ArticleGenes & development2005
p63 deficiency activates a program of cellular senescence and leads to accelerated aging.
Article in Genes & development, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 155 papers, 1 of them a synthesis that pooled it.
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
155 citing papers in PubMed, 1 synthesis or guideline pooled it, 298 citations in OpenAlex.
- A Reassessment of Genes Modulating Aging in Mice Using Demographic Measurements of the Rate of Aging.Genetics · 2018Pooled it
- Anti-skin aging effects of black ginseng extracts through regulating inflammatory factors and the CLOCK-ERK pathway in mice.Journal of ginseng research · 2026Article
- Article
- Deletion of p63 exon 13 in mice reveals C-terminal isoform-specific functions in epithelial development.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- p63 and ZNF148 cooperate to regulate head and neck squamous cell carcinoma.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- p63: A Master Regulator at the Crossroads Between Development, Senescence, Aging, and Cancer.Cells · 2025Review
- Dose-dependent effects of Nrf2 on the epidermis in chronic skin inflammation.Disease models & mechanisms · 2025Article
- p63 affects distinct metabolic pathways during keratinocyte senescence, evaluated by metabolomic profile and gene expression analysis.Cell death & disease · 2024Article
- p63 controls metabolic activation of hepatic stellate cells and fibrosis via an HER2-ACC1 pathway.Cell reports. Medicine · 2024Article
- ΔNp63 Regulates Homeostasis, Stemness, and Suppression of Inflammation in the Adult Epidermis.The Journal of investigative dermatology · 2024Article
- ΔNp63α-mediated epigenetic regulation in keratinocyte senescence.Epigenetics · 2023Article
- Review
- Obesity, Senescence, and Senolytics.Handbook of experimental pharmacology · 2022Article
- Structural and Functional Changes and Possible Molecular Mechanisms in Aged Skin.International journal of molecular sciences · 2021Review
- ΔNp63α promotes Epstein-Barr virus latency in undifferentiated epithelial cells.PLoS pathogens · 2021Article
- Age and Sex: Impact on adipose tissue metabolism and inflammation.Mechanisms of ageing and development · 2021Review
- Transcriptional and signalling regulation of skin epithelial stem cells in homeostasis, wounds and cancer.Experimental dermatology · 2021Review
- TP63 links chromatin remodeling and enhancer reprogramming to epidermal differentiation and squamous cell carcinoma development.Cellular and molecular life sciences : CMLS · 2020Review
- Adenosine/A2B Receptor Signaling Ameliorates the Effects of Aging and Counteracts Obesity.Cell metabolism · 2020Article
- TAp63γ influences mouse cartilage development.Aging · 2020Article
95 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
6 authors at 2 institutions in 1 country.
Funding
Abstract
The p53 tumor suppressor plays a key role in organismal aging. A cellular mechanism postulated to drive the aging process is cellular senescence, mediated in part by p53. Although senescent cells accumulate in elderly individuals, most studies have relied on correlating in vitro senescence assays with in vivo phenotypes of aging. Here, using two different mouse models in which the p53-related protein p63 is compromised, we demonstrate that cellular senescence and organismal aging are intimately linked and that these processes are mediated by p63 loss. We found that p63(+/-) mice have a shortened life span and display features of accelerated aging. Both germline and somatically induced p63 deficiency activates widespread cellular senescence with enhanced expression of senescent markers SA-beta-gal, PML, and p16(INK4a). Using an inducible tissue-specific p63 conditional model, we further show that p63 deficiency induces cellular senescence and causes accelerated aging phenotypes in the adult. Our results thus suggest a causative link between cellular senescence and aging in vivo, and demonstrate that p63 deficiency accelerates this process.
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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.