Fig. P1.

GPCR-induced reversible translocation of G-protein βγ-subunits. In the basal state, the combination of lipid moieties on the α- and γ-subunits stably binds inactive heterotrimers to the plasma membrane. G-protein activation releases the βγ-complex from the α-subunit. The single lipid group on the γ-subunit imparts transient membrane binding, and free βγ-subunits constantly explore the cytosolic surfaces of the plasma membrane and intracellular membranes. Receptor deactivation leads to reversal of translocation and the accumulation of inactive heterotrimers at the plasma membrane.