Mohran et al. show that calcium has a direct effect on thick filament activation in myocardium rather than an indirect effect due to calcium-mediated crosstalk between the thick and thin filaments. Their findings should be considered in developing future drug candidates to treat heart diseases.

Two connexins, Cx26 and Cx30, are expressed in the cochlea and play vital roles in hearing. Sanchez et al. identified a sequence difference in their E1 domains that differentially affects their abilities to operate as hemichannnels and function in transmembrane signaling.

Kraujaliene et al. used modeling and dye uptake/transfer studies to show that an Ala/Glu difference in the E1 domains of Cx26 and Cx30 can account for their differential permeabilities to anionic permeants. The permeability profiles are conserved in gap junction channels and hemichannel configurations.

Using a mathematical model, Stephenson tests the hypothesis that the characteristic response to Ca²⁺ of RyR channels is key not only for the Ca²⁺ release mechanism in cardiac muscle and other tissues, but also for the DHPR-dependent Ca²⁺ release in skeletal muscles.

Mott et al. evaluate two click-chemistry protein labeling tools based on genetic code expansion technology and circularly permutated Halotag, respectively, for their utility in TRPV1 cell surface expression studies.

Kooiker et al. investigate the mechanisms of a novel cardiac myosin inhibitor that depends on the presence of a myosin regulatory light chain (RLC-1). They show that RLC-1 destabilizes myosin interactions to inhibit force and accelerate kinetics in cardiac muscle.

The ω-grammotoxin-SIA peptide (GrTx-SIA) was originally found in tarantula venom and shown to inhibit voltage-gated Ca²⁺ channels. Here, Collaço et al. report that GrTx-SIA can also potently inhibit voltage-gated Na⁺ channel currents, with Na_V1.6 being the most susceptible subtype.