Encyclopedia of Cancer

Living Edition
| Editors: Manfred Schwab

p53 Family

  • Jacky K. H. Chung
  • Meredith S. Irwin
Living reference work entry
DOI: https://doi.org/10.1007/978-3-642-27841-9_4332-2



The p53 family consists of p53 and its two homologues, p63 and p73. All three proteins are transcription factors that bind specific DNA sequences to mediate gene expression involved in cell cycle arrest, apoptosis, and differentiation. p63 and p73 map to chromosomes 3q27 and 1p36, respectively. The three p53 family genes and their protein products share many characteristics, including some “p53-like activities.” However, some differences in structure and function suggest that each protein has unique roles in various biological and pathological processes from development to oncogenesis.


Molecular Structure and Function

In the late 1990s, two decades after the initial discovery of the p53 tumor suppressor protein, the p53 homologues p63 and p73 were identified. The p63 and p73 genes give rise to multiple mRNA, which are translated into several distinct isoforms (Fig. 1). Different isoforms...


Ectodermal Dysplasia Syndrome Binding Sequence Preference Promoter Binding Sequence 
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  1. Irwin MS, Miller FD (2004) p73: regulator in cancer and neural development. Cell Death Differ 11(Suppl 1):S17–S22CrossRefPubMedGoogle Scholar
  2. McKeon F, Melino G (2007) Fog of war: the emerging p53 family. Cell Cycle 6(3):229–232CrossRefPubMedGoogle Scholar
  3. Mills AA (2006) p63: oncogene or tumor suppressor? Curr Opin Genet Dev 16(1):38–44CrossRefPubMedGoogle Scholar
  4. Moll UM, Slade N (2004) p63 and p73: roles in development and tumor formation. Mol Cancer Res 2(7):371–386PubMedGoogle Scholar
  5. Stiewe T (2007) The p53 family in differentiation and tumorigenesis. Nat Rev Cancer 7(3):165–168CrossRefPubMedGoogle Scholar

Copyright information

© Springer-Verlag Berlin Heidelberg 2014

Authors and Affiliations

  1. 1.Department of Medical Genetics and MicrobiologyUniversity of TorontoTorontoCanada
  2. 2.Cell Biology Program and Division of Hematology-Oncology Hospital for Sick ChildrenUniversity of TorontoTorontoCanada