ArticleNucleic acids research2016
Control of alternative end joining by the chromatin remodeler p400 ATPase.
Article in Nucleic acids research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 20 citations in OpenAlex.
- Genome rearrangements induced by the stimulation of end-joining of DNA double strand breaks through multiple phosphorylation of MRE11 by the kinase PKB/AKT1.Nucleic acids research · 2025Article
- Chromatin Modifier EP400 Regulates Oocyte Quality and Zygotic Genome Activation in Mice.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- DNA Double-Strand Breaks as Pathogenic Lesions in Neurological Disorders.International journal of molecular sciences · 2022Review
- Zinc finger protein ZNF384 is an adaptor of Ku to DNA during classical non-homologous end-joining.Nature communications · 2021Article
- NuA4 and SAGA acetyltransferase complexes cooperate for repair of DNA breaks by homologous recombination.PLoS genetics · 2021Article
- MRGBP, a member of the NuA4 complex, inhibits DNA double-strand break repair.FEBS open bio · 2021Article
- CHD7 and 53BP1 regulate distinct pathways for the re-ligation of DNA double-strand breaks.Nature communications · 2020Article
- Loss of ZBTB24 impairs nonhomologous end-joining and class-switch recombination in patients with ICF syndrome.The Journal of experimental medicine · 2020Article
- Review
- JMJD6 participates in the maintenance of ribosomal DNA integrity in response to DNA damage.PLoS genetics · 2020Article
- PHF6 promotes non-homologous end joining and G2 checkpoint recovery.EMBO reports · 2020Article
- H2AX facilitates classical non-homologous end joining at the expense of limited nucleotide loss at repair junctions.Nucleic acids research · 2017Article
- Bromodomain proteins: repairing DNA damage within chromatin.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2017Review
- Inactivation of Pol θ and C-NHEJ eliminates off-target integration of exogenous DNA.Nature communications · 2017Article
- Acetylation Reader Proteins: Linking Acetylation Signaling to Genome Maintenance and Cancer.PLoS genetics · 2016Review
Corrections and comments
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Authors and funding
9 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Repair of DNA double-strand breaks occurs in a chromatin context that needs to be modified and remodeled to allow suitable access to the different DNA repair machineries. Of particular importance for the maintenance of genetic stability is the tight control of error-prone pathways, such as the alternative End Joining pathway. Here, we show that the chromatin remodeler p400 ATPase is a brake to the use of alternative End Joining. Using specific intracellular reporter susbstrates we observed that p400 depletion increases the frequency of alternative End Joining events, and generates large deletions following repair of double-strand breaks. This increase of alternative End Joining events is largely dependent on CtIP-mediated resection, indicating that it is probably related to the role of p400 in late steps of homologous recombination. Moreover, p400 depletion leads to the recruitment of poly(ADP) ribose polymerase (PARP) and DNA ligase 3 at DNA double-strand breaks, driving to selective killing by PARP inhibitors. All together these results show that p400 acts as a brake to prevent alternative End Joining-dependent genetic instability and underline its potential value as a clinical marker.
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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.