ArticleDNA repair2009
Apex1 can cleave complex clustered DNA lesions in cells.
Article in DNA repair, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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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
21 citing papers in PubMed, 50 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
- Track to the future: historical perspective on the importance of radiation track structure and DNA as a radiobiological target.International journal of radiation biology · 2018Review
- Comments on potential health effects of MRI-induced DNA lesions: quality is more important to consider than quantity.European heart journal. Cardiovascular Imaging · 2016Review
- Correlation of bistranded clustered abasic DNA lesion processing with structural and dynamic DNA helix distortion.Nucleic acids research · 2016Article
- Multiscale approach predictions for biological outcomes in ion-beam cancer therapy.Scientific reports · 2016Article
- Xeroderma Pigmentosum Group A Suppresses Mutagenesis Caused by Clustered Oxidative DNA Adducts in the Human Genome.PloS one · 2015Article
- Distinct roles of Ape1 protein, an enzyme involved in DNA repair, in high or low linear energy transfer ionizing radiation-induced cell killing.The Journal of biological chemistry · 2014Article
- Nonhomologous end joining: a good solution for bad ends.DNA repair · 2014Review
- 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
- 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
- Specificity of the dRP/AP lyase of Ku promotes nonhomologous end joining (NHEJ) fidelity at damaged ends.The Journal of biological chemistry · 2012Article
- Clustered DNA lesion repair in eukaryotes: relevance to mutagenesis and cell survival.Mutation research · 2011Review
- Distinct roles of Ape1 protein in the repair of DNA damage induced by ionizing radiation or bleomycin.The Journal of biological chemistry · 2011Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Current data indicate that clustered DNA damage generated by ionizing radiation contains 2-5 damages within 20 bps. The complexity of clustered damage is also believed to increase as the linear energy transfer of the radiation increases. Complex lesions are therefore biologically relevant especially with the use of carbon ion beam therapy to treat cancer. Since two closely opposed AP site analogs (furans) are converted to a double strand break (DSB) in cells, we hypothesized that breakage could be compromised by increasing the complexity of the cluster. We have examined the repair of clusters containing three and four lesions in mouse fibroblasts using a luciferase reporter plasmid. The addition of a third furan did reduce but not eliminate cleavage, while a tandem 8-oxo-7,8-dihydroguanine (8oxoG) immediately 5' to one furan in a two or three furan cluster decreased DSB formation by a small amount. In vitro studies using nuclear extracts demonstrated that the tandem 8oxoG was not removed under conditions where the furan was cleaved, but the presence of the 8oxoG reduced cleavage at the furan. Interestingly, a cluster of an 8oxoG opposite a furan did not form a DSB in cells. We have shown that Apex1 can cleave these complex clustered lesions in cells. This therefore indicates that Apex1 can generate complex DSBs from clustered lesions consisting of base damage and AP sites. Repair of these complex DSBs may be compromised by the nearby oxidative damage resulting in potentially lethal and biologically relevant 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.