ReviewChemical research in toxicology2017
Repair-Resistant DNA Lesions.
Review in Chemical research in toxicology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 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
44 citing papers in PubMed, 65 citations in OpenAlex.
- Transcription-coupled nucleotide excision repair protects against genomic instability and cell death induced by the liver toxin methyleugenol.Cell death & disease · 2026Article
- Altered benzo[a]pyrene adduct formation in nucleosomes establishes distinct mutational patterns in lung cancer.The Journal of biological chemistry · 2026Article
- Chemical and biological characterization of glycidamide-adducted adenine in DNA.The Journal of biological chemistry · 2025Article
- Transcription-Coupled Nucleotide Excision Repair: A Faster Solution or the Only Option?Biomolecules · 2025Review
- The mycobiome in human cancer: analytical challenges, molecular mechanisms, and therapeutic implications.Molecular cancer · 2025Review
- Evidence for intrinsic DNA dynamics and deformability in damage sensing by the Rad4/XPC nucleotide excision repair complex.Nucleic acids research · 2025Article
- Local sequence context atFrontiers in molecular biosciences · 2025Article
- DNA Adductomics: A Narrative Review of Its Development, Applications, and Future.Biomolecules · 2024Review
- Relative genotoxicity of polycyclic aromatic hydrocarbons inferred from free energy perturbation approaches.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Variable Inhibition of DNA Unwinding Rates Catalyzed by the SARS-CoV-2 Helicase Nsp13 by Structurally Distinct Single DNA Lesions.International journal of molecular sciences · 2024Article
- Differing structures and dynamics of two photolesions portray verification differences by the human XPD helicase.Nucleic acids research · 2023Article
- Risk assessment of aflatoxin BGenes and environment : the official journal of the Japanese Environmental Mutagen Society · 2023Article
- Inhibition ofInternational journal of molecular sciences · 2022Article
- Chemical Tools for the Study of DNA Repair.Accounts of chemical research · 2022Article
- Treatment of Human HeLa Cells with Black Raspberry Extracts Enhances the Removal of DNA Lesions by the Nucleotide Excision Repair Mechanism.Antioxidants (Basel, Switzerland) · 2022Article
- Establishing Linkages Among DNA Damage, Mutagenesis, and Genetic Diseases.Chemical research in toxicology · 2022Review
- Cruciferous Vegetable Intake and Bulky DNA Damage within Non-Smokers and Former Smokers in the Gen-Air Study (EPIC Cohort).Nutrients · 2022Article
- Smokeless tobacco and cigarette smoking: chemical mechanisms and cancer prevention.Nature reviews. Cancer · 2022Review
- Molecular Modeling Study of the Genotoxicity of the Sudan I and Sudan II Azo Dyes and Their Metabolites.Frontiers in chemistry · 2022Article
- Xeroderma Pigmentosum Complementation Group C (XPC): Emerging Roles in Non-Dermatologic Malignancies.Frontiers in oncology · 2022Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The eukaryotic global genomic nucleotide excision repair (GG-NER) pathway is the major mechanism that removes most bulky and some nonbulky lesions from cellular DNA. There is growing evidence that certain DNA lesions are repaired slowly or are entirely resistant to repair in cells, tissues, and in cell extract model assay systems. It is well established that the eukaryotic DNA lesion-sensing proteins do not detect the damaged nucleotide, but recognize the distortions/destabilizations in the native DNA structure caused by the damaged nucleotides. In this article, the nature of the structural features of certain bulky DNA lesions that render them resistant to NER, or cause them to be repaired slowly, is compared to that of those that are good-to-excellent NER substrates. Understanding the structural features that distinguish NER-resistant DNA lesions from good NER substrates may be useful for interpreting the biological significance of biomarkers of exposure of human populations to genotoxic environmental chemicals. NER-resistant lesions can survive to replication and cause mutations that can initiate cancer and other diseases. Furthermore, NER diminishes the efficacy of certain chemotherapeutic drugs, and the design of more potent pharmaceuticals that resist repair can be advanced through a better understanding of the structural properties of DNA lesions that engender repair-resistance.
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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.