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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.


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

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

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.

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