ArticleCell death and differentiation2012
Diverse p63 and p73 isoforms regulate Δ133p53 expression through modulation of the internal TP53 promoter activity.
Article in Cell death and differentiation, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 54 citations in OpenAlex.
- The TP53 gene contains a diversity box that makes it more than a tumor suppressor.Cell death and differentiation · 2026Review
- Associative memory plays a role in ER-1α positive breast cancers.Cell death and differentiation · 2026Review
- Review
- Exploring p53 isoforms: unraveling heterogeneous p53 tumor suppressor functionality in uveal melanoma.Cell death discovery · 2025Article
- Re-appraising the evidence for the source, regulation and function of p53-family isoforms.Nucleic acids research · 2024Review
- p53 Dysregulation in Breast Cancer: Insights on Mutations in theInternational journal of molecular sciences · 2023Article
- Review
- P63 and P73 Activation in Cancers with p53 Mutation.Biomedicines · 2022Review
- Adaptive homeostasis and the p53 isoform network.EMBO reports · 2021Review
- Δ133p53β isoform pro-invasive activity is regulated through an aggregation-dependent mechanism in cancer cells.Nature communications · 2021Article
- Review
- Δ133p53α enhances metabolic and cellular fitness of TCR-engineered T cells and promotes superior antitumor immunity.Journal for immunotherapy of cancer · 2021Article
- The Δ133p53 Isoforms, Tuners of the p53 Pathway.Cancers · 2020Review
- p53-Related Transcription Targets of TAp73 in Cancer Cells-Bona Fide or Distorted Reality?International journal of molecular sciences · 2020Review
- Discovery and characterization of a novel splice variant of the p53 tumor suppressor gene in a human T cell leukemia cellline.International journal of clinical and experimental pathology · 2020Article
- The Diverse Functions of Mutant 53, Its Family Members and Isoforms in Cancer.International journal of molecular sciences · 2019Review
- p53 Isoforms in Cellular Senescence- and Ageing-Associated Biological and Physiological Functions.International journal of molecular sciences · 2019Review
- Somatic and GermlineClinical cancer research : an official journal of the American Association for Cancer Research · 2017Article
- Damage-inducible intragenic demethylation of the human TP53 tumor suppressor gene is associated with transcription from an alternative intronic promoter.Molecular carcinogenesis · 2016Article
- Emerging Non-Canonical Functions and Regulation by p53: p53 and Stemness.International journal of molecular sciences · 2016Review
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
Abstract
In response to stress, p53 binds and transactivates the internal TP53 promoter, thus regulating the expression of its own isoform, Δ133p53α. Here, we report that, in addition to p53, at least four p63/p73 isoforms regulate Δ133p53 expression at transcriptional level: p63β, ΔNp63α, ΔNp63β and ΔNp73γ. This regulation occurs through direct DNA-binding to the internal TP53 promoter as demonstrated by chromatin immunoprecipitation and the use of DNA-binding mutant p63. The promoter regions involved in the p63/p73-mediated transactivation were identified using deleted, mutant and polymorphic luciferase reporter constructs. In addition, we observed that transient expression of p53 family members modulates endogenous Δ133p53α expression at both mRNA and protein levels. We also report concomitant variation of p63 and Δ133p53 expression during keratinocyte differentiation of HaCat cells and induced pluripotent stem cells derived from mutated p63 ectodermal dysplasia patients. Finally, proliferation assays indicated that Δ133p53α isoform regulates the anti-proliferative activities of p63β, ΔNp63α, ΔNp63β and ΔNp73γ. Overall, this study shows a strong interplay between p53, p63 and p73 isoforms to orchestrate cell fate outcome.
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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.