Fig. 8.

Schematic model for the regulation of FAK activity by β-arrs under basal and GPCR-stimulated conditions. Under basal conditions, both β-arr1 and β-arr2 form molecular complexes with a pool of non-autophosphorylated FAK in the cytoplasm, inhibiting its catalytic activity and negatively regulating both the amount of pY397-FAK in FA and FA number. Agonist (A)-mediated GPCR activation triggers G-protein activation (illustrated by GDP to GTP exchange); the receptors are then phosphorylated (P) by GRKs (not shown) and recruit β-arr–FAK complexes. β-arr interaction with AP-2 results in the release of FAK from its complex with β-arr, which relieves the inhibition exerted by β-arr on FAK, followed by FAK activation by the G protein