Issues

JGP study shows that the subendocardium is more susceptible to spontaneous Ca²⁺ release events that can initiate arrhythmias, and this may be reduced by local CaMKII inhibition.

Na,K ATPases are modulated by FXYD subunits. What do the FXYDs affect, how do they do it, and what are their physiological impacts?

Romer et al. explored T-tubules in skeletal muscle.

Inwardly rectifying potassium channels are generally thought to achieve their physiological voltage dependence via an “extrinsic” mechanism involving voltage-dependent block by polyamines. A surprising finding of polyamine-independent gating of Kir4.1/Kir5.1 heteromeric channels suggests a mechanism of voltage dependence arising from interactions with permeating ions.

Dries et al. show that injured myocardial slices from the subendocardium are more susceptible to spontaneous Ca²⁺ release events and whole-slice contractions than those from the subepicardium, and that this is reduced by CaMKII inhibition.

The cardiac KCNQ1 channel is a promising anti-arrhythmic target. Yazdi et al. report on how PUFAs interact with two binding sites in KCNQ1 to trigger channel activation. These findings further our mechanistic understanding of how to modulate KCNQ1 activity.

Inoue et al. use site-directed mutagenesis and reconstitution experiments to uncover critical residues within the zinc-binding motif of TRPM7 that are essential for the Mg²⁺-dependent regulation of the channel activity in conditions of oxidative stress.

Szanto et al. use heavy water and Shaker-IR K⁺ channel mutants to establish that structural water molecules contribute to the inactivation of the selectivity filter of the channel. Their experimental evidence supports previous predictions stemming from molecular dynamics simulations.