Fig. 7
From: Lack of beta-arrestin signaling in the absence of active G proteins
Designer receptor-mediated ERK1/2 activation and DMR response. a–c Clozapine-N-oxide (CNO)- and epidermal growth factor (EGF)-mediated ERK1/2 phosphorylation and total ERK1/2 in wild-type HEK293 cells (WT) expressing M3D-WT (a), M3D-Gq (b) or M3D-βArr (c). d–f CNO- and EGF-mediated ERK1/2 phosphorylation and total ERK1/2 in G protein-deficient (ΔGsix+PTX) HEK293 cells by M3D-WT (d), M3D-Gq (e) or M3D-β-arr (f). g–i CNO-mediated and EGF-mediated ERK1/2 phosphorylation and total ERK1/2 in β-arrestin-deficient (Δβarr1/2) cells by M3D-WT (g), M3D-Gq (h) or M3D-βArr (i). j–l Real-time DMR traces in CNO-stimulated cells expressing M3D-WT (j), M3D-Gq (k) or M3D-βArr (l). a–i Data are mean +/± s.e.m. of three independent experiments (three technical replicates). j–l Shown are representative traces (mean + s.e.m.) of three independent experiments, each measured in triplicates. For statistical analysis, two-sample paired Wilcoxon test (g) was applied to paired points at different times. *P < 0.05
