ArticleNature communications2016
Coordinated nuclease activities counteract Ku at single-ended DNA double-strand breaks.
Article in Nature communications, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 86 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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
86 citing papers in PubMed, 140 citations in OpenAlex.
- Mechanisms and disease relevance of DNA break repair pathway choice.Nature reviews. Molecular cell biology · 2026Review
- Interaction of NDRG1 and TGM2 Modulates DNA Replication and Repair.Molecular cancer research : MCR · 2026Article
- Structural basis of Ku-mediated activation of WRN exonuclease activity.Nature communications · 2026Article
- Dynamic Assemblies in Genome Maintenance.Advances in experimental medicine and biology · 2026Review
- Emerging insights into alternative end‑joining: Mechanisms, genome instability and therapeutic opportunities in cancer (Review).International journal of oncology · 2025Review
- Pathogenic variants in MAEA disrupt DNA replication fork stability and are associated with developmental abnormalities in humans.Science advances · 2025Article
- Mechanisms and regulation of DNA end resection in the maintenance of genome stability.Nature reviews. Molecular cell biology · 2025Review
- Review
- DNA nicks in both leading and lagging strand templates can trigger break-induced replication.Molecular cell · 2025Article
- Inhibition of Aberrantly Overexpressed Polo-like Kinase 4 Is a Potential Effective Treatment for DNA Damage Repair-Deficient Uterine Leiomyosarcoma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2024Article
- Endogenous base damage as a driver of genomic instability in homologous recombination-deficient cancers.DNA repair · 2024Review
- Identification of the main barriers to Ku accumulation in chromatin.Cell reports · 2024Article
- Exo1 cooperates with Tel1/ATM in promoting recombination events at DNA replication forks.iScience · 2024Article
- ATM and 53BP1 regulate alternative end joining-mediated V(D)J recombination.Science advances · 2024Article
- A novel role for the peptidyl-prolyl cis-trans isomerase Cyclophilin A in DNA-repair following replication fork stalling via the MRE11-RAD50-NBS1 complex.EMBO reports · 2024Article
- Identification of the main barriers to Ku accumulation in chromatin.bioRxiv : the preprint server for biology · 2024Article
- Short-range end resection requires ATAD5-mediated PCNA unloading for faithful homologous recombination.Nucleic acids research · 2023Article
- Multi-step processing of replication stress-derived nascent strand DNA gaps by MRE11 and EXO1 nucleases.Nature communications · 2023Article
- DNA-PK and the TRF2 iDDR inhibit MRN-initiated resection at leading-end telomeres.Nature structural & molecular biology · 2023Article
- Short Double-Stranded DNA (≤40-bp) Affects Repair Pathway Choice.International journal of molecular sciences · 2023Article
26 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issued
Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
Repair of single-ended DNA double-strand breaks (seDSBs) by homologous recombination (HR) requires the generation of a 3' single-strand DNA overhang by exonuclease activities in a process called DNA resection. However, it is anticipated that the highly abundant DNA end-binding protein Ku sequesters seDSBs and shields them from exonuclease activities. Despite pioneering works in yeast, it is unclear how mammalian cells counteract Ku at seDSBs to allow HR to proceed. Here we show that in human cells, ATM-dependent phosphorylation of CtIP and the epistatic and coordinated actions of MRE11 and CtIP nuclease activities are required to limit the stable loading of Ku on seDSBs. We also provide evidence for a hitherto unsuspected additional mechanism that contributes to prevent Ku accumulation at seDSBs, acting downstream of MRE11 endonuclease activity and in parallel with MRE11 exonuclease activity. Finally, we show that Ku persistence at seDSBs compromises Rad51 focus assembly but not DNA resection.
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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.