Fig. 5: Distinct AT1R–β-arrestin2 complex configurations are mediated by GRK2/3, GRK5/6 or PKC.

a–f To identify the contribution of the individual GRKs to the complex formation of β-arrestin2 (βarr2) with AT1R, Control or ΔQ-GRK cells were transfected with AT1R-NanoLuc, Halo-Tag-βarr2 and either GRK2, 3, 5, 6 or the empty vector (EV) as indicated, in absence or presence of PKC inhibitor Gö6983 (500 nM). Additionally, the GRK-specific βarr2 recruitment to the AT1R was measured utilising a Halo-Tag-βarr2 construct lacking the finger loop region (dFLR). Angiotensin II (AngII)-induced dynamic BRET changes are shown as concentration-response curves. All data points are calculated as Δ net BRET fold change normalised to baseline values and vehicle control, represented as the mean of n = 3 independent experiments ± SEM. The data are also presented in respective bar graphs, displaying the mean BRET values + SEM before (baseline) and after stimulation with 1 µM AngII (stimulated), normalised to the basal BRET ratio derived from the corresponding ΔQ-GRK + EV condition in (b). The results of the statistical analysis of displayed data are listed in Supplementary Table 4. All test statistics, effect sizes, confidence intervals and degrees of freedom are provided in the Source Data files. g Schematic summary of the kinase-specific complex configurations between AT1R and βarr1 or 2 either in the absence of GRKs, mediated by GRK2/3 or GRK5/6 overexpression as observed in (a–f; Supplementary Fig. 11).