ArticleThe Journal of clinical investigation2013
p53 isoforms regulate aging- and tumor-associated replicative senescence in T lymphocytes.
Article in The Journal of clinical investigation, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 117 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
117 citing papers in PubMed, 160 citations in OpenAlex.
- The p53 Isoforms as Potential Biomarkers in Different Cancer Entities.International journal of molecular sciences · 2026Review
- The senescence-inhibitory p53 isoform Δ133p53α: enhancing cancer immunotherapy and exploring novel therapeutic approaches for senescence-associated diseases.GeroScience · 2026Review
- Targeting immunosenescence in lung diseases: mechanistic insights and clinical interventions.BMC medicine · 2026Review
- Immunosenescence and Cancer: Cellular Aging Programs That Reshape Antitumor Immunity.Immune network · 2026Review
- Regulation of oncogenic C-terminal truncated p53β protein isoform expression by SRSF3-UPF1 splicing and surveillance axis.Cell & bioscience · 2026Article
- Senescence-inhibitory Δ133p53α counteracts accelerated ageing and mortality.bioRxiv : the preprint server for biology · 2026Article
- Biology of p53 protein isoforms and their significance in hematological malignancies.Frontiers in oncology · 2026Review
- Dual roles of immunosenescence in cancer immunotherapy.Frontiers in immunology · 2026Review
- Aging and vaccines: impact of immunosenescence and inflammaging in vaccine response.Frontiers in aging · 2026Review
- Article
- SRSF3 knockdown-induced cellular senescence as a possible therapeutic strategy for non-small cell lung cancer.Carcinogenesis · 2025Article
- Article
- Δ133p53α-mediated inhibition of astrocyte senescence and neurotoxicity as a possible therapeutic approach for neurodegenerative diseases.Neuroscience · 2025Review
- Article
- A Quantitative High-Throughput Screen Identifies Compounds that Upregulate the p53 Isoform Δ133p53α and Inhibit Cellular Senescence.ACS pharmacology & translational science · 2025Article
- Metabolic reprogramming in T cell senescence: a novel strategy for cancer immunotherapy.Cell death discovery · 2025Review
- The Emerging Role of CD8Cancers · 2025Review
- The Role of Senescence in Experimental Periodontitis at the Causal Level: An in Vivo Study.Cells · 2025Article
- Pharmacologic activation of Δ133p53α reduces cellular senescence in progeria patients-derived cells.Aging pathobiology and therapeutics · 2025Article
- Immunosenescence, Physical Exercise, and their Implications in Tumor Immunity and Immunotherapy.International journal of biological sciences · 2025Review
57 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
12 authors at 5 institutions in 3 countries.
Funding
Abstract
Cellular senescence contributes to aging and decline in tissue function. p53 isoform switching regulates replicative senescence in cultured fibroblasts and is associated with tumor progression. Here, we found that the endogenous p53 isoforms Δ133p53 and p53β are physiological regulators of proliferation and senescence in human T lymphocytes in vivo. Peripheral blood CD8+ T lymphocytes collected from healthy donors displayed an age-dependent accumulation of senescent cells (CD28-CD57+) with decreased Δ133p53 and increased p53β expression. Human lung tumor-associated CD8+ T lymphocytes also harbored senescent cells. Cultured CD8+ blood T lymphocytes underwent replicative senescence that was associated with loss of CD28 and Δ133p53 protein. In poorly proliferative, Δ133p53-low CD8+CD28- cells, reconstituted expression of either Δ133p53 or CD28 upregulated endogenous expression of each other, which restored cell proliferation, extended replicative lifespan and rescued senescence phenotypes. Conversely, Δ133p53 knockdown or p53β overexpression in CD8+CD28+ cells inhibited cell proliferation and induced senescence. This study establishes a role for Δ133p53 and p53β in regulation of cellular proliferation and senescence in vivo. Furthermore, Δ133p53-induced restoration of cellular replicative potential may lead to a new therapeutic paradigm for treating immunosenescence disorders, including those associated with aging, cancer, autoimmune diseases, and HIV infection.
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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.