title: Signalling pathways in pemphigus vulgaris.
abstract: Acantholysis in pemphigus vulgaris is induced by binding of autoantibodies to desmoglein 3 (Dsg3). The roles of signalling pathways on development of acantholysis have recently been extensively studied. In the study by Sayar et al., recently published in Exp Dermatol, epidermal growth factor receptor (EGFR) signalling was activated in both in vivo and in vitro pemphigus vulgaris experimental models. However, while EGFR inhibitors suppressed activity of p38 mitogen-activated protein kinase (p38MAPK) linearly, they suppressed activity of c-Myc and acantholysis in a non-linear, V-shaped relationship. These findings indicated complicated interactions among EGFR, p38MAPK and c-Myc in pemphigus vulgaris pathology.
authors.affiliation: Department of Dermatology, Kurume University School of Medicine and Kurume University Institute of Cutaneous Cell Biology, Kurume, Fukuoka, Japan.
authors.forename: Xiaoguang
authors.initials: X
authors.lastname: Li
authors.forename: Norito
authors.initials: N
authors.lastname: Ishii
authors.forename: Chika
authors.initials: C
authors.lastname: Ohata
authors.forename: Minao
authors.initials: M
authors.lastname: Furumura
authors.forename: Takashi
authors.initials: T
authors.lastname: Hashimoto
mesh_terms: D000818:Animals; D066246:ErbB Receptors / Q000037:antagonists & inhibitors*; D006801:Humans; D010392:Pemphigus / Q000188:drug therapy*; D011799:Quinazolines / Q000494:pharmacology*
chemical_list: D011799:Quinazolines; D066246:ErbB Receptors
keywords: acantholysis; pemphigus vulgaris; signalling pathway