Gene Summary

Gene:TP63; tumor protein p63
Aliases: AIS, KET, LMS, NBP, RHS, p40, p51, p63, EEC3, OFC8, p73H, p73L, SHFM4, TP53L, TP73L, p53CP, TP53CP, B(p51A), B(p51B)
Summary:This gene encodes a member of the p53 family of transcription factors. The functional domains of p53 family proteins include an N-terminal transactivation domain, a central DNA-binding domain and an oligomerization domain. Alternative splicing of this gene and the use of alternative promoters results in multiple transcript variants encoding different isoforms that vary in their functional properties. These isoforms function during skin development and maintenance, adult stem/progenitor cell regulation, heart development and premature aging. Some isoforms have been found to protect the germline by eliminating oocytes or testicular germ cells that have suffered DNA damage. Mutations in this gene are associated with ectodermal dysplasia, and cleft lip/palate syndrome 3 (EEC3); split-hand/foot malformation 4 (SHFM4); ankyloblepharon-ectodermal defects-cleft lip/palate; ADULT syndrome (acro-dermato-ungual-lacrimal-tooth); limb-mammary syndrome; Rap-Hodgkin syndrome (RHS); and orofacial cleft 8. [provided by RefSeq, Aug 2016]
Databases:OMIM, HGNC, Ensembl, GeneCard, Gene
Protein:tumor protein 63
Source:NCBIAccessed: 01 September, 2019


What does this gene/protein do?
Show (63)

Cancer Overview

Research Indicators

Publications Per Year (1994-2019)
Graph generated 01 September 2019 using data from PubMed using criteria.

Literature Analysis

Mouse over the terms for more detail; many indicate links which you can click for dedicated pages about the topic.

  • Zinc Fingers
  • Cell Differentiation
  • Apoptosis
  • Trans-Activators
  • DNA-Binding Proteins
  • Gene Expression Profiling
  • MicroRNAs
  • Phosphoproteins
  • Tumor Suppressor Gene
  • Triple Negative Breast Cancer
  • Messenger RNA
  • Adenocarcinoma
  • Squamous Cell Carcinoma
  • Wounds and Injuries
  • Bladder Cancer
  • Neoplastic Cell Transformation
  • Chromosome 3
  • Genetic Predisposition
  • United Kingdom
  • Single Nucleotide Polymorphism
  • Neoplasm Invasiveness
  • Protein Isoforms
  • Cell Proliferation
  • Down-Regulation
  • Biomarkers, Tumor
  • Transcriptional Activation
  • Breast Cancer
  • Transcription Factors
  • Urothelium
  • Promoter Regions
  • Nuclear Proteins
  • Sensitivity and Specificity
  • Mutation
  • Young Adult
  • Cancer Gene Expression Regulation
  • Uveal Neoplasms
  • Lung Cancer
  • Tumor Protein p73
  • Head and Neck Cancers
  • Immunohistochemistry
Tag cloud generated 01 September, 2019 using data from PubMed, MeSH and CancerIndex

Specific Cancers (6)

Data table showing topics related to specific cancers and associated disorders. Scope includes mutations and abnormal protein expression.

Note: list is not exhaustive. Number of papers are based on searches of PubMed (click on topic title for arbitrary criteria used).

Latest Publications: TP63 (cancer-related)

Yamaguchi H, Inokuchi K, Sakuma Y, Dan K
Mutation of the p51/p63 gene is associated with blastic crisis in chronic myelogenous leukemia.
Leukemia. 2001; 15(11):1729-34 [PubMed] Related Publications
The p51/p63 gene, a novel member of the p53 gene family, has recently been identified at 3q27-9. There are at least six major isotypes of p51/p63 mRNA transcripts. p51A/TAp63gamma has the potential to induce apoptosis and growth suppression in a manner similar to p53, and other isotypes may suppress the p53 and p51A1TAp63gamma genes in a dominant-negative manner. We analyzed the mutation and expression of the p51/p63 gene in 80 cases of chronic myelogenous leukemia (CML) to evaluate its role in blastic transformation. Expression of the p51/p63 gene was detected in 74 cases. The alpha isotype of p51/p63 transcripts was dominantly expressed in 72 of these 74 cases. There was no correlation between the isotypes of p51/p63 transcripts and the clinical phase. Mutations of the p51/p63 gene were found in six cases. All these mutated cases expressed p51B/TAp63 alpha. In four of the six cases, the mutations were within a limited region (codon 151-170) corresponding to the DNA-binding domain. We hypothesized that this limited region is a hot spot for mutation of the p51/p63 gene. Mutations of the p53 gene were found in four cases of CML in blastic crisis (BC). Frequencies of the p51/p63 and p53 gene mutations were higher in BC (p51/p63 gene, 11.8%; p53 gene, 7.8%) than in the chronic phase (p51/p63 gene, 1.5%; p53 gene, 0%). The p51/p63 gene mutation may act similarly to the p53 gene mutation as a genetic alteration potentially responsible for the progression of CML.

Ishida S, Yamashita T, Nakaya U, Tokino T
Adenovirus-mediated transfer of p53-related genes induces apoptosis of human cancer cells.
Jpn J Cancer Res. 2000; 91(2):174-80 [PubMed] Free Access to Full Article Related Publications
Two p53-related genes, p73 and p51, were recently identified as structural homologues of the p53 tumor suppressor gene, suggesting that the roles of these two genes may be similar to those of p53, including growth suppression and induction of apoptosis. Here we show that introduction of p73 or p51 cDNAs into cultured human cancer cells suppressed colony formation in the presence of G418. We then examined the ability of various isoforms of p73 and p51 to activate transcription of a reporter gene. This assay showed that p73beta and p51A activated transcription through a consensus p53 binding sequence, while p73alpha and p51B isoforms minimally transactivated the p53 reporter gene. To characterize further the biological functions of the p53-related genes, we constructed recombinant adenoviruses containing the p73 and p51 cDNAs. Ad-p73beta and Ad-p51A induced endogenous p21 gene expression more effectively than Ad-p73alpha and Ad-p51B, respectively. To evaluate the mode of cell death induced by p53-related genes, Ad-p73 and Ad-p51 were used to infect human cancer cells. Infection of Ad-p73beta, Ad-p51A or Ad-p51B resulted in DNA fragmentation in a subset of cancer cell lines more efficiently than did infection of Ad-p53. We then examined the combined effect of each p53-related gene and the E1A oncogene in the induction of apoptosis. The E1A oncogene cooperated with p51 as well as p53 to induce apoptosis, while p73 resulted in a weak induction of apoptosis by E1A. Overall, apoptosis induction by p51B and p73alpha isoforms may be due to mechanisms other than transcriptional activation of p53-target genes. Our results suggest that p53-related genes are both similar to and different from p53 in their pathways leading to growth suppression.

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Cite this page: Cotterill SJ. TP63, Cancer Genetics Web: Accessed:

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