TBX5-loss associated cardiomyocyte ectopy and atrial fibrillation is prevented by augmentation of SERCA2 activity, establishing a mechanism underlying the genetic basis for a Ca²⁺-dependent pathway for AF risk.

Customization of ion channel gating enhances homeostatic regulation through automatic detection and correction of abnormal physiological changes, as illustrated by self-restoration of excitation rhythm in cardiac arrhythmias.

Enhancing mitochondrial Ca²⁺ uptake effectively suppresses aberrant Ca²⁺ induced arrhythmogenic events in zebrafish, mouse and human cardiomyocytes, demonstrating a critical role for mitochondria in the regulation of cardiac rhythmicity.

An auxiliary subunit alters the effect of a family of small-molecule openers on a voltage-gated potassium channel by inducing structural re-arrangements that promote protonation of the drug molecule.

Usage-dependent inhibition breakdown and neural adaptation underpins the key spatiotemporal dynamics of human focal seizures.

The ability of lipid nanodiscs to trap different types of amyloid intermediates, as successfully demonstrated in this study for human-IAPP, could become one of the most powerful approaches to dissect the complicated misfolding pathways of protein aggregation.

High-resolution live imaging reveals how and when the mouse heart first starts to beat during development and how the onset of beating impacts on heart muscle cell maturation and heart formation.

X-ray crystallography reveals new conceptual insights into the location of the β2-subunit in the Na_v channel signaling complex.

The GIRK1 subunit contains a defective Na⁺-binding site but behaves as if it is permanently bound to a sodium ion, and therefore increases the affinity of Gβγ to GIRK1/4 hetero-tetrameric channels in lipid membranes.

A mouse with a defined mutation in an extracellular matrix protein that is expressed in selected neurons sheds light on circuit abnormalities producing transient hyperkinetic movements.