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TAp63 prevents premature aging by promoting adult stem cell maintenance.

Cell stem cell | Jul 2, 2009

http://www.ncbi.nlm.nih.gov/pubmed/19570515

The cellular mechanisms that regulate the maintenance of adult tissue stem cells are still largely unknown. We show here that the p53 family member, TAp63, is essential for maintenance of epidermal and dermal precursors and that, in its absence, these precursors senesce and skin ages prematurely. Specifically, we have developed a TAp63 conditional knockout mouse and used it to ablate TAp63 in the germline (TAp63(-/-)) or in K14-expressing cells in the basal layer of the epidermis (TAp63(fl/fl);K14cre+). TAp63(-/-) mice age prematurely and develop blisters, skin ulcerations, senescence of hair follicle-associated dermal and epidermal cells, and decreased hair morphogenesis. These phenotypes are likely due to loss of TAp63 in dermal and epidermal precursors since both cell types show defective proliferation, early senescence, and genomic instability. These data indicate that TAp63 serves to maintain adult skin stem cells by regulating cellular senescence and genomic stability, thereby preventing premature tissue aging.

Pubmed ID: 19570515 RIS Download

Mesh terms: Adult Stem Cells | Aging, Premature | Animals | Cell Aging | DNA Damage | Dermis | Epidermis | Genes, p53 | Genomic Instability | Hair Follicle | Keratinocytes | Mice | Mice, Knockout | Phosphoproteins | Skin Aging | Trans-Activators | Wound Healing

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Associated grants

  • Agency: NCI NIH HHS, Id: CA-16672
  • Agency: NCI NIH HHS, Id: CA16672
  • Agency: NCI NIH HHS, Id: R01 CA160394

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