p63 and p73, the Ancestors of p53
- 1Institute of Biophysical Chemistry, Goethe University, Frankfurt am Main, Germany
- 2IDI-IRCCS Biochemistry Laboratory, Department of Experimental Medicine and Biochemical Sciences, University of Rome “Tor Vergata”, Via Montpellier 1, 00133 Rome, Italy
- 3Medical Research Council, Toxicology Unit, Hodgkin Building, Leicester University, Lancaster Road, P.O. Box 138, Leicester LE1 9HN, United Kingdom
- Correspondence: gm89{at}leicester.ac.uk
Abstract
p73 and p63 are two homologs of the tumor suppressive transcription factor p53. Given the high degree of structural similarity shared by the p53 family members, p73 and p63 can bind and activate transcription from the majority of the p53-responsive promoters. Besides overlapping functions shared with p53 (i.e., induction of apoptosis in response to cellular stress), the existence of extensive structural variability within the family determines unique roles for p63 and p73. Their crucial and specific functions in controlling development and differentiation are well exemplified by the p63 and p73 knockout mouse phenotypes. Here, we describe the contribution of p63 and p73 to human pathology with emphasis on their roles in tumorigenesis and development.
Footnotes
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Editors: Arnold J. Levine and David P. Lane
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Additional Perspectives on The p53 Family available at www.cshperspectives.org
- Copyright © 2010 Cold Spring Harbor Laboratory Press; all rights reserved
