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. 2021 May 24;9:687489. doi: 10.3389/fcell.2021.687489

FIGURE 1.

FIGURE 1

G proteins, GRKs, and arrestins share similar structural features to engage active GPCR folds. (A) Schematic depiction of how active GPCRs (PDB: 3SN6) interact with trimeric G proteins (PDB: 3SN6), GRKs (PDB: 3NYN), and arrestins (PDB: 5DGY), as most prominent mediators and regulators of GPCR signaling. On the cartoon structures of the intracellular effector proteins, helices that interact with active GPCR folds are highlighted in red. (B) Structure of the endosomal complex (PDB: 6NI2) between an active GPCR, a trimeric G protein, and β-arrestin1.