Analysis of iconic and gating currents of wild type and mutated BK channels reveals a strong inhibition of this channel by extracellular acidification and elucidates the underlying mechanism that is potentially applicable to other voltage-dependent cation channels.
Gating currents analysis at different Ca2+ concentrations of BK channels reveals a strong allosteric coupling between Ca2+- and voltage-sensing modules via equivalent contributions exerted by the RCK1 and RCK2 Ca2+-sites.
Computation and experiment together demonstrate that nonspecific membrane–protein interactions could regulate transmembrane protein function and suggest that covalent linkers can be an integral component of the sensing apparatus.
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.
An inducedpluripotent stem cell (iPSC)-based model of KCNQ2-associated developmental epileptic encephalopathy suggests that disease is driven by dyshomeostaic neuronal mechanisms that are downstream of loss of M-current.
Acetylcholine, a common modulator in the brain, controls spike-frequency adaptation by specifically attenuating Ether-a-go-go related K+ currents, thereby explaining many cortical network statistical changes often observed in vivo.