ReviewGenes2022
53BP1: Keeping It under Control, Even at a Distance from DNA Damage.
Review in Genes, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
24 citing papers in PubMed, 38 citations in OpenAlex.
- Mechanisms and disease relevance of DNA break repair pathway choice.Nature reviews. Molecular cell biology · 2026Review
- Significance of p53-binding protein 1 as an in situ DNA damage marker for ulcerative colitis.Medical molecular morphology · 2026Article
- Pulsed Low-Dose-Rate Chemoradiation Induces Stromal Reprogramming in Pancreatic CAF-Generated ECM: Quantification by the HOST-Factor.Gastro hep advances · 2026Article
- Article
- GSK3B directs DNA repair choice and determines tumor response to PARP1 inhibition independent of BRCA1.The Journal of clinical investigation · 2025Article
- Molecular and Cellular Effects of CT Scans in Human Adipose Mesenchymal Stem Cells.International journal of molecular sciences · 2025Article
- Histone Phosphorylation in DNA Damage Response.International journal of molecular sciences · 2025Review
- CRISPR-Cas9-mediated homology-directed repair for precise gene editing.Molecular therapy. Nucleic acids · 2024Review
- 53BP1-the 'Pandora's box' of genome integrity.DNA repair · 2024Review
- Elucidation of the molecular mechanism of the breakage-fusion-bridge (BFB) cycle using a CRISPR-dCas9 cellular model.Nucleic acids research · 2024Article
- YIPF2 regulates genome integrity.Cell & bioscience · 2024Article
- Application of PARP inhibitors combined with immune checkpoint inhibitors in ovarian cancer.Journal of translational medicine · 2024Review
- Promising Effects of Novel Supplement Formulas in Preventing Skin Aging in 3D Human Keratinocytes.Nutrients · 2024Article
- CSB and SMARCAL1 compete for RPA32 at stalled forks and differentially control the fate of stalled forks in BRCA2-deficient cells.Nucleic acids research · 2024Article
- SUMO and the DNA damage response.Biochemical Society transactions · 2024Review
- NUDT16 regulates CtIP PARylation to dictate homologous recombination repair.Nucleic acids research · 2024Article
- Phase separation-mediated biomolecular condensates and their relationship to tumor.Cell communication and signaling : CCS · 2024Review
- Decline of DNA damage response along with myogenic differentiation.Life science alliance · 2024Article
- Engineered FHA domains can bind to a variety of Phosphothreonine-containing peptides.Protein engineering, design & selection : PEDS · 2024Article
- IDR-targeting compounds suppress HPV genome replication via disruption of phospho-BRD4 association with DNA damage response factors.Molecular cell · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Double-strand breaks (DSBs) are toxic lesions that can be generated by exposure to genotoxic agents or during physiological processes, such as during V(D)J recombination. The repair of these DSBs is crucial to prevent genomic instability and to maintain cellular homeostasis. Two main pathways participate in repairing DSBs, namely, non-homologous end joining (NHEJ) and homologous recombination (HR). The P53-binding protein 1 (53BP1) plays a pivotal role in the choice of DSB repair mechanism, promotes checkpoint activation and preserves genome stability upon DSBs. By preventing DSB end resection, 53BP1 promotes NHEJ over HR. Nonetheless, the balance between DSB repair pathways remains crucial, as unscheduled NHEJ or HR events at different phases of the cell cycle may lead to genomic instability. Therefore, the recruitment of 53BP1 to chromatin is tightly regulated and has been widely studied. However, less is known about the mechanism regulating 53BP1 recruitment at a distance from the DNA damage. The present review focuses on the mechanism of 53BP1 recruitment to damage and on recent studies describing novel mechanisms keeping 53BP1 at a distance from 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.