ArticleOncogene2005
Nonhomologous end-joining of site-specific but not of radiation-induced DNA double-strand breaks is reduced in the presence of wild-type p53.
Article in Oncogene, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 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
30 citing papers in PubMed, 73 citations in OpenAlex.
- The E3 ubiquitin ligase DTX3L and the deubiquitinase USP28 fine-tune DNA repair through mutual regulation of their protein levels.iScience · 2025Article
- Photodynamic Therapy and Dietary Antioxidants: A Dual Strategy for Genome Stability and DNA Damage Repair.Cancer medicine · 2025Review
- Negative feedback loop in the activation of non-homologous end joining DNA repair pathway in Helicobacter pylori infected patients with gastritis.Scientific reports · 2024Article
- Dual inhibition of DNA-PK and DNA polymerase theta overcomes radiation resistance induced by p53 deficiency.NAR cancer · 2020Article
- Drugging in the absence of p53.Journal of molecular cell biology · 2019Review
- Article
- Targeting Cyclin-Dependent Kinases for Treatment of Gynecologic Cancers.Frontiers in oncology · 2018Review
- TRIMming p53's anticancer activity.Oncogene · 2016Review
- DNA Damage and Pulmonary Hypertension.International journal of molecular sciences · 2016Review
- Use of the HPRT gene to study nuclease-induced DNA double-strand break repair.Human molecular genetics · 2015Article
- 53BP1 promotes microhomology-mediated end-joining in G1-phase cells.Nucleic acids research · 2015Article
- Regulation of the DNA damage response by ubiquitin conjugation.Frontiers in genetics · 2015Review
- EGFR-mediated chromatin condensation protects KRAS-mutant cancer cells against ionizing radiation.Cancer research · 2014Article
- Article
- Chromosome instability and deregulated proliferation: an unavoidable duo.Cellular and molecular life sciences : CMLS · 2012Review
- Article
- EGF receptor inhibition radiosensitizes NSCLC cells by inducing senescence in cells sustaining DNA double-strand breaks.Cancer research · 2011Article
- Article
- The alternative end-joining pathway for repair of DNA double-strand breaks requires PARP1 but is not dependent upon microhomologies.Nucleic acids research · 2010Article
- Synthesis-dependent microhomology-mediated end joining accounts for multiple types of repair junctions.Nucleic acids research · 2010Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
Nonhomologous end-joining (NHEJ) of DNA double-strand breaks (DSBs) entails two principal mechanisms: modification of DNA ends prior to ligation (error-prone rejoining) or precise ligation without modification if the DNA ends are complementary (error-free repair). Error-prone rejoining is mutagenic, because it can lead to destruction of coding sequence or to chromosomal aberrations, and therefore must be tightly regulated. Previous studies on the role of the p53 tumor suppressor in the regulation of NHEJ have yielded conflicting results, but a rigorous analysis of NHEJ proficiency and fidelity in a purely chromosomal context has not been carried out. To this end, we created novel repair plasmid substrates that integrate into the genome. DSBs generated by the I-SceI endonuclease within these substrates were repaired by either error-prone rejoining or precise ligation. We found that the expression of wild-type p53 inhibited any repair-associated DNA sequence deletion, including a more than 250-fold inhibition of error-prone rejoining events compared to p53-null cells, while any promoting effect of p53 on precise ligation could not be directly evaluated. The role of p53 in NHEJ appeared to involve a direct transactivation-independent mechanism, possibly restricting DNA end-modification by blocking the annealing of single strands along flanking stretches of microhomology. The inhibition of error-prone rejoining by p53 did not apply to the rejoining of DSBs induced by ionizing radiation. In conclusion, our data suggest that p53 restricts the mutagenic effects of NHEJ without compromising repair proficiency or cell survival, thereby maintaining genomic stability.
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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.