Human mutations in Ca_V1.2 underlie life-threatening arrhythmias and neurodevelopmental disorders. Through in-depth biophysical analysis, this study identifies divergent mechanistic alterations linked to Ca_V1.2 channelopathies and reveals an association between changes in channel function and patient phenotypes.

The present study reports on a novel effect of denervation at the neuromuscular junction level. It shows that the absence of nerve causes a reduction in the subsynaptic type 1 inositol 1,4,5-trisphosphate-stained region likely involved in the stabilization of the endplate.

PIEZO1, a mechanically gated ion channel, transduces mechanical cues in neural stem cells. Here, we show the impact of Piezo1 knockout on neural development in vivo and find that cholesterol biosynthesis and lipid membrane composition are regulated by Piezo1.

Compared to the “ventricular” essential myosin light chain MLC1sb/v, the longer and more positively charged MLC1sa present in slow-twitch M. soleus fibers decelerates actin filament gliding on β-myosin molecules presumably by a decreased dissociation rate from actin filaments.

Using a novel assay chamber to inject myosin light chain phosphatase during laser trap measurements, tonic smooth muscle force maintenance is observed at the myosin molecular level, marking an important step toward elucidating the underlying mechanisms of the latch state.

The present numerical modeling study shows that disorder in locations of Ca release units in cardiac pacemaker cells has substantial functional impact by creating release clusters, similar to Poisson clumping, and opportunity of Ca release to propagate within the clusters.

Epithelial Na⁺ channels are major regulators of fluid volumes and ultimately blood pressure in terrestrial vertebrates. We found that the amounts of protein comprising these channels in the kidneys and colons of rats and mice exceed what is required to explain the transport of Na⁺ by these tissues. This excess may facilitate regulation of the channels.