNA. It is generally believed that small non-bulky oxidatively generated DNA base modifications are removed by BER pathways, whereas DNA helix-distorting bulky lesions derived from the attack of chemical carcinogens or UV irradiation are repaired by the NER machinery. However, existing and growing experimental evidence indicates that oxidatively generated DNA lesions can be repaired by competitive BER and NER pathways in human cell extracts and intact human cells. Here, we focus on the interplay and competition of BER and NER pathways in excising oxidatively generated guanine lesions site-specifically positioned in plasmid DNA templates constructed by a gapped-vector technology. These experiments demonstrate a significant enhancement of the NER yields in covalently closed circular DNA plasmids (relative to the same, but linearized form of the same plasmid) harboring certain oxidatively generated guanine lesions. The interplay between the BER and NER pathways that remove oxidatively generated guanine lesions are reviewed and discussed in terms of competitive binding of the BER proteins and the DNA damage-sensing NER factor XPC-RAD23B to these lesions.
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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.