Cryo-EM structures of the gating cycle of bestrophin reveal the molecular underpinnings of activation and inactivation gating in this calcium-activated chloride channel and reveal a surprisingly wide pore.
Customization of ion channel gating enhances homeostatic regulation through automatic detection and correction of abnormal physiological changes, as illustrated by self-restoration of excitation rhythm in cardiac arrhythmias.
The 3Å structure and correlated functional analysis of the TRPM2 cation channel from Nematostella vectensis shed light on the molecular mechanisms of TRPM2 regulation by intra- and extracellular Ca2+, and of inactivation of human TRPM2.
Contrary to a generally accepted principle, the pore properties of KCNQ1 channels depend on the states of voltage-sensing domains activation; KCNE1 alters the voltage-sensing domains-pore coupling to modulate KCNQ1 channel properties.
Two mutations in TRPM3 resulting in developmental and epileptic encephalopathies result in a gain-of-channel function, which may lie at the basis of epileptic activity and neurodevelopmental symptoms in the patients.