ArticleNucleic acids research2008
Hierarchy of nonhomologous end-joining, single-strand annealing and gene conversion at site-directed DNA double-strand breaks.
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 91 papers, 1 of them a synthesis that pooled it.
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Who cites it
91 citing papers in PubMed, 1 synthesis or guideline pooled it, 152 citations in OpenAlex.
- Parp Inhibitors and Radiotherapy: A New Combination for Prostate Cancer (Systematic Review).International journal of molecular sciences · 2023Pooled it
- Overexpression of the ERG oncogene in prostate cancer identifies candidates for PARP inhibitor-based radiosensitization.The Journal of clinical investigation · 2026Article
- Exploring the complexity of genome size reduction in angiosperms.Plant molecular biology · 2024Review
- 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
- Gene expression of non-homologous end-joining pathways in the prognosis of ovarian cancer.iScience · 2023Article
- High-efficiency and multilocus targeted integration in CHO cells using CRISPR-mediated donor nicking and DNA repair inhibitors.Biotechnology and bioengineering · 2023Article
- APTX acts in DNA double-strand break repair in a manner distinct from XRCC4.Journal of radiation research · 2023Article
- The contribution of DNA repair pathways to genome editing and evolution in filamentous pathogens.FEMS microbiology reviews · 2022Review
- TRAIL Receptor Targeting Agents Potentiate PARP Inhibitor Efficacy in Pancreatic Cancer Independently ofCancers · 2022Article
- A Lack of Effectiveness in the ATM-Orchestrated DNA Damage Response Contributes to the DNA Repair Defect of HPV-Positive Head and Neck Cancer Cells.Frontiers in oncology · 2022Article
- RBM6 splicing factor promotes homologous recombination repair of double-strand breaks and modulates sensitivity to chemotherapeutic drugs.Nucleic acids research · 2021Article
- Comprehensive optimization of a reporter assay toolbox for three distinct CRISPR-Cas systems.FEBS open bio · 2021Article
- Marker-free quantification of repair pathway utilization at Cas9-induced double-strand breaks.Nucleic acids research · 2021Article
- The cancer-testis gene,Cancer biology & medicine · 2021Article
- Dual Inhibition of PARP and the Intra-S/G2 Cell Cycle Checkpoints Results in Highly Effective Radiosensitization of HPV-Positive HNSCC Cells.Frontiers in oncology · 2021Article
- Genomic Reporter Constructs to Monitor Pathway-Specific Repair of DNA Double-Strand Breaks.Frontiers in genetics · 2021Review
- A robust CRISPR-Cas9-based fluorescent reporter assay for the detection and quantification of DNA double-strand break repair.Nucleic acids research · 2020Article
- The chromatin remodeler ALC1 underlies resistance to PARP inhibitor treatment.Science advances · 2020Article
- RIF1 controls replication initiation and homologous recombination repair in a radiation dose-dependent manner.Journal of cell science · 2020Article
- Article
31 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In mammalian cells, DNA double-strand breaks (DSBs) are repaired by three pathways, nonhomologous end-joining (NHEJ), gene conversion (GC) and single-strand annealing (SSA). These pathways are distinct with regard to repair efficiency and mutagenic potential and must be tightly controlled to preserve viability and genomic stability. Here, we employed chromosomal reporter constructs to characterize the hierarchy of NHEJ, GC and SSA at a single I-SceI-induced DSB in Chinese hamster ovary cells. We discovered that the use of GC and SSA was increased by 6- to 8-fold upon loss of Ku80 function, suggesting that NHEJ is dominant over the other two pathways. However, NHEJ efficiency was not altered if GC was impaired by Rad51 knockdown. Interestingly, when SSA was made available as an alternative mode for DSB repair, loss of Rad51 function led to an increase in SSA activity at the expense of NHEJ, implying that Rad51 may indirectly promote NHEJ by limiting SSA. We conclude that a repair hierarchy exists to limit the access of the most mutagenic mechanism, SSA, to the break site. Furthermore, the cellular choice of repair pathways is reversible and can be influenced at the level of effector proteins such as Ku80 or Rad51.
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