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1. Functional Epicardial Conduction Disturbances Due to a SCN5A Variant Associated With Brugada Syndrome

2. C-terminal phosphorylation of NaV1.5 impairs FGF13-dependent regulation of channel inactivation

10. Fluorescent‐ and tagged‐protoxin II peptides: potent markers of the Na v 1.7 channel pain target

11. Human model of IRX5 mutations reveals key role for this transcription factor in ventricular conduction

12. Human model of IRX5 mutations reveals key role for this transcription factor in ventricular conduction

13. Proteomic and functional mapping of cardiac NaV1.5 channel phosphorylation sites

14. Human model of IRX5 mutations reveals key role for this transcription factor in ventricular conduction

15. Proteomic and functional mapping of cardiac NaV1.5 channel phosphorylation reveals multisite regulation of surface expression and gating

20. Human model of IRX5 mutations reveals key role for this transcription factor in ventricular conduction.

21. Fluorescent- and tagged-protoxin II peptides: potent markers of the Nav 1.7 channel pain target.

22. RRAD mutation causes electrical and cytoskeletal defects in cardiomyocytes derived from a familial case of Brugada syndrome

24. Voltage-gated sodium channels assemble and gate as dimers

25. Dysfunction of the Voltage-Gated K + Channel b2 Subunit in a Familial Case of Brugada Syndrome

26. Mutant voltage-gated Na+ channels can exert a dominant negative effect through coupled gating.

27. Dysfunction of the Voltage‐Gated K + Channel β2 Subunit in a Familial Case of Brugada Syndrome

30. Physiological and Pathophysiological Insights of Nav1.4 and Nav1.5 Comparison

32. A Long QT Mutation Substitutes Cholesterol for Phosphatidylinositol-4,5-Bisphosphate in KCNQ1 Channel Regulation

33. In KCNQ1 Channels, a Long QT Mutation Induces a Regulation by Cholesterol Instead of Phosphatidylinositol-4,5-Bisphosphate

35. Physiological and pathophysiological insights of Nav1.4 and Nav1.5 comparison.

40. Variable Nav1.5 Protein Expression from the Wild-Type Allele Correlates with the Penetrance of Cardiac Conduction Disease in the Scn5a+/− Mouse Model

48. Mouse Model of SCN5A -Linked Hereditary Lenègre’s Disease

50. Long-Term Amiodarone Administration Remodels Expression of Ion Channel Transcripts in the Mouse Heart

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