ArticleNucleic acids research2003
Repair of a minimal DNA double-strand break by NHEJ requires DNA-PKcs and is controlled by the ATM/ATR checkpoint.
Article in Nucleic acids research, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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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
24 citing papers in PubMed, 36 citations in OpenAlex.
- ATR and CDK4/6 inhibition target the growth of methotrexate-resistant choriocarcinoma.Oncogene · 2022Article
- Individual Response to Radiation of Individuals with Neurofibromatosis Type I: Role of the ATM Protein and Influence of Statins and Bisphosphonates.Molecular neurobiology · 2022Article
- Genotoxicity-Stimulated and CYLD-Driven Malignant Transformation.Cancer management and research · 2022Article
- Antiviral strategies targeting herpesviruses.Journal of virus eradication · 2021Review
- Review
- MiR-584-5p potentiates vincristine and radiation response by inducing spindle defects and DNA damage in medulloblastoma.Nature communications · 2018Article
- ATM-dependent pathways of chromatin remodelling and oxidative DNA damage responses.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2017Review
- Differential expression profile analysis of DNA damage repair genes in CD133Oncology letters · 2017Article
- Inhibiting DNA-PKBiochemical and biophysical research communications · 2017Article
- CRISPaint allows modular base-specific gene tagging using a ligase-4-dependent mechanism.Nature communications · 2016Article
- Functional interplay between ATM/ATR-mediated DNA damage response and DNA repair pathways in oxidative stress.Cellular and molecular life sciences : CMLS · 2014Review
- Article
- Downregulated Ku70 and ATM associated to poor prognosis in colorectal cancer among Chinese patients.OncoTargets and therapy · 2014Article
- Enhanced genotoxicity of silver nanoparticles in DNA repair deficient Mammalian cells.Frontiers in genetics · 2012Article
- Unique and redundant functions of ATM and DNA-PKcs during V(D)J recombination.Cell cycle (Georgetown, Tex.) · 2011Review
- Biochemical characterization of metnase's endonuclease activity and its role in NHEJ repair.Biochemistry · 2011Article
- Specific and nonhomologous isofunctional enzymes of the genetic information processing pathways as potential therapeutical targets for tritryps.Enzyme research · 2011Article
- Increase in double-stranded DNA break-related foci in early-stage thymocytes of aged mice.Experimental gerontology · 2009Article
- Suppression of nonhomologous end joining repair by overexpression of HMGA2.Cancer research · 2009Article
- IGFBP2 is overexpressed by pediatric malignant astrocytomas and induces the repair enzyme DNA-PK.Journal of child neurology · 2008Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mammalian cells primarily rejoin DNA double-strand breaks (DSBs) by the non-homologous end-joining (NHEJ) pathway. The joining of the broken DNA ends appears directly without template and accuracy is ensured by the NHEJ factors that are under ATM/ATR regulated checkpoint control. In the current study we report the engineering of a mono-specific DNA damaging agent. This was used to study the molecular requirements for the repair of the least complex DSB in vivo. Single-chain PvuII restriction enzymes fused to protein delivery sequences transduce cells efficiently and induce blunt end DSBs in vivo. We demonstrate that beside XRCC4/LigaseIV and KU, the DNA-PK catalytic subunit (DNA-PKcs) is also essential for the joining of this low complex DSB in vivo. The appearance of blunt end 3'-hydroxyl and 5'-phosphate DNA DSBs induces a significantly higher frequency of anaphase bridges in cells that do not contain functional DNA-PKcs, suggesting an absolute requirement for DNA-PKcs in the control of chromosomal stability during end joining. Moreover, these minimal blunt end DSBs are sufficient to induce a p53 and ATM/ATR checkpoint function.
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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.