N-Glycosylation of the voltage-gated sodium channel β2 subunit is required for efficient trafficking of Na_V1.5/β2 to the plasma membrane.

ABSTRACT: The voltage-gated sodium channel is critical for cardiomyocyte function and consists of a protein complex comprising a pore-forming α subunit and two associated β subunits. It has been shown previously that the associated β2 subunits promote cell surface expression of the α subunit. The major α isoform in the adult human heart is Na_V1.5, and germline mutations in the Na_V1.5-encoding gene, sodium voltage-gated channel α subunit 5 (SCN5A), often cause inherited arrhythmias. Here, we investigated the mechanisms that regulate β2 trafficking and how they may determine proper Na_V1.5 cell surface localization. Using heterologous expression in polarized Madin-Darby canine kidney cells, we show that β2 is N-glycosylated in vivo and in vitro</

SUBMITTER: Cortada E 

PROVIDER: S-EPMC6827310 | biostudies-literature | 2019 Nov

REPOSITORIES: biostudies-literature