ArticleNucleic acids research2013
Human LIGIV is synthetically lethal with the loss of Rad54B-dependent recombination and is required for certain chromosome fusion events induced by telomere dysfunction.
Article in Nucleic acids research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 47 citations in OpenAlex.
- Nonhomologous end-joining uses distinct mechanisms to repair each strand of a double strand break.Nature communications · 2025Article
- Lig3-dependent rescue of mouse viability and DNA double-strand break repair by catalytically inactive Lig4.Nucleic acids research · 2025Article
- Polλ promotes microhomology-mediated end-joining.Nature structural & molecular biology · 2023Article
- Review
- Suppression of non-homologous end joining does not rescue DNA repair defects in Fanconi anemia patient cells.Cell cycle (Georgetown, Tex.) · 2020Article
- Strong suppression of gene conversion with increasing DNA double-strand break load delimited by 53BP1 and RAD52.Nucleic acids research · 2020Article
- Absence of XRCC4 and its paralogs in human cells reveal differences in outcomes for DNA repair and V(D)J recombination.DNA repair · 2020Article
- DNA-PKcs promotes chromatin decondensation to facilitate initiation of the DNA damage response.Nucleic acids research · 2019Article
- Chromothripsis during telomere crisis is independent of NHEJ, and consistent with a replicative origin.Genome research · 2019Article
- Both the classical and alternative non-homologous end joining pathways contribute to the fusion of drastically shortened telomeres induced by TRF2 overexpression.Cell cycle (Georgetown, Tex.) · 2019Article
- PARP1 is required for preserving telomeric integrity but is dispensable for A-NHEJ.Oncotarget · 2018Article
- FANCI and FANCD2 have common as well as independent functions during the cellular replication stress response.Nucleic acids research · 2017Article
- DNA Ligase IV Guides End-Processing Choice during Nonhomologous End Joining.Cell reports · 2017Article
- Human somatic cells deficient for RAD52 are impaired for viral integration and compromised for most aspects of homology-directed repair.DNA repair · 2017Article
- The synthetic lethal killing of RAD54B-deficient colorectal cancer cells by PARP1 inhibition is enhanced with SOD1 inhibition.Oncotarget · 2016Article
- Sister chromatid telomere fusions, but not NHEJ-mediated inter-chromosomal telomere fusions, occur independently of DNA ligases 3 and 4.Genome research · 2016Article
- LIG4 mediates Wnt signalling-induced radioresistance.Nature communications · 2016Article
- Radiosensitization by PARP Inhibition in DNA Repair Proficient and Deficient Tumor Cells: Proliferative Recovery in Senescent Cells.Radiation research · 2016Article
- Complex interactions between the DNA-damage response and mammalian telomeres.Nature structural & molecular biology · 2015Review
- Cockayne syndrome group B protein regulates DNA double-strand break repair and checkpoint activation.The EMBO journal · 2015Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Classic non-homologous end joining (C-NHEJ) is the predominant DNA double-strand break repair pathway in humans. Although seven genes Ku70, Ku86, DNA-PK(cs), Artemis, DNA Ligase IV (LIGIV), X-ray cross-complementing group 4 and XRCC4-like factor are required for C-NHEJ, several of them also have ancillary functions. For example, Ku70:Ku86 possesses an essential telomere maintenance activity. In contrast, LIGIV is believed to function exclusively in C-NHEJ. Moreover, a viable LIGIV-null human B-cell line and LIGIV-reduced patient cell lines have been described. Together, these observations suggest that LIGIV (and hence C-NHEJ), albeit important, is nonetheless dispensable, whereas Ku70:Ku86 and telomere maintenance are essential. To confirm this hypothesis, we inactivated LIGIV in the epithelial human cell line, HCT116. The resulting LIGIV-null cell line was viable, verifying that the gene and C-NHEJ are not essential. However, functional inactivation of RAD54B, a key homologous recombination factor, in the LIGIV-null background yielded no viable clones, suggesting that the combined absence of RAD54B/homologous recombination and C-NHEJ is synthetically lethal. Finally, we demonstrate that LIGIV is differentially required for certain chromosome fusion events induced by telomere dysfunction-used for those owing to the overexpression of a dominant negative version of telomere recognition factor 2, but not used for those owing to absence of Ku70:Ku86.
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