ArticleNucleic acids research2009
The formation of double-strand breaks at multiply damaged sites is driven by the kinetics of excision/incision at base damage in eukaryotic cells.
Article in Nucleic acids research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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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
33 citing papers in PubMed, 61 citations in OpenAlex.
- Deciphering repair pathways of clustered DNA damage in human TK6 cells: insights from atomic force microscopy direct visualization.Nucleic acids research · 2025Article
- Chromatin and the Cellular Response to Particle Radiation-Induced Oxidative and Clustered DNA Damage.Frontiers in cell and developmental biology · 2022Review
- Article
- Dynamic structural insights into the molecular mechanism of DNA unwinding by the bacteriophage T7 helicase.Nucleic acids research · 2020Article
- Dual Inhibitors of 8-Oxoguanine Surveillance by OGG1 and NUDT1.ACS chemical biology · 2019Article
- Linking high GC content to the repair of double strand breaks in prokaryotic genomes.PLoS genetics · 2019Article
- Visualization and prediction of CRISPR incidence in microbial trait-space to identify drivers of antiviral immune strategy.The ISME journal · 2019Article
- Enhanced Cleavage at Abasic Sites within Clustered Lesions in Nucleosome Core Particles.Chembiochem : a European journal of chemical biology · 2018Article
- Vicinal abasic site impaired processing of a Tg:G mismatch and 8-oxoguanine lesions in three-component bistranded clustered DNA damage.RSC advances · 2018Article
- Potent and Selective Inhibitors of 8-Oxoguanine DNA Glycosylase.Journal of the American Chemical Society · 2018Article
- Complex DNA Damage: A Route to Radiation-Induced Genomic Instability and Carcinogenesis.Cancers · 2017Review
- Correlation of bistranded clustered abasic DNA lesion processing with structural and dynamic DNA helix distortion.Nucleic acids research · 2016Article
- Gamma radiation at a human relevant low dose rate is genotoxic in mice.Scientific reports · 2016Article
- Reactivity of Nucleic Acid Radicals.Advances in physical organic chemistry · 2016Article
- Article
- Influenza infection induces host DNA damage and dynamic DNA damage responses during tissue regeneration.Cellular and molecular life sciences : CMLS · 2015Article
- Double-strand breaks from a radical commonly produced by DNA-damaging agents.Chemical research in toxicology · 2015Article
- Xeroderma Pigmentosum Group A Suppresses Mutagenesis Caused by Clustered Oxidative DNA Adducts in the Human Genome.PloS one · 2015Article
- Reduced repair capacity of a DNA clustered damage site comprised of 8-oxo-7,8-dihydro-2'-deoxyguanosine and 2-deoxyribonolactone results in an increased mutagenic potential of these lesions.Mutation research · 2014Article
- 5,6-Dihydropyrimidine peroxyl radical reactivity in DNA.Journal of the American Chemical Society · 2014Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
It has been stipulated that repair of clustered DNA lesions may be compromised, possibly leading to the formation of double-strand breaks (DSB) and, thus, to deleterious events. Using a variety of model multiply damaged sites (MDS), we investigated parameters that govern the formation of DSB during the processing of MDS. Duplexes carrying MDS were inserted into replicative or integrative vectors, and used to transform yeast Saccharomyces cerevisiae. Formation of DSB was assessed by a relevant plasmid survival assay. Kinetics of excision/incision and DSB formation at MDS was explored using yeast cell extracts. We show that MDS composed of two uracils or abasic sites, were rapidly incised and readily converted into DSB in yeast cells. In marked contrast, none of the MDS carrying opposed oG and hU separated by 3-8 bp gave rise to DSB, despite the fact that some of them contained preexisting single-strand break (a 1-nt gap). Interestingly, the absence of DSB formation in this case correlated with slow excision/incision rates of lesions. We propose that the kinetics of the initial repair steps at MDS is a major parameter that direct towards the conversion of MDS into DSB. Data provides clues to the biological consequences of MDS in eukaryotic cells.
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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.