TRPV5 and TRPV6 are unique among TRP channels due to their high Ca²⁺ selectivity, while most other members of this ion channel family do not select for a specific cation type. Ives et al. used biomolecular simulations and in silico electrophysiology to determine the mechanism underlying this unusual Ca²⁺ selectivity.

Intracellular fibroblast growth factors (iFGF) regulate voltage-gated sodium (Na_V) channel expression and gating. Using a mouse model and heterologous expression in Xenopus oocytes, we describe mechanisms of how iFGF alters Na_V channel activation and inactivation.

This manuscript reports discovery of voltage-dependent inhibition of TRPV channels by intracellular polyamines and develops a kinetic model of this process. Polyamines are inhibitors of each TRPV sub-type.

Similar to HCM-causing truncation mutations, CRISPR-mediated cMyBP-C ablation in iPSC-derived human engineered cardiac tissue constructs causes cMyBP-C haploinsufficiency in the heterozygous state. While cMyBP-C ablation causes early hypercontractility, developing Ca²⁺-handling abnormalities leads to progressive contractile dysfunction.

This article reports that restrictive deletion of the N-terminal extension of cardiac troponin I as seen in adaptation to heart failure enhances Frank-Starling response of the heart by increasing myofilament sensitivity to passive tension rather than resting sarcomere length.

Probenecid, an FDA-approved gout medication of therapeutic interest for other disease conditions, depresses sarcoplasmic reticulum Ca²⁺ release and contractile activation in mouse skeletal muscle. The effects are unrelated to its capacity to block ATP release through pannexin-1 channels.

Occupation of the uppermost ion-binding site of the selectivity filter of K⁺ channels by external K⁺ promotes channel activity. Such a phenomenon is not observed in KCNQ1 voltage-gated channels, allowing a deeper understanding of their conduction and permeability mechanism.