The GIRK1 subunit contains a defective Na+-binding site but behaves as if it is permanently bound to a sodium ion, and therefore increases the affinity of Gβγ to GIRK1/4 hetero-tetrameric channels in lipid membranes.
The functional interaction of Na+ and KATP channels at the intercalated disk of cardiomyocytes depends on Ankyrin G and is clinically relevant since KATP channel mutations affect Na+ channel expression.
Determining how GIRK2 activity depends on the concentration of Gβγ subunits in lipid membranes at different Na+ concentrations has allowed the Gβγ concentration generated during GABAB activation in neurons to be estimated.
The G protein subunits Gβγ and the signaling lipid PIP2 are simultaneously needed to activate the potassium ion channel GIRK2 to control the voltage across a lipid bilayer, while sodium ions modulate these molecules' effects.
Genetic analysis of how neuropeptides control C. elegans reproductive behavior shows how T-type calcium channels engage and disengage target neurons from these critical regulators of neural circuits and behavior.
In mouse brain slices, native delta glutamate receptors carry ionic current and underlie the α1-adrenergic receptor-mediated depolarization of dorsal raphe neurons that drives action potential firing in vivo.
The engagement of DNA crossings is shown to license ATP hydrolysis and DNA cleavage by topoisomerase VI, a finding with mechanistic ramifications for related GHKL ATPases and meiotic recombination machineries.