Issues

JGP study suggests that tropomyosin regulates the crossbridge cycle in muscle by pivoting around relatively fixed points on actin thin filaments.

Recent papers by Nelson et al. and Pilagov et al. provide important new information on the ever-expanding role of myosin heads in the regulation of contraction.

In this review, we discuss the role of Zn²⁺ and zinc transporters in regulating cellular Ca²⁺ dynamics in cardiac muscle.

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.

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.

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.

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.

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.