Lehman and Rynkiewicz show that, in the absence of Ca²⁺, troponin-I causes tropomyosin to pivot over relatively fixed points on actin subunits, blocking myosin-head binding sites on actin and thereby causing muscle relaxation.

Lewis et al. investigate how training status influences relaxed myosin conformations known to play a role in skeletal muscle metabolism. Their findings indicate that individuals with moderate activity levels have a shift in the relaxed conformations of their type II myosin molecules, lowering the basal ATP consumption.

Szanto et al. provide data that support the idea that rearrangement of S6, including its rotation, may mediate the communication between the activation gate and the inactivation gate controlling slow inactivation in K_V channels.

Histone proteins are known to be elevated in circulation where they contribute to vascular dysfunction. However, many details regarding the mechanism of action are unknown. Here, the authors show that P2XR7 channel current is activated by extracellularly applied histone proteins in a heterologous expression system.

This work demonstrates that the opening of lateralize cardiac connexin-43 hemichannels, in the absence of a cardiac pathology, is still sufficient to alter cardiac membrane excitability and promote arrhythmias upon β-adrenergic cardiac stress.

The intracellular C-terminal positively charged regions of the γ subunits play important roles in BK channel modulation. This work identifies positively charged peptides as BK channel modulators and reveals a role for the Ca²⁺-bowl site in BK channel modulation by positively charged peptides and the auxiliary γ subunits.

Diastolic dysfunction was induced in guinea pigs by pressure overload. We found myofilament dysfunction that included depressed force development, reduced tension-dependent ATP consumption rate, prolonged K_tr, and prolonged myofibril relaxation in the absence of a change in myosin isoform composition. Blunted cross-bridge cycle kinetics may be an important contributor to diastolic heart failure.