ArticleNature structural & molecular biology2010
Alternative end-joining is suppressed by the canonical NHEJ component Xrcc4-ligase IV during chromosomal translocation formation.
Article in Nature structural & molecular biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 180 papers.
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Who cites it
180 citing papers in PubMed.
- Emerging insights into alternative end‑joining: Mechanisms, genome instability and therapeutic opportunities in cancer (Review).International journal of oncology · 2025Review
- The zinc finger of DNA ligase 3α binds to nucleosomes via an arginine anchor.Nature communications · 2025Article
- Megabase-scale loss of heterozygosity provoked by CRISPR-Cas9 DNA double-strand breaks.Molecular cell · 2025Article
- CRISPR/Cas9 generated DSB clusters mimic complex lesions induced by high-LET radiation and shift repair from c-NHEJ to mutagenic repair pathways.Scientific reports · 2025Article
- Single-molecule techniques in studying the molecular mechanisms of DNA synapsis in non-homologous end-joining repair.Biophysics reports · 2025Article
- Engineering recombination machinery facilitates the construction of yeast cell factories.FEMS yeast research · 2025Review
- Chromosomal Instability and Chromoanagenesis as Forces for Genomic Evolution.Methods in molecular biology (Clifton, N.J.) · 2025Review
- Microhomology-mediated repair machinery and its relationship with HPV-mediated oncogenesis.Journal of medical virology · 2024Review
- Developmental progression of DNA double-strand break repair deciphered by a single-allele resolution mutation classifier.Nature communications · 2024Article
- Novel insights into the ecDNA formation mechanism involving MSH3 in methotrexate‑resistant human colorectal cancer cells.International journal of oncology · 2023Article
- Modeling sarcoma relevant translocations using CRISPR-Cas9 in human embryonic stem derived mesenchymal precursors.Genes, chromosomes & cancer · 2023Review
- Specificity of cancer-related chromosomal translocations is linked to proximity after the DNA double-strand break and subsequent selection.NAR cancer · 2023Article
- DNA damage response signaling: A common link between cancer and cardiovascular diseases.Cancer medicine · 2023Review
- Article
- Review
- Ku70 affects the frequency of chromosome translocation in human lymphocytes after radiation and T-cell acute lymphoblastic leukemia.Radiation oncology (London, England) · 2022Article
- Impact of DNA damage response defects in cancer cells on response to immunotherapy and radiotherapy.Journal of medical imaging and radiation oncology · 2022Review
- Alternative end-joining in BCR gene rearrangements and translocations.Acta biochimica et biophysica Sinica · 2022Review
- Breaking the paradigm: early insights from mammalian DNA breakomes.The FEBS journal · 2022Review
- Beta human papillomavirus 8 E6 allows colocalization of non-homologous end joining and homologous recombination repair factors.PLoS pathogens · 2022Article
120 more citing papers are in PubMed but not listed here.
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Funding
Abstract
Chromosomal translocations in hematologic and mesenchymal tumors form overwhelmingly by nonhomologous end-joining (NHEJ). Canonical NHEJ, essential for the repair of radiation-induced and some programmed double-strand breaks (DSBs), requires the Xrcc4-ligase IV complex. For other DSBs, the requirement for Xrcc4-ligase IV is less stringent, suggesting the existence of alternative end-joining (alt-NHEJ) pathways. To understand the contributions of the canonical NHEJ and alt-NHEJ pathways, we examined translocation formation in cells deficient in Xrcc4-ligase IV. We found that Xrcc4-ligase IV is not required for but rather suppresses translocations. Translocation breakpoint junctions have similar characteristics in wild-type cells and cells deficient in Xrcc4-ligase IV, including an unchanged bias toward microhomology, unlike what is observed for intrachromosomal DSB repair. Complex insertions in some junctions show that joining can be iterative, encompassing successive processing steps before joining. Our results imply that alt-NHEJ is the primary mediator of translocation formation in mammalian cells.
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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.