An interaction between PRRT2 and Na⁺/K⁺ ATPase contributes to the control of neuronal excitability.

ABSTRACT: Mutations in PRoline Rich Transmembrane protein 2 (PRRT2) cause pleiotropic syndromes including benign infantile epilepsy, paroxysmal kinesigenic dyskinesia, episodic ataxia, that share the paroxysmal character of the clinical manifestations. PRRT2 is a neuronal protein that plays multiple roles in the regulation of neuronal development, excitability, and neurotransmitter release. To better understand the physiopathology of these clinical phenotypes, we investigated PRRT2 interactome in mouse brain by a pulldown-based proteomic approach and identified α1 and α3 Na⁺/K⁺ ATPase (NKA) pumps as major PRRT2-binding proteins. We confirmed PRRT2 and NKA interaction by biochemical approaches and showed their colocalization at neuronal plasma membrane. The acute or constitutive

SUBMITTER: Sterlini B 

PROVIDER: S-EPMC7969623 | biostudies-literature | 2021 Mar

REPOSITORIES: biostudies-literature