The role of RIPK4 in epidermis physiology.

Abstract

Proteins which regulate morphogenesis of the epidermis ensure its proper construction and function and mutations or abnormal expression
of those proteins impact epidermal function. One recently described protein is Receptor Interacting Serine/Threonine Kinase 4 (RIPK4).
Mutations in RIPK4 cause the autosomal-recessive form of Bartsocas-Papas syndrome and Popliteal Pterygium Syndrome the Aslan type. In mice, deletion of Ripk4 (Ripk4-/-) leads to premature death of neonates caused by numerous skin adhesions. RIPK4 regulates development and maintenance of differentiation and proliferation homeostasis of keratinocytes, as well as inflammation. RIPK4 also appears to act as a tumor suppressor in skin, since expression is decreased in squamous skin carcinoma and inducible deletion in mice facilitates induction and growth of papillomas and squamous skin carcinomas in chemical carcinogenesis. The review describes the RIP family, the engagement of RIPK4 in differentiation of the epidermis and consequences resulting from its improper expression.