ArticleNucleic acids research2008
DNA repair of clustered lesions in mammalian cells: involvement of non-homologous end-joining.
Article in Nucleic acids research, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 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
33 citing papers in PubMed, 73 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
- Condensed Matter Systems Exposed to Radiation: Multiscale Theory, Simulations, and Experiment.Chemical reviews · 2024Review
- A perspective on tumor radiation resistance following high-LET radiation treatment.Journal of cancer research and clinical oncology · 2024Review
- Article
- Sodium sulfide selectively induces oxidative stress, DNA damage, and mitochondrial dysfunction and radiosensitizes glioblastoma (GBM) cells.Redox biology · 2019Article
- Bacterial Ligase D preternary-precatalytic complex performs efficient abasic sites processing at double strand breaks during nonhomologous end joining.Nucleic acids research · 2019Article
- Ape1 guides DNA repair pathway choice that is associated with drug tolerance in glioblastoma.Scientific reports · 2017Article
- Evidence for double-strand break mediated mitochondrial DNA replication in Saccharomyces cerevisiae.Nucleic acids research · 2017Article
- Review
- Article
- Efficient processing of abasic sites by bacterial nonhomologous end-joining Ku proteins.Nucleic acids research · 2014Article
- The functional landscape of Hsp27 reveals new cellular processes such as DNA repair and alternative splicing and proposes novel anticancer targets.Molecular & cellular proteomics : MCP · 2014Article
- 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
- Requirements for 5'dRP/AP lyase activity in Ku.Nucleic acids research · 2014Article
- Replication fork collapse is a major cause of the high mutation frequency at three-base lesion clusters.Nucleic acids research · 2013Article
- DNA double-strand-break complexity levels and their possible contributions to the probability for error-prone processing and repair pathway choice.Nucleic acids research · 2013Review
- Homologous recombination rescues ssDNA gaps generated by nucleotide excision repair and reduced translesion DNA synthesis in yeast G2 cells.Proceedings of the National Academy of Sciences of the United States of America · 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
- Resolution of complex ends by Nonhomologous end joining - better to be lucky than good?Genome integrity · 2012Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Clustered lesions are defined as >or=two lesions within 20 bps and are generated in DNA by ionizing radiation. In vitro studies and work in bacteria have shown that attempted repair of two closely opposed lesions can result in the formation of double strand breaks (DSBs). Since mammalian cells can repair DSBs by non-homologous end-joining (NHEJ), we hypothesized that NHEJ would repair DSBs formed during the removal of clustered tetrahydrofurans (furans). However, two opposing furans situated 2, 5 or 12 bps apart in a firefly luciferase reporter plasmid caused a decrease in luciferase activity in wild-type, Ku80 or DNA-PKcs-deficient cells, indicating the generation of DSBs. Loss of luciferase activity was maximal at 5 bps apart and studies using siRNA implicate the major AP endonuclease in the initial cleavage. Since NHEJ-deficient cells had equivalent luciferase activity to their isogenic wild-type cells, NHEJ was not involved in accurate repair of clustered lesions. However, quantitation and examination of re-isolated DNA showed that damage-containing plasmids were inaccurately repaired by Ku80-dependent, as well as Ku80-independent mechanisms. This work indicates that not even NHEJ can completely prevent the conversion of clustered lesions to potentially lethal DSBs, so demonstrating the biological relevance of ionizing radiation-induced clustered damage.
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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.