ReviewMethods in molecular biology (Clifton, N.J.)2013
Senescence regulation by the p53 protein family.
Review in Methods in molecular biology (Clifton, N.J.), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 90 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
90 citing papers in PubMed, 161 citations in OpenAlex.
- Unveiling Selenoprotein T as a novel regulator of cardiomyocyte senescence: pivotal role of the CD36 receptor in AC16 human cardiomyocytes.GeroScience · 2026Article
- Transcription-dependent and -independent functions of Drosophila p53 isoforms in the induction of apoptosis and senescence-associated tumorigenesis.Cell death & disease · 2026Article
- Colonic inflammatory response in a D-galactose-induced aging model: elevated IL-1β expression.Journal of molecular histology · 2026Article
- Biomarkers for Chronic Kidney Disease: An Updated Review of Innovative Detection Approaches.Current aging science · 2026Review
- SLy1-deficiency results in functional impaired, exhausted and senescent NK cells.Frontiers in immunology · 2026Article
- The Impact of Senescence-Associated Secretory Phenotype (SASP) on Head and Neck Cancers: From Biology to Therapy.Cancers · 2025Review
- Redox-Immune Axis and Ozone Pollution: From Oxidative Stress to Thymic Involution and Neurodegeneration.Medical sciences (Basel, Switzerland) · 2025Review
- Nanotoxicity of Porous Silica Nanoparticles: Physicochemical Properties and Mechanistic Cellular Endpoints.Nanomaterials (Basel, Switzerland) · 2025Review
- Reprogramming cellular senescence and aging clocks for advanced cancer immunotherapy.Molecular cancer · 2025Review
- Article
- A base editing platform for the correction of cancer driver mutations unmasks conserved p53 transcription programs.Genome biology · 2025Article
- Review
- Structural and mechanistic diversity in p53-mediated regulation of organismal longevity across taxonomical orders.PLoS computational biology · 2025Article
- Review
- Expression pattern of cancer-associated cellular senescence genes in clear cell renal cell carcinoma distinguishes tumor subclasses with clinical implications.Scientific reports · 2025Article
- Automated and Enclosed Three-Dimensional Biofabrication System for Mesenchymal Stem Cell Culture to Enhance Diabetic Wound Healing.Biomaterials research · 2025Article
- Probiotics and muscle health: the impact ofFrontiers in microbiology · 2025Review
- Decoding senescence of aging single cells at the nexus of biomaterials, microfluidics, and spatial omics.npj aging · 2024Review
- Filbertone Reduces Senescence in CNutrients · 2024Article
- Increased PTCHD4 expression via m6A modification of PTCHD4 mRNA promotes senescent cell survival.Nucleic acids research · 2024Article
30 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
2 authors at 1 institution in 1 country.
Funding
Abstract
p53, a guardian of the genome, exerts its tumor suppression activity by regulating a large number of downstream targets involved in cell cycle arrest, DNA repair, apoptosis, and cellular senescence. Although p53-mediated apoptosis is able to kill cancer cells, a role for cellular senescence in p53-dependent tumor suppression is becoming clear. Mouse studies showed that activation of p53-induced premature senescence promotes tumor regression in vivo. However, p53-mediated cellular senescence also leads to aging-related phenotypes, such as tissue atrophy, stem cell depletion, and impaired wound healing. In addition, several p53 isoforms and two p53 homologs, p63 and p73, have been shown to play a role in cellular senescence and/or aging. Importantly, p53, p63, and p73 are necessary for the maintenance of adult stem cells. Therefore, understanding the dual role the p53 protein family in cancer and aging is critical to solve cancer and longevity in the future. In this chapter, we provide an overview on how p53, p63, p73, and their isoforms regulate cellular senescence and aging.
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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.