TAp63: The fountain of youth
Author(s) -
Xiaohua Su,
Elsa R. Flores
Publication year - 2009
Publication title -
aging
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.473
H-Index - 90
ISSN - 1945-4589
DOI - 10.18632/aging.100095
Subject(s) - longevity , stem cell , senescence , premature aging , genome instability , biology , carcinogenesis , wound healing , stem cell theory of aging , microbiology and biotechnology , dna damage , immunology , genetics , cancer , dna , haematopoiesis , stem cell factor
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.
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