In vivo specificity of GPCR regulation in GRK-overexpressing transgenic mice
| GRK | Target GPCR | Phenotype | Reference |
|---|---|---|---|
| GRK2 | β1/β2-AR | Attenuation of agonist-stimulated cardiac contractility | Koch et al. (1995) |
| Attenuation of agonist-stimulated vasodilation | Eckhart et al. (2002) | ||
| α1B-AR | None | Eckhart et al. (2000) | |
| GRK3 | α1B-AR | Attenuation of agonist-stimulated signaling in heart | Eckhart et al. (2000) |
| Thrombin | Attenuation of myocardial thrombin-stimulated ERK1/2 signaling | Iaccarino et al. (1998) | |
| β1/β2-AR | None | Iaccarino et al. (1998) | |
| AT1AR | None | Iaccarino et al. (1998) | |
| GRK4(A142V) | D1 dopamine | Development of hypertension and impaired renal sodium excretion | Felder et al. (2002) |
| GRK5 | β1/β2-AR | Attenuation of isoproterenol stimulation of cardiac contractility | Rockman et al. (1996) |
| AT1AR | None | Rockman et al. (1996) |
GRK2 overexpression was targeted to either the heart or the vasculature. GRK4 gene polymorphism A142V was targeted to all tissues. All other GRK transgenic mice have targeted overexpression in the heart. No phenotype indicates that stimulation of the listed GPCR was carried out and the response was not different from wild-type animals
AT1R, angiotensin II type 1 receptor.