Fig. 3
From: Lack of beta-arrestin signaling in the absence of active G proteins
DMR biosensing of G protein- and arrestin-mediated cellular responses. DMR recordings in absence (a–c) and presence of G protein inhibitors (d–f) of agonist-mediated DP2 (a, d), GPR17 (b, e) and FFA2 (c, f) in wild-type (WT) HEK293 cells. Concentration-response-curves of DMR peak values in absence and presence of G protein inhibitors of DP2 (g), GPR17 (h), and FFA2 (i) response in wild-type HEK293 cells. j C3-mediated and forskolin-mediated DMR response of FFA2 in ΔG12/13 cells in the absence and presence of PTX/FR. k C3-induced DMR response of FFA2 in vector- or Gα12/13-transfected ΔG12/13 cells. l C3- or forskolin-mediated DMR response of FFA2 in vector- or β-arrestin2-transfected ΔG12/13 cells in the presence of PTX/FR. Inset shows βarr2-GFP transfected ΔG12/13 cells, scale bar 50 µm. m–o Agonist-induced DMR response of DP2 (m), GPR17 (n), or FFA2 (o) in vector- or β-arrestin2-transfected Δβarr1/2 cells in absence and presence of G protein inhibitors. a–f, j–o Shown are representative traces (mean + s.e.m.) of three independent experiments, each performed in triplicate. g–i Data are mean ± s.e.m. of three independent experiments (three technical replicates)
