J.-S. Rougier

Identification of a Binding Site for Small Molecule Inhibitors Targeting Human TRPM4

The paper identifies the binding site of small molecule inhibitors NBA and IBA in TRPM4 using cryo-EM and patch clamp experiments.

Role of 14-3-3 proteins in human cardiac sodium channel Nav1.5 regulation

This study investigates the role of 14-3-3 proteins in regulating the human cardiac sodium channel Nav1.5 using heterologous expression in tsA201 cells and finds no significant regulatory effect.

Species-specific effects of cation channel TRPM4 small-molecule inhibitors

This study compares the effects of TRPM4 inhibitors on human and mouse TRPM4 channels, revealing species-specific responses and highlighting the need for in vivo validation.

Deletion of Trpm4 alters the function and expression of NaV1.5 channel in murine cardiac myocytes

This study shows that Trpm4 deletion in mice reduces NaV1.5 expression and Na+ currents in cardiac myocytes, leading to altered electrophysiological properties.

Calmodulin binds to the N-terminal domain of the cardiac sodium channel Nav1.5

This study identifies calmodulin as a new binding partner of the Nav1.5 N-terminal domain and shows that mutations in this region impair the interaction, contributing to dominant-negative effects in Brugada Syndrome.

Nav1.5 single-molecule localization reveals different reorganization modes at cardiomyocyte domains

The paper uses single-molecule localization microscopy to study Nav1.5 localization in different cardiomyocyte domains and finds site-specific redistribution in disease models.

A distinct pool of Nav1.5 channels at the lateral membrane of murine ventricular cardiomyocytes

This study investigates the role of 1-syntrophin in regulating sodium current at the lateral membrane of cardiomyocytes and identifies a sub-pool of Nav1.5 channels independent of 1-syntrophin and the PDZ-binding motif.

Dystrophin and calcium current are decreased in cardiomyocytes expressing Cre enzyme driven by αMHC but not TNT promoter

This study shows that MHC-Cre mice exhibit reduced dystrophin and calcium current, unlike TNT-Cre mice, highlighting the need for Cre-only controls in experiments.