ArticlePLoS genetics2013
Defective repair of oxidative base lesions by the DNA glycosylase Nth1 associates with multiple telomere defects.
Article in PLoS genetics, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 60 citations in OpenAlex.
- Oxidative DNA lesions destabilize centromeres and drive chromosome instability.bioRxiv : the preprint server for biology · 2026Article
- Telomeric DNA damage landscapes distinguish oxidative from inflammatory cellular stress.Nucleic acids research · 2025Article
- Oxidative Stress and DNA Damage at Telomeres.Cold Spring Harbor perspectives in biology · 2025Review
- Telomere function and regulation from mouse models to human ageing and disease.Nature reviews. Molecular cell biology · 2025Review
- COProceedings of the National Academy of Sciences of the United States of America · 2024Article
- CObioRxiv : the preprint server for biology · 2024Article
- The crosstalk between telomeres and DNA repair mechanisms: an overview to mammalian somatic cells, germ cells, and preimplantation embryos.Journal of assisted reproduction and genetics · 2024Review
- DNA Glycosylases Define the Outcome of Endogenous Base Modifications.International journal of molecular sciences · 2023Review
- Article
- NTHL1 in genomic integrity, aging and cancer.DNA repair · 2020Review
- G-quadruplex ligands targeting telomeres do not inhibit HIV promoter activity and cooperate with latency reversing agents in killing latently infected cells.Cell cycle (Georgetown, Tex.) · 2020Article
- Telomeres Increasingly Develop Aberrant Structures in Aging Humans.The journals of gerontology. Series A, Biological sciences and medical sciences · 2020Article
- Back to the future: The intimate and evolving connection between telomere-related factors and genotoxic stress.The Journal of biological chemistry · 2019Review
- Telomere Trimming and DNA Damage as Signatures of High Risk Neuroblastoma.Neoplasia (New York, N.Y.) · 2019Article
- The impact of oxidative DNA damage and stress on telomere homeostasis.Mechanisms of ageing and development · 2019Review
- Telomere maintenance: regulatingMolecular & cellular oncology · 2019Article
- Association between plasma trans fatty acids concentrations and leucocyte telomere length in US adults.European journal of clinical nutrition · 2018Article
- The Good, the Bad, and the Ugly of ROS: New Insights on Aging and Aging-Related Diseases from Eukaryotic and Prokaryotic Model Organisms.Oxidative medicine and cellular longevity · 2018Review
- Age-Dependent Protective Effect of Selenium against UVA Irradiation in Primary Human Keratinocytes and the Associated DNA Repair Signature.Oxidative medicine and cellular longevity · 2018Article
- Molecular mechanisms by which oxidative DNA damage promotes telomerase activity.Nucleic acids research · 2017Article
Corrections and comments
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Authors and funding
4 authors at 4 institutions in 2 countries.
Funding
Abstract
Telomeres are chromosome end structures and are essential for maintenance of genome stability. Highly repetitive telomere sequences appear to be susceptible to oxidative stress-induced damage. Oxidation may therefore have a severe impact on telomere integrity and function. A wide spectrum of oxidative pyrimidine-derivatives has been reported, including thymine glycol (Tg), that are primarily removed by a DNA glycosylase, Endonuclease III-like protein 1 (Nth1). Here, we investigate the effect of Nth1 deficiency on telomere integrity in mice. Nth1 null (Nth1(-/-) ) mouse tissues and primary MEFs harbor higher levels of Endonuclease III-sensitive DNA lesions at telomeric repeats, in comparison to a non-telomeric locus. Furthermore, oxidative DNA damage induced by acute exposure to an oxidant is repaired slowly at telomeres in Nth1(-/-) MEFs. Although telomere length is not affected in the hematopoietic tissues of Nth1(-/-) adult mice, telomeres suffer from attrition and increased recombination and DNA damage foci formation in Nth1(-/-) bone marrow cells that are stimulated ex vivo in the presence of 20% oxygen. Nth1 deficiency also enhances telomere fragility in mice. Lastly, in a telomerase null background, Nth1(-/-) bone marrow cells undergo severe telomere loss at some chromosome ends and cell apoptosis upon replicative stress. These results suggest that Nth1 plays an important role in telomere maintenance and base repair against oxidative stress-induced base modifications. The fact that telomerase deficiency can exacerbate telomere shortening in Nth1 deficient mouse cells supports that base excision repair cooperates with telomerase to maintain telomere integrity.
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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.