title: Plakophilin-2 promotes activation of epidermal growth factor receptor.
abstract: While growth factor-driven dimerization of receptor tyrosine kinases (RTKs) is a simple and intuitive mechanism of activating RTKs, K.-I. Arimoto et al. (Mol. Cell. Biol. 34:3843-3854, 2014, doi:10.1128/MCB.00758-14) describe a novel means of promoting the activity of RTKs. Namely, plakophilin-2 (PKP2) associates with the epidermal growth factor receptor (EGFR) and enhances its ligand-dependent and ligand-independent activity. This discovery suggests that antagonizing PKP2 may be a new therapeutic opportunity to combat tumors in which activation of EGFR contributes to pathogenesis.
authors.affiliation: Schepens Eye Research Institute, Massachusetts Eye and Ear Infirmary, Harvard Medical School, Boston, Massachusetts, USA andrius_kazlauskas@meei.harvard.edu.
authors.forename: Andrius
authors.initials: A
authors.lastname: Kazlauskas
mesh_terms: D000818:Animals; D063646:Carcinogenesis / Q000378:metabolism*; D066246:ErbB Receptors / Q000378:metabolism*; D005260:Female; D006801:Humans; D008325:Mammary Neoplasms, Experimental / Q000378:metabolism*; D051191:Plakophilins / Q000502:physiology*
chemical_list: C495337:PKP2 protein, human; D051191:Plakophilins; C512478:EGFR protein, human; D066246:ErbB Receptors
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