Summary
Abstract Voltage-gated sodium channels (NaVs) maintain the electrical cadence in cardiac muscle tissues by selectively controlling the rapid inward passage of sodium. The NaV complex is comprised of a 260-kDa pore- forming α-subunit (encoded primarily by NaV1.5 in heart) that partners with β -subunits (β1-β4) comprised of a single transmembrane segment and exofacial immunoglobulin (Ig) fold. These β-subunits belong to a larger family of β/MPZ proteins that includes other single pass Ig proteins such as MPZ(P0). Defects in sodium channel function resulting from inherited mutations in either th
