Calmodulin binds to the N-terminal domain of the cardiac sodium channel Na1.5.

The cardiac voltage-gated sodium channel Na1.5 conducts the rapid inward sodium current crucial for cardiomyocyte excitability. Loss-of-function mutations in its gene are linked to cardiac arrhythmias such as Brugada Syndrome (BrS).

Single-Molecule Localization of the Cardiac Voltage-Gated Sodium Channel Reveals Different Modes of Reorganization at Cardiomyocyte Membrane Domains.

Background: Mutations in the gene encoding the cardiac voltage-gated sodium channel Na1.5 cause various cardiac arrhythmias. This variety may arise from different determinants of Na1.

Modeling Depolarization Delay, Sodium Currents, and Electrical Potentials in Cardiac Transverse Tubules.

T-tubules are invaginations of the lateral membrane of striated muscle cells that provide a large surface for ion channels and signaling proteins, thereby supporting excitation-contraction coupling. T-tubules are often remodeled in heart failure. To better understand the electrical behavior of T-tubules of cardiac cells in health and disease, this study addresses two largely unanswered questions regarding their electrical properties: (1) the delay of T-tubular membrane depolarization and (2) the effects of T-tubular sodium current on T-tubular potentials.

Plakophilin-2 Haploinsufficiency Causes Calcium Handling Deficits and Modulates the Cardiac Response Towards Stress.

Human variants in plakophilin-2 (PKP2) associate with most cases of familial arrhythmogenic cardiomyopathy (ACM). Recent studies show that PKP2 not only maintains intercellular coupling, but also regulates transcription of genes involved in Ca cycling and cardiac rhythm. ACM penetrance is low and it remains uncertain, which genetic and environmental modifiers are crucial for developing the cardiomyopathy.

Corrigendum: Transcriptomic analyses of murine ventricular cardiomyocytes.

This corrects the article DOI: 10.1038/sdata.2018.

Transcriptomic analyses of murine ventricular cardiomyocytes.

Mice are used universally as model organisms for studying heart physiology, and a plethora of genetically modified mouse models exist to study cardiac disease. Transcriptomic data for whole-heart tissue are available, but not yet for isolated ventricular cardiomyocytes. Our lab therefore collected comprehensive RNA-seq data from wildtype murine ventricular cardiomyocytes as well as from knockout models of the ion channel regulators CASK, dystrophin, and SAP97.

Refining the molecular organization of the cardiac intercalated disc.

This review presents an extensively integrated model of the cardiac intercalated disc (ID), a highly orchestrated structure that connects adjacent cardiomyocytes. Classically, three main structures are distinguished: gap junctions (GJs) metabolically and electrically connect cytoplasm of adjacent cardiomyocytes; adherens junctions (AJs) connect the actin cytoskeleton of adjacent cells; and desmosomes function as cell anchors and connect intermediate filaments. Furthermore, ion channels reside in the ID.