ArticleProceedings of the National Academy of Sciences of the United States of America2007
Cleavage of the transactivation-inhibitory domain of p63 by caspases enhances apoptosis.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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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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Who cites it
22 citing papers in PubMed, 42 citations in OpenAlex.
- STAT3 and p63 in the Regulation of Cancer Stemness.Frontiers in genetics · 2022Review
- Inhibition of Cytosolic Phospholipase A2α Induces Apoptosis in Multiple Myeloma Cells.Molecules (Basel, Switzerland) · 2021Article
- Tumor suppressor RBM24 inhibits nuclear translocation of CTNNB1 and TP63 expression in liver cancer cells.Oncology letters · 2021Article
- TA*p63 and GTAp63 achieve tighter transcriptional regulation in quality control by converting an inhibitory element into an additional transactivation domain.Cell death & disease · 2019Article
- Pir2/Rnf144b is a potential endometrial cancer biomarker that promotes cell proliferation.Cell death & disease · 2018Article
- STAT3, stem cells, cancer stem cells and p63.Cellular & molecular biology letters · 2018Review
- Requirement of zinc transporter ZIP10 for epidermal development: Implication of the ZIP10-p63 axis in epithelial homeostasis.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Interferon-Stimulated Gene 15 in the Control of Cellular Responses to Genotoxic Stress.Molecules and cells · 2017Review
- The Regulation of Tumor Suppressor p63 by the Ubiquitin-Proteasome System.International journal of molecular sciences · 2016Review
- Mutant p53 enhances MET trafficking and signalling to drive cell scattering and invasion.Oncogene · 2013Article
- Chemosensitivity is controlled by p63 modification with ubiquitin-like protein ISG15.The Journal of clinical investigation · 2012Article
- Regulation of p73 activity by post-translational modifications.Cell death & disease · 2012Review
- Distinct SNP combinations confer susceptibility to urinary bladder cancer in smokers and non-smokers.PloS one · 2012Article
- The role of p63 in cancer, stem cells and cancer stem cells.Cellular & molecular biology letters · 2011Review
- Tumour suppressor ING1b maintains genomic stability upon replication stress.Nucleic acids research · 2011Article
- Endogenous retrovirus drives hitherto unknown proapoptotic p63 isoforms in the male germ line of humans and great apes.Proceedings of the National Academy of Sciences of the United States of America · 2011Article
- Resveratrol-induced p53-independent apoptosis of human nasopharyngeal carcinoma cells is correlated with the downregulation of ΔNp63.Cancer gene therapy · 2010Article
- C-terminal cleavage of DeltaNp63alpha is associated with TSA-induced apoptosis in immortalized corneal epithelial cells.Investigative ophthalmology & visual science · 2010Article
- Differential control of TAp73 and DeltaNp73 protein stability by the ring finger ubiquitin ligase PIR2.Proceedings of the National Academy of Sciences of the United States of America · 2010Article
- p63 regulates the caspase-8-FLIP apoptotic pathway in epidermis.Cell death and differentiation · 2009Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 3 countries.
Funding
Abstract
p63 is a p53-related transcription factor. Utilization of two different promoters and alternative splicing at the C terminus lead to generation of six isoforms. The alpha isoforms of TAp63 and DeltaNp63 contain a transactivation-inhibitory (TI) domain at the C termini, which can bind to the transactivation (TA) domain and inhibit its transcriptional activity. Consequently, TAp63alpha can directly inhibit its activity through an intramolecular interaction; similarly, DeltaNp63alpha can inhibit the activity of the active TAp63 isoforms through an intermolecular interaction. In this work, we demonstrate that after induction of apoptosis, the TI domain of the p63alpha isoforms is cleaved by activated caspases. Cleavage of DeltaNp63alpha relieves its inhibitory effect on the transcriptionally active p63 proteins, and the cleavage of TAp63alpha results in production of a TAp63 protein with enhanced transcriptional activity. In agreement with these data, generation of the N-terminal TAp63 fragment has a role in apoptosis because stable cell lines expressing wild-type TAp63 are more sensitive to apoptosis compared with cells expressing the noncleavable mutant. We also used a model system in which TAp63 expression was induced by trichostatin-A treatment in HCT116 cells. Trichostatin-A sensitized these cells to apoptosis, and this sensitization was associated with cleavage of up-regulated p63.
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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.