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Journal of Biomedicine and Biotechnology
Volume 2011, Article ID 864904, 13 pages
Review Article

A Symphony of Regulations Centered on p63 to Control Development of Ectoderm-Derived Structures

1Department of Biomolecular Science and Biotechnology, University of Milan, 20133 Milano, Italy
2Department of Dermatology, University of Rome “Tor Vergata”, 00133 Rome, Italy
3Rome Oncogenomic Centre, Via Elio Chianesi 53, 00144 Rome, Italy
4Molecular Biotechnology Center, Dulbecco Telethon Institute, University of Torino, 10126 Torino, Italy

Received 5 October 2010; Revised 25 January 2011; Accepted 16 March 2011

Academic Editor: Thomas Lufkin

Copyright © 2011 Luisa Guerrini et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


The p53-related transcription factor p63 is critically important for basic cellular functions during development of the ectoderm and derived structure and tissues, including skin, limb, palate, and hair. On the one side, p63 is required to sustain the proliferation of keratinocyte progenitors, while on the other side it is required for cell stratification, commitment to differentiate, cell adhesion, and epithelial-mesenchymal signaling. Molecules that are components or regulators of the p63 pathway(s) are rapidly being identified, and it comes with no surprise that alterations in the p63 pathway lead to congenital conditions in which the skin and other ectoderm-derived structures are affected. In this paper, we summarize the current knowledge of the molecular and cellular regulations centered on p63, derived from the comprehension of p63-linked human diseases and the corresponding animal models, as well as from cellular models and high-throughput molecular approaches. We point out common themes and features, that allow to speculate on the possible role of p63 downstream events and their potential exploitation in future attempts to correct the congenital defect in preclinical studies.