A potassium channel, as a nonconducting function, organizes compartmentalized neuronal calcium signaling microdomains via structural and functional coupling of plasma membrane and endoplasmic reticulum calcium channels.
A high axonal chloride concentration explains why activation of light-gated chloride channels causes neurotransmitter release, and a novel hybrid somatodendritic targeting motif ameliorates this phenomenon and improves their inhibitory function.
Fatty acid analogues are interesting prototype compounds that may inspire the development of future IKs channel activators to treat patients with long QT syndrome caused by diverse arrhythmia-causing mutations in the IKs channel.
Global phosphoproteomic analysis in nerve terminal during exocytosis reveals 252 uniquely regulated phosphosites, highlighting complex regulation of active zone proteins at multiple sites and the role of specific kinases/phosphatases.
Phosphatidic acid influences the gating of voltage-gated K+ channels through a non-specific surface charge mechanism and through a specific interaction between a voltage sensor arginine and the primary phosphate head group on the cytoplasmic membrane leaflet.
Building on previous work (Pless, 2013), we argue that side-chain 'flip out' is a key event in potassium channel C-type inactivation, and propose a new method for encoding multiple noncanonical amino acids and controlling protein stoichiometry.