ReviewThe British journal of radiology2014
DNA DSB repair pathway choice: an orchestrated handover mechanism.
Review in The British journal of radiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 158 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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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
158 citing papers in PubMed, 280 citations in OpenAlex.
- Basic-patch mutations in bacteriophage T4 Rad50 uncouple ATPase activation from processive nuclease activity.Bioscience reports · 2026Article
- CDW19S coordinates phasic end processing via distinct enzymatic activities.Nucleic acids research · 2026Article
- Late toxicity after peposertib-enhanced chemoradiation in rectal cancer patients managed with organ preservation.Clinical and translational radiation oncology · 2026Article
- The relationship between DNA damage and repair and the occurrence and development of disease.Frontiers in genetics · 2026Review
- Search-and-remove genome editing allows selection of cells by DNA sequence.Nature communications · 2025Article
- Airborne PMInternational journal of molecular sciences · 2025Article
- TRIP12's role in the governance of DNA polymerase β involvement in DNA damage response and repair.Nucleic acids research · 2025Article
- Discovery and Characterization of Small Molecule Inhibitors Targeting Exonuclease 1 for Homologous Recombination-Deficient Cancer Therapy.ACS chemical biology · 2025Article
- A reciprocal relationship between markers of genomic DNA damage and alpha-synuclein pathology in dementia with Lewy bodies.Molecular neurodegeneration · 2025Article
- Review
- Towards Personalized Radiotherapy in Pelvic Cancer: Patient-Related Risk Factors for Late Radiation Toxicity.Current oncology (Toronto, Ont.) · 2025Review
- Gene Editing for Duchenne Muscular Dystrophy: From Experimental Models to Emerging Therapies.Degenerative neurological and neuromuscular disease · 2025Review
- Replication stress induces POLQ-mediated structural variant formation throughout common fragile sites after entry into mitosis.Nature communications · 2024Article
- Tissue microarray analyses of the essential DNA repair factors ATM, DNA-PKcs and Ku80 in head and neck squamous cell carcinoma.Radiation oncology (London, England) · 2024Article
- Structure-specific nucleases in genome dynamics and strategies for targeting cancers.Journal of molecular cell biology · 2024Review
- Cell-Penetrating Peptides and CRISPR-Cas9: A Combined Strategy for Human Genetic Disease Therapy.Human gene therapy · 2024Review
- Loss of tet methyl cytosine dioxygenase 3 (TET3) enhances cardiac fibrosis via modulating the DNA damage repair response.Clinical epigenetics · 2024Article
- Epigenetic and gene therapy in human and veterinary medicine.Environmental epigenetics · 2024Review
- Review
- Specificity of cancer-related chromosomal translocations is linked to proximity after the DNA double-strand break and subsequent selection.NAR cancer · 2023Article
98 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
DNA double strand breaks (DSBs) are potential lethal lesions but can also lead to chromosome rearrangements, a step promoting carcinogenesis. DNA non-homologous end-joining (NHEJ) is the major DSB rejoining process and occurs in all cell cycle stages. Homologous recombination (HR) can additionally function to repair irradiation-induced two-ended DSBs in G2 phase. In mammalian cells, HR predominantly uses a sister chromatid as a template for DSB repair; thus HR functions only in late S/G2 phase. Here, we review current insight into the interplay between HR and NHEJ in G2 phase. We argue that NHEJ represents the first choice pathway, repairing approximately 80% of X-ray-induced DSBs with rapid kinetics. However, a subset of DSBs undergoes end resection and repair by HR. 53BP1 restricts resection, thereby promoting NHEJ. During the switch from NHEJ to HR, 53BP1 is repositioned to the periphery of enlarged irradiation-induced foci (IRIF) via a BRCA1-dependent process. K63-linked ubiquitin chains, which also form at IRIF, are also repositioned as well as receptor-associated protein 80 (RAP80), a ubiquitin binding protein. RAP80 repositioning requires POH1, a proteasome component. Thus, the interfacing barriers to HR, 53BP1 and RAP80 are relieved by POH1 and BRCA1, respectively. Removal of RAP80 from the IRIF core is required for loss of the ubiquitin chains and 53BP1, and for efficient replication protein A foci formation. We propose that NHEJ is used preferentially to HR because it is a compact process that does not necessitate extensive chromatin changes in the DSB vicinity.
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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.