A Novel Strategy Using Cardiac Sodium Channel Polymorphic Fragments To Rescue Trafficking-Deficient <i>SCN5A</i> Mutations

Abstract

In the present study, we demonstrate that small peptides, spanning the H558R polymorphism, are sufficient to restore the trafficking defect of BrS-associated Na(v)1.5 mutations. Our findings suggest that it might be possible to use short cDNA constructs as a novel strategy tailored to specific disease-causing mutants of BrS.