ArticleOncogene2008
The proline-rich domain in p63 is necessary for the transcriptional and apoptosis-inducing activities of TAp63.
Article in Oncogene, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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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
18 citing papers in PubMed, 31 citations in OpenAlex.
- Article
- TAp63γ is the primary isoform of TP63 for tumor suppression but not development.Cell death discovery · 2025Article
- Differential Transcriptional Activity of ΔNp63β Is Encoded by an Isoform-Specific C-Terminus.Molecular and cellular biology · 2025Article
- Review
- ΔN63 suppresses the ability of pregnancy-identified mammary epithelial cells (PIMECs) to drive HER2-positive breast cancer.Cell death & disease · 2021Article
- A Novel Ferroptosis-Related Gene Model for Overall Survival Predictions of Bladder Urothelial Carcinoma Patients.Frontiers in oncology · 2021Article
- p63-related signaling at a glance.Journal of cell science · 2020Review
- FIH-1 engages novel binding partners to positively influence epithelial proliferation via p63.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
- The Roles of P53 and Its Family Proteins, P63 and P73, in the DNA Damage Stress Response in Organogenesis-Stage Mouse Embryos.Toxicological sciences : an official journal of the Society of Toxicology · 2018Article
- The Regulation of Tumor Suppressor p63 by the Ubiquitin-Proteasome System.International journal of molecular sciences · 2016Review
- Isolation and expression analysis of a LEAFY/FLORICAULA homolog and its promoter from London plane (Platanus acerifolia Willd.).Plant cell reports · 2012Article
- Tumor protein p63/nuclear factor κB feedback loop in regulation of cell death.The Journal of biological chemistry · 2011Article
- Manganese superoxide dismutase is a p53-regulated gene that switches cancers between early and advanced stages.Cancer research · 2011Article
- Abnormal hair follicle development and altered cell fate of follicular keratinocytes in transgenic mice expressing DeltaNp63alpha.Development (Cambridge, England) · 2010Article
- SCH529074, a small molecule activator of mutant p53, which binds p53 DNA binding domain (DBD), restores growth-suppressive function to mutant p53 and interrupts HDM2-mediated ubiquitination of wild type p53.The Journal of biological chemistry · 2010Article
- DEK proto-oncogene expression interferes with the normal epithelial differentiation program.The American journal of pathology · 2009Article
- Transcriptional regulation by AIRE: molecular mechanisms of central tolerance.Nature reviews. Immunology · 2008Review
- The p53 family and programmed cell death.Oncogene · 2008Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
p63 shares considerable sequence identity with p53, especially in its DNA-binding, activation and tetramerization domains. When the upstream promoter is used for p63 expression, three major transactivation p63 (TAp63) isoforms (alpha, beta and gamma) are produced. p63 is also expressed from an alternate promoter located in intron 3, producing three major DeltaNp63 isoforms. Recent studies demonstrated that p63 has the potential to function as a tumor suppressor or an oncoprotein. To further address this, we generated cell lines that inducibly express each TAp63 isoform. We showed that TAp63 isoforms are capable of inducing p53-responsive genes, inhibiting cell proliferation and promoting apoptosis. Interestingly, we discovered that both the activation domain (residues 1-59) and the proline-rich domain (residues 67-127) are required for TAp63 transcriptional activity. Likewise, TAp63beta(DeltaPRD), deleted of residues 60-133, possessed a greatly attenuated ability to induce endogenous target genes and promote apoptosis, but retained the ability to inhibit cell proliferation when expressed in stable, inducible cell lines. TAp63beta(DeltaPRD) also functioned as a dominant negative to wild-type p63beta in a dose-dependent manner. Furthermore, the loss of function seen with deletion of the proline-rich domain was not due to a DNA-binding defect, as TAp63beta(DeltaPRD) was found to strongly bind endogenous promoters using chromatin immunoprecipitation assay. Finally, mutational analysis revealed that a PXXP motif at residues 124-127 contributes to the transcriptional activity of TAp63. Altogether, our findings suggest that TAp63 transcriptional activity can be regulated by modification(s) of, or protein interactions with, the p63 proline-rich domain.
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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.