Targeting of the cardiac voltage-gated sodium channel 1.5 requires an ankyrin-G-dependent pathway

Abstract

The focus of this project is determining if an ankyrin-G-dependent pathway controls the membrnae expression of the voltage-gated sodium channel 1.5 in cardiomyocytes. Disruption of the normal localization of Nav1.5 can result in Brugada syndrome and has been linked to myopathic disease. This project defines that an ankyrin-G-based pathway is required for the expression, localization and function of Nav1.5 at the cariomyocyte plasma membrane.