![]() ![]() We speculate that adhesion/excitability nodes are key sites for crosstalk of the contractile and electrical molecular apparatus and may represent the structural substrate of cardiomyopathies in patients with mutations in molecules of the VGSC complex.įast sodium current is key to the generation of a rapidly conducting action potential in multiple tissues. We show that the N-cadherin-Na V1.5 association is not random, that Na V1.5 molecules in these clusters are major contributors to cardiac sodium current, and that loss of Na V1.5 expression reduces intercellular adhesion strength. ![]() ![]() Here we combine nanoscale-imaging (single-molecule localization microscopy electron microscopy and ‘angle view’ scanning patch clamp) with mathematical simulations to demonstrate distinct hubs at the cardiac intercalated disc, populated by clusters of the adhesion molecule N-cadherin and the VGSC Na V1.5. Demonstration of similar macromolecular organization in cardiac muscle is missing. Studies of myelinated fibres, however, show that voltage-gated sodium channels (VGSCs) aggregate with cell adhesion molecules at discrete subcellular locations, such as the nodes of Ranvier. Intercellular adhesion and electrical excitability are considered separate cellular properties. ![]()
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