Tumor Protein P63 is a Key Regulator of Skin Functions in Ectodermal Dysplasia
نویسنده
چکیده
Tumor protein (TP)-p63 has been discovered as TP53 homolog more than fifteen years ago and has become a master regulator of skin development, proliferation and stem cell maintenance. While TP53 is known to be the most mutated gene in human cancer, TP63 mutations are mostly associated with the various types of ectodermal dysplasia. All TP53 family members, TP53, TP63 and TP73, function as transcription factors that regulate the cell cycle arrest, apoptosis, autophagy or metabolism through activation/repression of downstream target genes or protein-protein interactions with other protein regulators of transcription and splicing. Several downstream target genes or protein interactors of TP63 are involved in the molecular mechanisms underlying the ectodermal dysplasia phenotypes. This mini-review underlines a few venues of investigations about the key role for TP63 in skin biology and pathology.
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