ArticleDNA repair2017
Synthetic lethality between murine DNA repair factors XLF and DNA-PKcs is rescued by inactivation of Ku70.
Article in DNA repair, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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.
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Who cites it
16 citing papers in PubMed, 29 citations in OpenAlex.
- Core NHEJ Factors Maintain Synapsis Across Diverse DNA End Structures.bioRxiv : the preprint server for biology · 2026Article
- DNA Repair and Immune Response: Editorial.Biomolecules · 2022Article
- Role of Paralogue of XRCC4 and XLF in DNA Damage Repair and Cancer Development.Frontiers in immunology · 2022Review
- Acetyltransferases GCN5 and PCAF Are Required for B Lymphocyte Maturation in Mice.Biomolecules · 2021Article
- DNA End Joining: G0-ing to the Core.Biomolecules · 2021Review
- Article
- Repair of DNA Double-Strand Breaks by the Nonhomologous End Joining Pathway.Annual review of biochemistry · 2021Review
- DNA Damage Response.Biomolecules · 2021Article
- Non-Homologous End Joining Factors XLF, PAXX and DNA-PKcs Maintain the Neural Stem and Progenitor Cell Population.Biomolecules · 2020Article
- Leaky severe combined immunodeficiency in mice lacking non-homologous end joining factors XLF and MRI.Aging · 2020Article
- Mediator of DNA Damage Checkpoint Protein 1 Facilitates V(D)J Recombination in Cells Lacking DNA Repair Factor XLF.Biomolecules · 2019Article
- Generation of a Mouse Model Lacking the Non-Homologous End-Joining Factor Mri/Cyren.Biomolecules · 2019Article
- Genetic interaction between DNA repair factors PAXX, XLF, XRCC4 and DNA-PKcs in human cells.FEBS open bio · 2019Article
- Nonhomologous DNA end-joining for repair of DNA double-strand breaks.The Journal of biological chemistry · 2018Review
- Robust DNA repair in PAXX-deficient mammalian cells.FEBS open bio · 2018Article
- Normal development of mice lacking PAXX, the paralogue of XRCC4 and XLF.FEBS open bio · 2018Article
Corrections and comments
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Authors and funding
5 authors at 4 institutions in 3 countries.
Funding
Abstract
DNA double-strand breaks (DSBs) are recognized and repaired by the Classical Non-Homologous End-Joining (C-NHEJ) and Homologous Recombination pathways. C-NHEJ includes the core Ku70 and Ku80 (or Ku86) heterodimer that binds DSBs and thus promotes recruitment of accessory downstream NHEJ factors XLF, PAXX, DNA-PKcs, Artemis and other core subunits, XRCC4 and DNA Ligase 4 (Lig4). In the absence of core C-NHEJ factors, DNA repair can be performed by Alternative End-Joining, which likely depends on DNA Ligase 1 and DNA Ligase 3. Genetic inactivation of C-NHEJ factors, such as Ku70, Ku80, XLF, PAXX and DNA-PKcs results in viable mice showing increased levels of genomic instability and sensitivity to DSBs. Knockouts of XRCC4 or Lig4, on the other hand, as well as combined inactivation of XLF and DNA-PKcs, or XLF and PAXX, result in late embryonic lethality in mice, which in most cases correlate with severe apoptosis in the central nervous system. Here, we demonstrate that inactivation of the Ku70 gene rescues the synthetic lethality between XLF and DNA-PKcs, resulting in triple knockout mice that are indistinguishable from Ku70-deficient littermates by size or levels of genomic instability. Moreover, we find that combined inactivation of Ku70 and XLF results in viable mice. Together, these findings suggest that Ku70 is epistatic with XLF and DNA-PKcs and support a model in which inactivation of Ku70 allows DNA lesions to become accessible to alternative DNA repair pathways.
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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.