ArticleNature cell biology2010
53BP1-dependent robust localized KAP-1 phosphorylation is essential for heterochromatic DNA double-strand break repair.
Article in Nature cell biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 203 papers.
What it found
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Who cites it
203 citing papers in PubMed, 331 citations in OpenAlex.
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- Chromatin Remodeling, DNA Double-Strand Break Repair, and Human Disease: How a Breakup Changes You.Biomolecules · 2026Review
- Chromatin Nano-Organization in Peripheral Blood Mononuclear Cells After In-Solution Irradiation with the Beta-Emitter Lu-177.Biomolecules · 2026Article
- Article
- From survival of irradiated mice to modern molecular insights: a seventy-year journey in radiobiology at the institute of biophysics, Czech academy of sciences.European biophysics journal : EBJ · 2025Review
- Structural insights into γH2Ax containing nucleosomes.Nucleic acids research · 2025Article
- Reclassification of ATM Missense Variants of Uncertain Significance by Integrating Results from Systematic Functional Assays into an ACMG Points-Based Framework.Clinical cancer research : an official journal of the American Association for Cancer Research · 2025Article
- EGFR-induced lncRNAProceedings of the National Academy of Sciences of the United States of America · 2025Article
- CHAMP1 complex directs heterochromatin assembly and promotes homology-directed DNA repair.Nature communications · 2025Article
- 53BP1-the 'Pandora's box' of genome integrity.DNA repair · 2024Review
- DNA double-strand break movement in heterochromatin depends on the histone acetyltransferase dGcn5.Nucleic acids research · 2024Article
- OTUD5 promotes end-joining of deprotected telomeres by promoting ATM-dependent phosphorylation of KAP1Nature communications · 2024Article
- The tripartite motif-containing 24 is a multifunctional player in human cancer.Cell & bioscience · 2024Review
- UBE2D3 facilitates NHEJ by orchestrating ATM signalling through multi-level control of RNF168.Nature communications · 2024Article
- Valosin-Containing Protein (VCP): A Review of Its Diverse Molecular Functions and Clinical Phenotypes.International journal of molecular sciences · 2024Review
- KAP1 stabilizes MYCN mRNA and promotes neuroblastoma tumorigenicity by protecting the RNA mJournal of experimental & clinical cancer research : CR · 2024Article
- HJURP is recruited to double-strand break sites and facilitates DNA repair by promoting chromatin reorganization.Oncogene · 2024Article
- Decline of DNA damage response along with myogenic differentiation.Life science alliance · 2024Article
- The Chromosome Passenger Complex (CPC) Components and Its Associated Pathways Are Promising Candidates to Differentiate Between Normosensitive and Radiosensitive ATM-Mutated Cells.Biomarker insights · 2024Article
- The impact of chromatin on double-strand break repair: Imaging tools and discoveries.DNA repair · 2024Article
143 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
7 authors at 3 institutions in 2 countries.
Funding
Abstract
DNA double-strand breaks (DSBs) trigger ATM (ataxia telangiectasia mutated) signalling and elicit genomic rearrangements and chromosomal fragmentation if misrepaired or unrepaired. Although most DSB repair is ATM-independent, approximately 15% of ionizing radiation (IR)-induced breaks persist in the absence of ATM-signalling. 53BP1 (p53-binding protein 1) facilitates ATM-dependent DSB repair but is largely dispensable for ATM activation or checkpoint arrest. ATM promotes DSB repair within heterochromatin by phosphorylating KAP-1 (KRAB-associated protein 1, also known as TIF1beta, TRIM28 or KRIP-1; ref. 2). Here, we show that the ATM signalling mediator proteins MDC1, RNF8, RNF168 and 53BP1 are also required for heterochromatic DSB repair. Although KAP-1 phosphorylation is critical for 53BP1-mediated repair, overall phosphorylated KAP-1 (pKAP-1) levels are only modestly affected by 53BP1 loss. pKAP-1 is transiently pan-nuclear but also forms foci overlapping with gammaH2AX in heterochromatin. Cells that do not form 53BP1 foci, including human RIDDLE (radiosensitivity, immunodeficiency, dysmorphic features and learning difficulties) syndrome cells, fail to form pKAP-1 foci. 53BP1 amplifies Mre11-NBS1 accumulation at late-repairing DSBs, concentrating active ATM and leading to robust, localized pKAP-1. We propose that ionizing-radiation induced foci (IRIF) spatially concentrate ATM activity to promote localized alterations in regions of chromatin otherwise inhibitory to repair.
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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.