ArticleNucleic acids research2007
Interplay between DNA N-glycosylases/AP lyases at multiply damaged sites and biological consequences.
Article in Nucleic acids research, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 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.
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Who cites it
22 citing papers in PubMed, 51 citations in OpenAlex.
- A combinatorial system to examine the enzymatic repair of multiply damaged DNA substrates.Nucleic acids research · 2022Article
- Article
- Article
- Vicinal abasic site impaired processing of a Tg:G mismatch and 8-oxoguanine lesions in three-component bistranded clustered DNA damage.RSC advances · 2018Article
- Effects of indirect actions and oxygen on relative biological effectiveness: estimate of DSB induction and conversion induced by gamma rays and helium ions.Journal of radiation research · 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
- Radiation-mediated formation of complex damage to DNA: a chemical aspect overview.The British journal of radiology · 2014Review
- Replication fork collapse is a major cause of the high mutation frequency at three-base lesion clusters.Nucleic acids research · 2013Article
- Quantification of 8-oxodGuo lesions in double-stranded DNA using a photoelectrochemical DNA sensor.Analytical chemistry · 2012Article
- Article
- Clustered DNA lesion repair in eukaryotes: relevance to mutagenesis and cell survival.Mutation research · 2011Review
- Delayed repair of radiation induced clustered DNA damage: friend or foe?Mutation research · 2011Review
- Saccharomyces cerevisiae-based system for studying clustered DNA damages.Radiation and environmental biophysics · 2010Article
- HO* radicals induce an unexpected high proportion of tandem base lesions refractory to repair by DNA glycosylases.Proceedings of the National Academy of Sciences of the United States of America · 2010Article
- Hierarchy of lesion processing governs the repair, double-strand break formation and mutability of three-lesion clustered DNA damage.Nucleic acids research · 2010Article
- Apex1 can cleave complex clustered DNA lesions in cells.DNA repair · 2009Article
- Processing of thymine glycol in a clustered DNA damage site: mutagenic or cytotoxic.Nucleic acids research · 2009Article
- The formation of double-strand breaks at multiply damaged sites is driven by the kinetics of excision/incision at base damage in eukaryotic cells.Nucleic acids research · 2009Article
- DNA repair of clustered lesions in mammalian cells: involvement of non-homologous end-joining.Nucleic acids research · 2008Article
- Human abasic endonuclease action on multilesion abasic clusters: implications for radiation-induced biological damage.Nucleic acids research · 2008Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Evidence has emerged that repair of clustered DNA lesions may be compromised, possibly leading to the formation of double-strand breaks (DSB) and, thus, to deleterious events. The first repair event occurring at a multiply damaged site (MDS) is of major importance and will largely contribute to the hazardousness of MDS. Here, using protein extracts from wild type or hOGG1-overexpressing Chinese hamster ovary cells, we investigated the initial incision rate at base damage and the formation of repair intermediates in various complex MDS. These MDS comprise a 1 nt gap and 3-4 base damage, including 8-oxoguanine (oG) and 5-hydroxyuracil (hU). We report a hierarchy in base excision that mainly depends on the nature and the distribution of the damage. We also show that excision at both oG and hU, and consequently DSB formation, can be modulated by hOGG1 overexpression. Anyhow, for all the MDS analyzed, DSB formation is limited, due to impaired base excision. Interestingly, repair intermediates contain a short single-stranded region carrying a potentially mutagenic base damage. This in vitro study provides new insight into the processing of MDS and suggests that repair intermediates resulting from the processing of such MDS are rather mutagenic than toxic.
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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.