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. Author manuscript; available in PMC: 2022 Jun 4.
Published in final edited form as: Mol Cell. 2021 Sep 27;81(22):4605–4621.e11. doi: 10.1016/j.molcel.2021.09.007

Figure 1. D6R and C5aR2 lack functional G protein coupling.

Figure 1

(A) Schematic representation of canonical GPCR and non-canonical 7TMR pairs activated by a common agonist. C5a, complement C5a; C5aR1, C5a receptor subtype 1; C5aR2, C5a receptor subtype 2; CCL7, chemokine CCL7; CCR2, C-C chemokine receptor subtype 2; D6R, decoy D6 receptor.

(B and C) Agonist-induced dissociation of heterotrimeric G proteins for C5aR1-C5aR2 and CCR2-D6R pairs measured using NanoBiT complementation assay. Data (mean ± SEM) represent three independent experiments, normalized with respect to baseline signal (i.e., vehicle treatment).

(D) Agonist-induced second messenger response measured using the GloSensor assay (cAMP stimulation and inhibition of forskolin-induced cAMP level) and Fluo-4 NW calcium mobilization assay. For each of the second messenger assays, a well-established prototypical GPCR was included as a reference (V2R, vasopressin receptor subtype 2; B2R, bradykinin receptor subtype 2). Data (mean ± SEM) represent four independent experiments, normalized with respect to maximum signal (treated as 100%). See also Figure S1.