ArticleNucleic acids research2009
Processing of thymine glycol in a clustered DNA damage site: mutagenic or cytotoxic.
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 23 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
23 citing papers in PubMed, 63 citations in OpenAlex.
- Multiple DNA damages induced by water radiolysis demonstrated using a dynamic Monte Carlo code.Communications chemistry · 2025Article
- The role of DNA polymerase I in tolerating single-strand breaks generated at clustered DNA damage in Escherichia coli.Scientific reports · 2024Article
- A perspective on tumor radiation resistance following high-LET radiation treatment.Journal of cancer research and clinical oncology · 2024Review
- Analysis of Nucleotide Variations in Human G-Quadruplex Forming Regions Associated with Disease States.Genes · 2023Article
- AOP report: Development of an adverse outcome pathway for oxidative DNA damage leading to mutations and chromosomal aberrations.Environmental and molecular mutagenesis · 2022Article
- Article
- Untargeted Metabolomics Identifies Key Metabolic Pathways Altered by Thymoquinone in Leukemic Cancer Cells.Nutrients · 2020Article
- Strand with mutagenic lesion is preferentially used as a template in the region of a bi-stranded clustered DNA damage site in Escherichia coli.Scientific reports · 2020Article
- Review
- The Influence of (5'Cells · 2019Article
- Occurrence, Biological Consequences, and Human Health Relevance of Oxidative Stress-Induced DNA Damage.Chemical research in toxicology · 2016Review
- Disruption of PARP1 function inhibits base excision repair of a sub-set of DNA lesions.Nucleic acids research · 2015Article
- Xeroderma Pigmentosum Group A Suppresses Mutagenesis Caused by Clustered Oxidative DNA Adducts in the Human Genome.PloS one · 2015Article
- Increased mutability and decreased repairability of a three-lesion clustered DNA-damaged site comprised of an AP site and bi-stranded 8-oxoG lesions.International journal of radiation biology · 2014Article
- 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
- Is thymidine glycol containing DNA a substrate of E. coli DNA mismatch repair system?PloS one · 2014Article
- Replication fork collapse is a major cause of the high mutation frequency at three-base lesion clusters.Nucleic acids research · 2013Article
- Irreparable complex DNA double-strand breaks induce chromosome breakage in organotypic three-dimensional human lung epithelial cell culture.Nucleic acids research · 2011Article
- Delayed repair of radiation induced clustered DNA damage: friend or foe?Mutation research · 2011Review
- Clustered DNA lesion repair in eukaryotes: relevance to mutagenesis and cell survival.Mutation research · 2011Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Localized clustering of damage is a hallmark of certain DNA-damaging agents, particularly ionizing radiation. The potential for genetic change arising from the effects of clustered damage sites containing combinations of AP sites, 8-oxo-7,8-dihydroguanine (8-oxoG) or 5,6-dihydrothymine is high. To date clusters containing a DNA base lesion that is a strong block to replicative polymerases, have not been explored. Since thymine glycol (Tg) is non-mutagenic but a strong block to replicative polymerases, we have investigated whether clusters containing Tg are highly mutagenic or lead to potentially cytotoxic lesions, when closely opposed to either 8-oxoG or an AP site. Using a bacterial plasmid-based assay and repair assays using cell extracts or purified proteins, we have shown that DNA double-strand breaks (DSBs) arise when Tg is opposite to an AP site, either through attempted base excision repair or at replication. In contrast, 8-oxoG opposite to Tg in a cluster 'protects' against DSB formation but does enhance the mutation frequency at the site of 8-oxoG relative to that at a single 8-oxoG, due to the decisive role of endonucleases in the initial stages of processing Tg/8-oxoG clusters, removing Tg to give an intermediate with an abasic site or single-strand break.
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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.