ArticleThe Journal of cell biology2000
p53 binding protein 1 (53BP1) is an early participant in the cellular response to DNA double-strand breaks.
Article in The Journal of cell biology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 465 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.
The trial behind it
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
465 citing papers in PubMed, 904 citations in OpenAlex.
- 53BP1 as a potential predictor of response in PARP inhibitor-treated homologous recombination-deficient ovarian cancer.Gynecologic oncology · 2019Trial
- STAT5A-RNF8 signaling regulates homologous recombination repair and cisplatin responsiveness in cervical cancer.Neoplasia (New York, N.Y.) · 2026Article
- Significance of p53-binding protein 1 as an in situ DNA damage marker for ulcerative colitis.Medical molecular morphology · 2026Article
- Quantifying Radiation Effects of Iodinated Contrast Media in Pediatric CT Using DNA Damage Biomarkers.International journal of molecular sciences · 2026Article
- Probiotic intervention mitigates radiation-induced intestinal injury by alleviating oxidative stress in a human gut-on-a-chip.Scientific reports · 2026Article
- Canonical autophagy remains inactive in induced pluripotent stem cells and neuronal progenitor cells following DNA damage induced by BPDE or etoposide.Scientific reports · 2026Article
- Not just splitting hairs-monitoring environmental chemical exposures, their biological effects and their social determinants with hair shafts and follicles: a narrative review.Environmental health : a global access science source · 2026Review
- A ZNF-nanobody fusion reveals SUMOylation-dependent changes in p53 protein localization.iScience · 2026Article
- Retarded DNA DSB repair kinetics and augmented radiation sensitivity in Wiskott Aldrich syndrome patients.Scientific reports · 2026Article
- Chromatin Nano-Organization in Peripheral Blood Mononuclear Cells After In-Solution Irradiation with the Beta-Emitter Lu-177.Biomolecules · 2026Article
- A busy BOD1-y: the diverse functions of an intracellular signaling regulatory protein family.Biochemical Society transactions · 2025Review
- 53BP1-RIF1 and DNA-PKcs show distinct genetic interactions with diverse chromosomal break repair outcomes.Nature communications · 2025Article
- Small Extracellular Vesicles From Radioresistant H3K27M-Pediatric Diffuse Midline Glioma Cells Modulate Tumor Phenotypes and Radiation Response.Journal of extracellular vesicles · 2025Article
- Genetically Encoded Cell Fate Reporter System for Multiplex Single-Cell Detection of DNA and Mitochondrial Damage.ACS omega · 2025Article
- Induced somatic mutation accumulation during skeletal muscle regeneration reduces muscle strength.Nature aging · 2025Article
- Fluorescence recovery in the super-resolution regime reveals subcompartments of 53BP1 foci.Cell reports methods · 2025Article
- Targeting CyclinD1-CDK6 to Mitigate Senescence-Driven Inflammation and Age-Associated Functional Decline.bioRxiv : the preprint server for biology · 2025Article
- WIP1 mutations suppress DNA damage triggered bypass of the mitotic timer.The EMBO journal · 2025Article
- Mitochondria-derived nuclear ATP surge protects against confinement-induced proliferation defects.Nature communications · 2025Article
- A cancer persistent DNA repair circuit driven by MDM2, MDM4 (MDMX), and mutant p53 for recruitment of MDC1 and 53BP1 on chromatin.Nucleic acids research · 2025Article
405 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
4 authors at 2 institutions in 2 countries.
Funding
Abstract
p53 binding protein 1 (53BP1), a protein proposed to function as a transcriptional coactivator of the p53 tumor suppressor, has BRCT domains with high homology to the Saccharomyces cerevisiae Rad9p DNA damage checkpoint protein. To examine whether 53BP1 has a role in the cellular response to DNA damage, we probed its intracellular localization by immunofluorescence. In untreated primary cells and U2OS osteosarcoma cells, 53BP1 exhibited diffuse nuclear staining; whereas, within 5-15 min after exposure to ionizing radiation (IR), 53BP1 localized at discreet nuclear foci. We propose that these foci represent sites of processing of DNA double-strand breaks (DSBs), because they were induced by IR and chemicals that cause DSBs, but not by ultraviolet light; their peak number approximated the number of DSBs induced by IR and decreased over time with kinetics that parallel the rate of DNA repair; and they colocalized with IR-induced Mre11/NBS and gamma-H2AX foci, which have been previously shown to localize at sites of DSBs. Formation of 53BP1 foci after irradiation was not dependent on ataxia-telangiectasia mutated (ATM), Nijmegen breakage syndrome (NBS1), or wild-type p53. Thus, the fast kinetics of 53BP1 focus formation after irradiation and the lack of dependency on ATM and NBS1 suggest that 53BP1 functions early in the cellular response to DNA DSBs.
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What OpenQuestion holds
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.