Aging
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Research Perspective|Volume 1, Issue 10|pp 866—869

TAp63: The fountain of youth

Xiaohua Su1, Elsa R. Flores1
  • 1Department of Molecular and Cellular Oncology, Graduate School of Biomedical Sciences, The University of Texas M.D. Anderson Cancer Center, Houston, TX 77030, USA
Received: September 21, 2009Accepted: October 19, 2009Published: October 21, 2009

Copyright: © 2009 Su et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

The mechanisms controlling organismal aging have yet to be clearly defined. In our recent paper [1], we revealed thatTAp63, the p53 family member, is a critical gene in preventing organismal aging by controlling the maintenance of dermal and epidermal precursor and stem cells critical for wound healing and hair growth. In the absence of TAp63, dermal stem cells (skin-derived precursors or SKPs) in young mice are hyperproliferative. As early as one month of age, SKPs and epidermal precursor cells exhibit signs of premature aging including a marked increase in senescence, DNA damage, and genomic instability resulting in an exhaustion of these cells and an overall acceleration in aging. Here, we discuss our findings and its relevance to longevity, regenerative medicine, and tumorigenesis.