ArticleDNA repair2006
Closely opposed apurinic/apyrimidinic sites are converted to double strand breaks in Escherichia coli even in the absence of exonuclease III, endonuclease IV, nucleotide excision repair and AP lyase cleavage.
Article in DNA repair, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 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
30 citing papers in PubMed, 51 citations in OpenAlex.
- Tripleknock: predicting lethal effect of three-gene knockout in bacteria by deep learning.Scientific reports · 2026Article
- Base excision repair inFrontiers in microbiology · 2026Review
- Development of a reverse transcription recombinase polymerase amplification combined with lateral flow assay for equipment-free on-site field detection of tomato chlorotic spot virus.Virology journal · 2023Article
- Recombinase Polymerase Amplification Assay with and without Nuclease-Dependent-Labeled Oligonucleotide Probe.International journal of molecular sciences · 2021Article
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- The Influence of 5'Molecules (Basel, Switzerland) · 2021Article
- DNA damage accumulates and responses are engaged in human ALS brain and spinal motor neurons and DNA repair is activatable in iPSC-derived motor neurons with SOD1 mutations.Acta neuropathologica communications · 2020Article
- Human RAD51 paralogue RAD51C fosters repair of alkylated DNA by interacting with the ALKBH3 demethylase.Nucleic acids research · 2019Article
- Expanded Substrate Scope of DNA Polymerase θ and DNA Polymerase β: Lyase Activity on 5'-Overhangs and Clustered Lesions.Biochemistry · 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
- Genome-wide map of Apn1 binding sites under oxidative stress in Saccharomyces cerevisiae.Yeast (Chichester, England) · 2017Article
- Ape1 guides DNA repair pathway choice that is associated with drug tolerance in glioblastoma.Scientific reports · 2017Article
- 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
- Replication fork collapse is a major cause of the high mutation frequency at three-base lesion clusters.Nucleic acids research · 2013Article
- Artemis is required to improve the accuracy of repair of double-strand breaks with 5'-blocked termini generated from non-DSB-clustered lesions.Mutagenesis · 2013Article
- 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
- Specific and nonhomologous isofunctional enzymes of the genetic information processing pathways as potential therapeutical targets for tritryps.Enzyme research · 2011Article
- Article
- Hierarchy of lesion processing governs the repair, double-strand break formation and mutability of three-lesion clustered DNA damage.Nucleic acids research · 2010Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Multiply damaged sites (MDSs) consist of two or more damages within 20 base pairs (bps) and are introduced into DNA by ionizing radiation. Using a plasmid assay, we previously demonstrated that repair in Escherichia coli generated a double strand break (DSB) from two closely opposed uracils when uracil DNA glycosylase initiated repair. To identify the enzymes that converted the resulting apurinic/apyrimidinic (AP) sites to DSBs, repair was examined in bacteria deficient in AP site cleavage. Since exonuclease III (xth) and endonuclease IV (nfo) mutant bacteria were able to introduce DSBs at the MDSs, we generated unique bacterial mutants deficient in UvrA, Xth and Nfo. However, the additional disruption of nucleotide excision repair (NER) did not prevent DSB formation. xth- nfo- nfi- bacteria also converted the MDSs to DSBs, ruling out endonuclease V as the candidate AP endonuclease. By using MDSs containing tetrahydrofuran (an AP site analog), it was determined that even in the absence of Xth, Nfo, NER and AP lyase cleavage, DSBs were formed from closely opposed AP sites. This finding implies that there is an unknown enzyme/repair pathway for MDSs, and multiple underlying repair systems in cells that can process closely opposed DNA damage into lethal lesions following exposure to ionizing radiation.
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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.