The cardiac sodium channel is post-translationally modified by arginine methylation.

摘要: The α subunit of the cardiac sodium channel (Nav1.5) is an essential protein in initial depolarization phase cardiomyocyte action potential. Post-translational modifications such as phosphorylation are known to regulate Nav1.5 function. Here, we used a proteomic approach for study post-translational using tsA201 cells model system. We generated stable cell line expressing Nav1.5, purified channel, and analyzed by MALDI-TOF LC–MS/MS. report identification arginine methylation novel modification Nav1.5. R513, R526, R680, located linker between domains I II were found mono- or dimethylated states. functional relevance underscored fact that R526H R680H mutations causing Brugada long QT type 3 syndromes, respectively. Our work describes first time voltage-gated ion...