ReviewNature reviews. Molecular cell biology2017
Non-homologous DNA end joining and alternative pathways to double-strand break repair.
Review in Nature reviews. Molecular cell biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1,053 papers, 1 of them a synthesis that pooled it.
What it found
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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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1,053 citing papers in PubMed, 1 synthesis or guideline pooled it.
- CRISPR for cystic fibrosis: Advances and insights from a systematic review.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Pooled it
- DNA Repair Mechanisms.Methods in molecular biology (Clifton, N.J.) · 2027Review
- Article
- CRISPR-mediated gap-based replacement enables site-specific DNA lesion insertion into long DNA and nucleosomes.Nucleic acids research · 2026Article
- Chromatin Modifications Orchestrate DNA Repair Pathway Choice: Epigenetics Strategies for Enhancing CRISPR-Cas9-Mediated Knock-In Efficiency.Cell proliferation · 2026Review
- BTAF1: a key regulator of DNA end resection and predictor of chemotherapy sensitivity in gastric cancer.Cell death and differentiation · 2026Article
- BRIP1, a G-quadruplex DNA helicase, protects against AID-induced genomic instability by limiting R-loop accumulation.Molecular medicine (Cambridge, Mass.) · 2026Article
- Synthetic lethality in cancer: mechanisms, therapeutic exploitation and clinical translation.Signal transduction and targeted therapy · 2026Review
- Interfering with DNA repair pathways to enhance CRISPR-Cas9-mediated homology-directed repair in a chelicerate genetic model.iScience · 2026Article
- Mechanisms and disease relevance of DNA break repair pathway choice.Nature reviews. Molecular cell biology · 2026Review
- Chromosomal instability in cancer: sources, consequences and new therapeutic opportunities.Signal transduction and targeted therapy · 2026Review
- Modulation of DNA Damage by Epstein-Barr Virus (EBV).Viruses · 2026Review
- A novel combination approach targeting P300 and DNA-PK exploits epigenetic dependencies in acute myeloid leukemia.Molecular therapy. Oncology · 2026Article
- Transgenerational chromosome repair in the asexual bdelloid rotiferScience advances · 2026Article
- Base editing for precision therapeutics.Cell genomics · 2026Review
- Enhanced γ-globin reactivation and sickle cell correction through a repressor-to-activator motif switch in theMolecular therapy. Nucleic acids · 2026Article
- Programmable enzymes for targeted gene insertion.Nature reviews. Genetics · 2026Review
- Review
- CRISPR-Cas9 and precision editing technologies linking functional genomics to clinical translation in genetic diseases.Clinical and translational medicine · 2026Review
- GNL3 SUMOylation is essential for DNA double-strand break repair by homologous recombination.Nature communications · 2026Article
993 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
4 authors.
Funding
Abstract
DNA double-strand breaks (DSBs) are the most dangerous type of DNA damage because they can result in the loss of large chromosomal regions. In all mammalian cells, DSBs that occur throughout the cell cycle are repaired predominantly by the non-homologous DNA end joining (NHEJ) pathway. Defects in NHEJ result in sensitivity to ionizing radiation and the ablation of lymphocytes. The NHEJ pathway utilizes proteins that recognize, resect, polymerize and ligate the DNA ends in a flexible manner. This flexibility permits NHEJ to function on a wide range of DNA-end configurations, with the resulting repaired DNA junctions often containing mutations. In this Review, we discuss the most recent findings regarding the relative involvement of the different NHEJ proteins in the repair of various DNA-end configurations. We also discuss the shunting of DNA-end repair to the auxiliary pathways of alternative end joining (a-EJ) or single-strand annealing (SSA) and the relevance of these different pathways to human disease.
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What OpenQuestion holds
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.