ArticleCell proliferation2023
DNA damage-induced cellular senescence is regulated by 53BP1 accumulation in the nuclear foci and phase separation.
Article in Cell proliferation, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 29 citations in OpenAlex.
- GW9508-Induced Activation of GPR40 in Thymic Epithelial Cells: A Therapeutic Strategy to Delay Thymic Aging.Aging cell · 2026Article
- The cGAS-STING pathway in senescence and aging-related diseases: mechanisms and therapeutic opportunities.Cell communication and signaling : CCS · 2026Review
- Therapy-induced senescent cancer cells as bidirectional regulators of antitumor immunity and resistance in the tumor microenvironment.Cell death & disease · 2026Review
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- Condensatopathies as a mechanistic framework for disease and integrated theranostic intervention.Theranostics · 2026Review
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- Article
- Oxidative Stress, Inflammation, and Cellular Senescence in Neuropathic Pain: Mechanistic Crosstalk.Antioxidants (Basel, Switzerland) · 2025Review
- ACSL5 regulated acetyl-CoA to promote bladder cancer cellular senescence via 53BP1 acetylation.Oncogene · 2025Article
- Doxorubicin Induces a Senescent Phenotype in Murine and Human Astrocytes.Journal of neurochemistry · 2025Article
- Hepatocytes as Model for Investigating Natural Senotherapeutic Compounds and Their Effects on Cell Cycle Dynamics and Genome Stability.International journal of molecular sciences · 2025Review
- Biomolecular Condensates in Telomere Maintenance of ALT Cancer Cells.Journal of molecular biology · 2025Review
- Cellular Senescence in Health, Disease, and Lens Aging.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Liquid-liquid phase separation in cell physiology and cancer biology: recent advances and therapeutic implications.Frontiers in oncology · 2025Review
- Studying Cellular Senescence Using the Model Organism Drosophila melanogaster.Methods in molecular biology (Clifton, N.J.) · 2025Article
- Phase separation in DNA repair: orchestrating the cellular response to genomic stability.PeerJ · 2025Review
- Study on the In Vitro and In Vivo Antioxidant Activity and Potential Mechanism ofAntioxidants (Basel, Switzerland) · 2025Article
- Benzyl isothiocyanate provokes senolysis by targeting AKT in senescent IPF fibroblasts and reverses persistent pulmonary fibrosis in aged mice.Frontiers in pharmacology · 2025Article
- Article
- Effects of MMP2 and its inhibitor TIMP2 on DNA damage, apoptosis and senescence of human lens epithelial cells induced by oxidative stress.Journal of bioenergetics and biomembranes · 2024Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Cellular senescence is linked to a wide range of age-related diseases and can be triggered by a variety of stresses, including DNA damage. A variety of genotoxic stressors, such as anti-cancer drugs, cause DNA double-strand breaks (DSBs), which trigger the accumulation of the tumour suppressor protein p53 in the nucleus. Cellular stresses stabilize and activate the p53 signalling pathway, which regulates various cellular processes, such as apoptosis, DNA repair, and senescence. Although p53 signalling is a well-known tumour suppressor pathway, it remains unclear how it is regulated during cellular senescence. Here, we show that p53-binding protein 1 (53BP1) accumulation in the nuclear foci is required for DNA damage-induced cellular senescence via p53 activation. In human immortalized fibroblast, shRNA-mediated 53BP1 depletion decreased not only the expression of p53-target genes but also the cellular senescence induced by adriamycin treatment. Furthermore, we confirmed that DSBs trigger the hyperaccumulation of 53BP1 in the nuclear foci, which plays a key role in the regulation of cellular senescence. To prevent the accumulation of 53BP1 in the nuclear foci, we used phase separation inhibitors, and siRNA against RNF168, which accumulates at DSB loci and forms complexes with 53BP1. This blocks the formation of 53BP1 nuclear foci and DNA damage-induced cellular senescence by activating the p53 signaling pathway. In conclusion, we demonstrated that increased accumulation of 53BP1 in the nuclear foci following DNA damage activates p53 and governs cellular senescence via a liquid-liquid phase separation mechanism.
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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.