Small GTPases SAR1A and SAR1B regulate the trafficking of the cardiac sodium channel Na_v1.5.

ABSTRACT:

Background

The cardiac sodium channel Na_v1.5 is essential for the physiological function of the heart and causes cardiac arrhythmias and sudden death when mutated. Many disease-causing mutations in Na_v1.5 cause defects in protein trafficking, a cellular process critical to the targeting of Na_v1.5 to cell surface. However, the molecular mechanisms underlying the trafficking of Na_v1.5, in particular, the exit from the endoplasmic reticulum (ER) for cell surface trafficking, remain poorly understood.

Methods and results

Here we investigated the role of the SAR1 GTPases in trafficking of Na_v1.5. Overexpression of dominant-negative mutant SAR1A (T39N or H79G) or SAR1B (T39N or H79G) significantly reduces the expression level

SUBMITTER: Wang Z 

PROVIDER: S-EPMC6168416 | biostudies-literature | 2018 Nov

REPOSITORIES: biostudies-literature