ArticlePLoS genetics2008
Alternative-NHEJ is a mechanistically distinct pathway of mammalian chromosome break repair.
Article in PLoS genetics, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 595 papers.
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Who cites it
595 citing papers in PubMed, 848 citations in OpenAlex.
- ALYREF binds to poly-ADP-ribose at double strand breaks impairing repair in tumoral cells.EMBO reports · 2026Article
- MPP8 Facilitates DNA DSB Repair via NHEJ to Promote Chemoresistance of TNBC Independent of Methyl-H3K9 Binding.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Article
- PCNA-RECQL5-RPRD1B recruit repair components to stressed replication forks to promote survival of BRCA1-deficient cancer cells.Nucleic acids research · 2026Article
- The tumor suppressor menin is a key scaffold mediator for homologous recombination repair.Nucleic acids research · 2026Article
- Reciprocal compensation of caspase-2 and p53 regulates the DNA damage response in HCT116 colon cancer cells.The Journal of biological chemistry · 2026Article
- CRISPR/Cas9-Based Genome Editing: Understanding Differences in DNA Repair Pathways, Profiles, and Outcomes.International journal of molecular sciences · 2026Review
- Overexpression of the BRC repeat 8 of BRCA2 hyperstabilizes RAD51 and alters DNA repair dynamics.Molecular biology reports · 2026Article
- ALK Knock-In Reporter Reveals APE1 as a Negative Regulator ofInternational journal of molecular sciences · 2026Article
- Profilin-1 Deficiency Activates STING to Drive T Cell-Mediated Anti-Tumor Immunity in Breast Cancer.bioRxiv : the preprint server for biology · 2026Article
- FET Fusion Oncoproteins Disrupt Physiologic DNA Repair and Create a Targetable Opportunity for ATR Inhibitor Therapy.Cancer research · 2026Article
- Pan-Cancer Genomic Scars of Alternative End Joining and Single-Strand Annealing.bioRxiv : the preprint server for biology · 2026Article
- Dysfunctional DNA Mismatch Repair Drives the Evolution of Gene Amplification in MTX-Resistant Human Colorectal Cancer Cells.International journal of molecular sciences · 2026Article
- Discovery of an Endonuclease G-inhibitory Ku80-peptide protecting against leukemogenic rearrangements at the MLL breakpoint cluster.Nature communications · 2026Article
- Targeting IPNature communications · 2026Article
- Multiomic single-cell perturbation screens reveal critical lncRNA regulators of senescence.Nature aging · 2026Article
- Caffeine inhibits nonhomologous end joining by impairing ligase IV/XRCC4 function.Nucleic acids research · 2026Article
- Identification of HMCES as the Core Genetic Determinant Underlying theInternational journal of molecular sciences · 2026Article
- PARP1 and PARP2 are dispensable for DNA repair by microhomology-mediated end-joining at double-ended DSBs.Nucleic acids research · 2026Article
- Dynamic Assemblies in Genome Maintenance.Advances in experimental medicine and biology · 2026Review
535 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
Abstract
Characterizing the functional overlap and mutagenic potential of different pathways of chromosomal double-strand break (DSB) repair is important to understand how mutations arise during cancer development and treatment. To this end, we have compared the role of individual factors in three different pathways of mammalian DSB repair: alternative-nonhomologous end joining (alt-NHEJ), single-strand annealing (SSA), and homology directed repair (HDR/GC). Considering early steps of repair, we found that the DSB end-processing factors KU and CtIP affect all three pathways similarly, in that repair is suppressed by KU and promoted by CtIP. In contrast, both KU and CtIP appear dispensable for the absolute level of total-NHEJ between two tandem I-SceI-induced DSBs. During later steps of repair, we find that while the annealing and processing factors RAD52 and ERCC1 are important to promote SSA, both HDR/GC and alt-NHEJ are significantly less dependent upon these factors. As well, while disruption of RAD51 causes a decrease in HDR/GC and an increase in SSA, inhibition of this factor did not affect alt-NHEJ. These results suggest that the regulation of DSB end-processing via KU/CtIP is a common step during alt-NHEJ, SSA, and HDR/GC. However, at later steps of repair, alt-NHEJ is a mechanistically distinct pathway of DSB repair, and thus may play a unique role in mutagenesis during cancer development and therapy.
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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.