Structure modeling, site-directed mutagenesis, and current recordings revealed the mechanism by which stabilization of voltage sensors in the resting and activated states determines the gating properties of the CaV1.1 calcium channel.
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.
A characterization of LGN-V1 synaptic transmission properties demonstrates thalamocortical synapses in vivo are weak and unreliable, but biologically constrained models show they efficiently drive cortex.
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.
The structures of Slo1 in complex with b4 imply that the auxiliary beta subunits modulate the channel's gating properties through stabilizing ‘pre-existing’ conformations rather than creating new ones.
Individual nonmuscle myosin 2 filaments in cells may differ their mechanical and kinetic properties depending on the myosin paralog composition giving the cells a mechanism for fine tuning the output of a given nonmuscle myosin filament.