ArticleNucleic acids research1998
Multiply damaged sites in DNA: interactions with Escherichia coli endonucleases III and VIII.
Article in Nucleic acids research, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 106 citations in OpenAlex.
- Fluorescence anisotropy study of radiation-induced DNA damage clustering based on FRET.Analytical and bioanalytical chemistry · 2021Article
- Recognition of a tandem lesion by DNA bacterial formamidopyrimidine glycosylases explored combining molecular dynamics and machine learning.Computational and structural biotechnology journal · 2021Article
- Carbon Ion Radiotherapy: A Review of Clinical Experiences and Preclinical Research, with an Emphasis on DNA Damage/Repair.Cancers · 2017Review
- Base Excision Repair of NBiochemistry · 2016Article
- Role of isolated and clustered DNA damage and the post-irradiating repair process in the effects of heavy ion beam irradiation.Journal of radiation research · 2015Article
- FANCD2 influences replication fork processes and genome stability in response to clustered DSBs.Cell cycle (Georgetown, Tex.) · 2015Article
- Nucleosomes suppress the formation of double-strand DNA breaks during attempted base excision repair of clustered oxidative damages.The Journal of biological chemistry · 2014Article
- Irreparable complex DNA double-strand breaks induce chromosome breakage in organotypic three-dimensional human lung epithelial cell culture.Nucleic acids research · 2011Article
- Mechanism of cluster DNA damage repair in response to high-atomic number and energy particles radiation.Mutation research · 2011Review
- Alkylation base damage is converted into repairable double-strand breaks and complex intermediates in G2 cells lacking AP endonuclease.PLoS genetics · 2011Article
- Processing of thymine glycol in a clustered DNA damage site: mutagenic or cytotoxic.Nucleic acids research · 2009Article
- Going ape as an approach to cancer therapeutics.Antioxidants & redox signaling · 2009Review
- The transition of closely opposed lesions to double-strand breaks during long-patch base excision repair is prevented by the coordinated action of DNA polymerase delta and Rad27/Fen1.Molecular and cellular biology · 2009Article
- Human abasic endonuclease action on multilesion abasic clusters: implications for radiation-induced biological damage.Nucleic acids research · 2008Article
- Non-problematic risks from low-dose radiation-induced DNA damage clusters.Dose-response : a publication of International Hormesis Society · 2008Article
- Interplay between DNA N-glycosylases/AP lyases at multiply damaged sites and biological consequences.Nucleic acids research · 2007Article
- Article
- Endogenous DNA damage clusters in human skin, 3-D model, and cultured skin cells.Free radical biology & medicine · 2005Article
- Processing of a complex multiply damaged DNA site by human cell extracts and purified repair proteins.Nucleic acids research · 2005Article
- Enhanced mutagenic potential of 8-oxo-7,8-dihydroguanine when present within a clustered DNA damage site.Nucleic acids research · 2004Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Bursts of free radicals produced by ionization of water in close vicinity to DNA can produce clusters of opposed DNA lesions and these are termed multiply damaged sites (MDS). How MDS are processed by the Escherichia coli DNA glycosylases, endonuclease (endo) III and endo VIII, which recognize oxidized pyrimidines, is the subject of this study. Oligonucleotide substrates were constructed containing a site of pyrimidine damage or an abasic (AP) site in close proximity to a single nucleotide gap, which simulates a free radical-induced single-strand break. The gap was placed in the opposite strand 1, 3 or 6 nt 5' or 3' of the AP site or base lesion. Endos III and VIII were able to cleave an AP site in the MDS, no matter what the position of the opposed strand break, although cleavage at position one 5' or 3' was reduced compared with cleavage at positions three or six 5' or 3'. Neither endo III nor endo VIII was able to remove the base lesion when the gap was positioned 1 nt 5' or 3' in the opposite strand. Cleavage of the modified pyrimidine by endo III increased as the distance increased between the base lesion and the opposed strand break. With endo VIII, however, DNA breakage at the site of the base lesion was equivalent to or less when the gap was positioned 6 nt 3' of the lesion than when the gap was 3 nt 3' of the lesion. Gel mobility shift analysis of the binding of endo VIII to an oligonucleotide containing a reduced AP (rAP) site in close opposition to a single nucleotide gap correlated with cleavage of MDS substrates by endo VIII. If the strand break in the MDS was replaced by an oxidized purine, 7,8-dihydro-8-oxoguanine (8-oxoG), neither endo VIII cleavage nor binding were perturbed. These data show that processing of oxidized pyrimidines by endos III and VIII was strongly influenced by the position and type of lesion in the opposite strand, which could have a significant effect on the biological outcome of the MDS lesion.
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