JGP, in partnership with the Society of General Physiologists, announces a new networking and mentoring program for junior faculty.
Barro-Soria et al. highlight work that reveals how β1 and β3 subunits modulate NaV1.5 channel function.
Chromaffin cells release transmitters from populations of granules to which synaptotagmin-1 and synaptotagmin-7 are selectively sorted. Rao et al. characterize the functional properties of these granules and show that synaptotagmin-7 confers fast kinetics and high efficacy to the exocytotic event.
IKs channels are important for repolarization of cardiac action potentials during stress, but the mechanism has not been described microscopically. Thompson et al. show that cAMP facilitates voltage sensor activation in single channels, causing fewer silent sweeps, reduced first latency to opening, and occupancy of higher-subconductance states in open channels.
G protein–gated inwardly rectifying potassium (GIRK) channels are activated by the phospholipid phosphatidylinositol 4,5 bisphosphate (PIP2). Using functional and computational experiments, Lacin et al. reveal that PIP2 interacts with the tether helix of the neuronal GIRK channel in a dynamic way.
Voltage-gated NaV channels are modulated by two different noncovalent accessory subunits: β1 and β3. Zhu et al. present data showing that β1 and β3 cause distinct effects on channel gating because they interact with NaV channels at different locations. β3 regulates the voltage sensor in domain III, whereas β1 regulates the one in domain IV.