Figure 1
GRKs are involved in cellular signaling that is independent of G protein activation. Biased agonist activates either G protein signaling or GRK/β-arrestin-dependent signaling. Each agonist promotes distinct conformational changes of GPCRs. Unbiased agonists activate both G protein signaling and GRK/β-arrestin-dependent signaling, whereas biased agonists activate either G protein- or GRK/β-arrestin-dependent signaling as shown in bold arrows. Physiological responses mediated by GRK/β-arrestin-dependent signaling are believed to be distinct from those by G protein activation.
Figure 2
Binding partners with GRKs. GRKs regulate diverse signaling pathways by the interaction with intracellular proteins, resulting in various physiological responses.
Table 1
Interactions of each GRKs with intracellular proteins
| GRK isoform | Binding partner | Function | Reference |
|---|---|---|---|
| GRK6 | GIT1 | GRK6 cooperates with GIT1 to enhance Rac1 activity, and promotes engulfment of apoptotic cells | [43] |