ArticleDNA repair2014
DNA ligase III and DNA ligase IV carry out genetically distinct forms of end joining in human somatic cells.
Article in DNA repair, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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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.
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Who cites it
36 citing papers in PubMed, 55 citations in OpenAlex.
- Cell Type Specific Suppression of Hyper-Recombination by Human RAD18 Is Linked to Proliferating Cell Nuclear Antigen K164 Ubiquitination.Biomolecules · 2025Article
- Lig3-dependent rescue of mouse viability and DNA double-strand break repair by catalytically inactive Lig4.Nucleic acids research · 2025Article
- Fanconi anemia-associated chromosomal radial formation is dependent on POLθ-mediated alternative end joining.Cell reports · 2023Article
- BMN673 Is a PARP Inhibitor with Unique Radiosensitizing Properties: Mechanisms and Potential in Radiation Therapy.Cancers · 2022Review
- Catalytically inactive DNA ligase IV promotes DNA repair in living cells.Nucleic acids research · 2022Article
- Article
- Mismatch discrimination and sequence bias during end-joining by DNA ligases.Nucleic acids research · 2022Article
- UPF1 promotes the formation of R loops to stimulate DNA double-strand break repair.Nature communications · 2021Article
- Genome-wide Nucleotide-Resolution Mapping of DNA Replication Patterns, Single-Strand Breaks, and Lesions by GLOE-Seq.Molecular cell · 2020Article
- Article
- Absence of XRCC4 and its paralogs in human cells reveal differences in outcomes for DNA repair and V(D)J recombination.DNA repair · 2020Article
- Can Designer Indels Be Tailored by Gene Editing?: Can Indels Be Customized?BioEssays : news and reviews in molecular, cellular and developmental biology · 2019Article
- 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
- DNA Ligase 1 is an essential mediator of sister chromatid telomere fusions in G2 cell cycle phase.Nucleic acids research · 2019Article
- PARP1 is required for preserving telomeric integrity but is dispensable for A-NHEJ.Oncotarget · 2018Article
- Structure-activity relationships among DNA ligase inhibitors: Characterization of a selective uncompetitive DNA ligase I inhibitor.DNA repair · 2017Article
- FANCI and FANCD2 have common as well as independent functions during the cellular replication stress response.Nucleic acids research · 2017Article
- Telomeres in cancer: tumour suppression and genome instability.Nature reviews. Molecular cell biology · 2017Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Ku-dependent C-NHEJ (classic non-homologous end joining) is the primary DNA EJing (end joining) repair pathway in mammals. Recently, an additional EJing repair pathway (A-NHEJ; alternative-NHEJ) has been described. Currently, the mechanism of A-NHEJ is obscure although a dependency on LIGIII (DNA ligase III) is often implicated. To test the requirement for LIGIII in A-NHEJ we constructed a LIGIII conditionally-null human cell line using gene targeting. Nuclear EJing activity appeared unaffected by a deficiency in LIGIII as, surprisingly, so were random gene targeting integration events. In contrast, LIGIII was required for mitochondrial function and this defined the gene's essential activity. Human Ku:LIGIII and Ku:LIGIV (DNA ligase IV) double knockout cell lines, however, demonstrated that LIGIII is required for the enhanced A-NHEJ activity that is observed in Ku-deficient cells. Most unexpectedly, however, the majority of EJing events remained LIGIV-dependent. In conclusion, although human LIGIII has an essential function in mitochondrial maintenance, it is dispensable for most types of nuclear DSB repair, except for the A-NHEJ events that are normally suppressed by Ku. Moreover, we describe that a robust Ku-independent, LIGIV-dependent repair pathway exists in human somatic cells.
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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.