ArticleNucleic acids research2011
Ku counteracts mobilization of PARP1 and MRN in chromatin damaged with DNA double-strand breaks.
Article in Nucleic acids research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers, 1 of them a synthesis that pooled it.
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Who cites it
67 citing papers in PubMed, 1 synthesis or guideline pooled it, 114 citations in OpenAlex.
- Efficacy and Safety of PARP Inhibitor Therapy in Advanced Ovarian Cancer: A Systematic Review and Network Meta-analysis of Randomized Controlled Trials.Current computer-aided drug design · 2024Pooled it
- Nucleotide Metabolism in Health and Disease.MedComm · 2026Review
- Cryo-EM structures of NHEJ assemblies with nucleosomes.Nature communications · 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
- Review
- Structural and functional insights into the interaction between Ku70/80 and Pol X family polymerases in NHEJ.Nature communications · 2025Article
- SMAD4 Limits PARP1 dependent DNA Repair to Render Pancreatic Cancer Cells Sensitive to Radiotherapy.Cell death & disease · 2024Article
- Olaparib combined with CDK12-IN-3 to promote genomic instability and cell death in ovarian cancer.International journal of biological sciences · 2024Article
- Structural and functional basis of inositol hexaphosphate stimulation of NHEJ through stabilization of Ku-XLF interaction.Nucleic acids research · 2023Article
- Molecular mechanisms of tumor resistance to radiotherapy.Molecular cancer · 2023Review
- PAXX binding to the NHEJ machinery explains functional redundancy with XLF.Science advances · 2023Article
- Article
- CRISPR-based gene editing of non-homologous end joining factors biases DNA repair pathway choice toward single-strand annealing inCurrent research in biotechnology · 2023Article
- PARP-1: a critical regulator in radioprotection and radiotherapy-mechanisms, challenges, and therapeutic opportunities.Frontiers in pharmacology · 2023Review
- Poly(ADP) ribose polymerase promotes DNA polymerase theta-mediated end joining by activation of end resection.Nature communications · 2022Article
- Inhibition of DNA Repair by Inappropriate Activation of ATM, PARP, and DNA-PK with the Drug Agonist AsiDNA.Cells · 2022Article
- The Multifaceted Roles of Ku70/80.International journal of molecular sciences · 2021Review
- It Is Just a Matter of Time: Balancing Homologous Recombination and Non-homologous End Joining at the rDNA Locus During Meiosis.Frontiers in plant science · 2021Review
- The molecular basis and disease relevance of non-homologous DNA end joining.Nature reviews. Molecular cell biology · 2020Review
- ATM antagonizes NHEJ proteins assembly and DNA-ends synapsis at single-ended DNA double strand breaks.Nucleic acids research · 2020Article
7 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In mammalian cells, the main pathway for DNA double-strand breaks (DSBs) repair is classical non-homologous end joining (C-NHEJ). An alternative or back-up NHEJ (B-NHEJ) pathway has emerged which operates preferentially under C-NHEJ defective conditions. Although B-NHEJ appears particularly relevant to genomic instability associated with cancer, its components and regulation are still largely unknown. To get insights into this pathway, we have knocked-down Ku, the main contributor to C-NHEJ. Thus, models of human cell lines have been engineered in which the expression of Ku70/80 heterodimer can be significantly lowered by the conditional induction of a shRNA against Ku70. On Ku reduction in cells, resulting NHEJ competent protein extracts showed a shift from C- to B-NHEJ that could be reversed by addition of purified Ku protein. Using a cellular fractionation protocol after treatment with a strong DSBs inducer followed by western blotting or immunostaining, we established that, among C-NHEJ factors, Ku is the main counteracting factor against mobilization of PARP1 and the MRN complex to damaged chromatin. In addition, Ku limits PAR synthesis and single-stranded DNA production in response to DSBs. These data support the involvement of PARP1 and the MRN proteins in the B-NHEJ route for the repair of DNA DSBs.
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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.