ArticleDNA repair2011
XRCC1 and base excision repair balance in response to nitric oxide.
Article in DNA repair, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 2 of them syntheses 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
30 citing papers in PubMed, 2 syntheses or guidelines pooled it, 48 citations in OpenAlex.
- XRCC1 R399Q polymorphism and colorectal cancer risk in the Chinese Han population: a meta-analysis.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015Pooled it
- XRCC1 and XPD genetic polymorphisms and susceptibility to age-related cataract: a meta-analysis.Molecular vision · 2015Pooled it
- Utilization of the CometChip assay for detecting PAH-induced DNA bulky adducts in a 3D primary human bronchial epithelial cell model.Toxicology · 2025Article
- The role of protein lactylation in brain health and disease: current advances and future directions.Cell death discovery · 2025Review
- Measuring DNA modifications with the comet assay: a compendium of protocols.Nature protocols · 2023Review
- Transgenic mice harboring direct repeat substrates reveal key underlying causes of homologous recombination in vivo.DNA repair · 2022Review
- A high-throughput 384-well CometChip platform reveals a role for 3-methyladenine in the cellular response to etoposide-induced DNA damage.NAR genomics and bioinformatics · 2022Article
- Lung Pneumonitis and Fibrosis in Cancer Therapy: A Review on Cellular and Molecular Mechanisms.Current drug targets · 2022Review
- The Role of Nitric Oxide in Cancer: Master Regulator or NOt?International journal of molecular sciences · 2020Review
- Applications of CometChip for Environmental Health Studies.Chemical research in toxicology · 2020Review
- The DNA repair enzyme MUTYH potentiates cytotoxicity of the alkylating agent MNNG by interacting with abasic sites.The Journal of biological chemistry · 2020Article
- The splicing component ISY1 regulates APE1 in base excision repair.DNA repair · 2020Article
- Oxidative damage and DNA damage in lungs of an ovalbumin-induced asthmatic murine model.Journal of thoracic disease · 2018Article
- Towards precision prevention: Technologies for identifying healthy individuals with high risk of disease.Mutation research · 2017Review
- Article
- A multi-targeted approach to suppress tumor-promoting inflammation.Seminars in cancer biology · 2015Review
- HSP90 regulates DNA repair via the interaction between XRCC1 and DNA polymerase β.Nature communications · 2014Article
- Genetic polymorphisms of XRCC1 gene and susceptibility to hepatocellular carcinoma in Chinese population.Medical oncology (Northwood, London, England) · 2014Article
- XRCC1 Arg399Gln variation and leukemia susceptibility: evidence from 2,647 cases and 5,518 controls.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
Inflammation associated reactive oxygen and nitrogen species (RONs), including peroxynitrite (ONOO(-)) and nitric oxide (NO), create base lesions that potentially play a role in the toxicity and large genomic rearrangements associated with many malignancies. Little is known about the role of base excision repair (BER) in removing these endogenous DNA lesions. Here, we explore the role of X-ray repair cross-complementing group 1 (XRCC1) in attenuating RONs-induced genotoxicity. XRCC1 is a scaffold protein critical for BER for which polymorphisms modulate the risk of cancer. We exploited CHO and human glioblastoma cell lines engineered to express varied levels of BER proteins to study XRCC1. Cytotoxicity and the levels of DNA repair intermediates (single-strand breaks; SSB) were evaluated following exposure of the cells to the ONOO(-) donor, SIN-1, and to gaseous NO. XRCC1 null cells were slightly more sensitive to SIN-1 than wild-type cells. We used small-scale bioreactors to expose cells to NO and found that XRCC1-deficient CHO cells were not sensitive. However, using a molecular beacon assay to test lesion removal in vitro, we found that XRCC1 facilitates AAG-initiated excision of two key NO-induced DNA lesions: 1,N(6)-ethenoadenine and hypoxanthine. Furthermore, overexpression of AAG rendered XRCC1-deficient cells sensitive to NO-induced DNA damage. These results show that AAG is a key glycosylase for BER of NO-induced DNA damage and that XRCC1's role in modulating sensitivity to RONs is dependent upon the cellular level of AAG. This demonstrates the importance of considering the expression of other components of the BER pathway when evaluating the impact of XRCC1 polymorphisms on cancer risk.
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What OpenQuestion holds
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.