Functional cross-talk between phosphorylation and disease-causing mutations in the cardiac sodium channel Na_v1.5.

ABSTRACT: The voltage-gated sodium channel Na_v1.5 initiates the cardiac action potential. Alterations of its activation and inactivation properties due to mutations can cause severe, life-threatening arrhythmias. Yet despite intensive research efforts, many functional aspects of this cardiac channel remain poorly understood. For instance, Na_v1.5 undergoes extensive posttranslational modification in vivo, but the functional significance of these modifications is largely unexplored, especially under pathological conditions. This is because most conventional approaches are unable to insert metabolically stable posttranslational modification mimics, thus preventing a precise elucidation of the contribution by these modifications to channel function. Here, we overcome this limitatio

SUBMITTER: Galleano I 

PROVIDER: S-EPMC8379932 | biostudies-literature | 2021 Aug

REPOSITORIES: biostudies-literature