title: Connexin hemichannels influence genetically determined inflammatory and hyperproliferative skin diseases.
abstract: Connexin mutations underlie numerous human genetic diseases. Several connexin genes have been linked to skin diseases, and mechanistic studies have indicated that a gain of abnormal channel function may be responsible for pathology. The topical accessibility of the epidermal connexins, the existence of several mouse models of human skin disease, and the ongoing identification of pharmacological inhibitors targeting connexins provide an opportunity to test new therapeutic approaches.
authors.affiliation: Department of Physiology and Biophysics, Stony Brook University, Stony Brook, NY 11794, United States.
authors.forename: Noah A
authors.initials: NA
authors.lastname: Levit
authors.affiliation: Department of Physiology and Biophysics, Stony Brook University, Stony Brook, NY 11794, United States. Electronic address: thomas.white@stonybrook.edu.
authors.forename: Thomas W
authors.initials: TW
authors.lastname: White
mesh_terms: D000818:Animals; D017630:Connexins / Q000235:genetics*; D030342:Genetic Diseases, Inborn / Q000235:genetics; D006801:Humans; D007249:Inflammation / Q000235:genetics*; D009154:Mutation / Q000235:genetics; D012871:Skin Diseases / Q000235:genetics*
chemical_list: D017630:Connexins
keywords: Connexin; Gap junctions; Genetic disease; Inflammation; Inhibitor; KID syndrome; Skin