Fig. 4: Comparison of agonist-induced mouse µ-opioid receptor (MOP) phosphorylation, G protein signaling, and GRK and arrestin binding. | Communications Biology

Fig. 4: Comparison of agonist-induced mouse µ-opioid receptor (MOP) phosphorylation, G protein signaling, and GRK and arrestin binding.

From: A bead-based GPCR phosphorylation immunoassay for high-throughput ligand profiling and GRK inhibitor screening

Fig. 4

Cells were exposed to increasing concentrations of DAMGO (a, c, e, g) or morphine (b, d, f, h). Total MOP phosphorylation was determined according to the standard assay protocol and depicted as the mean of pT370-, pS375-, pT376- and pT379-MOP phosphorylation assays (red). G protein signaling was determined using GIRK-mediated changes in membrane potential (gray). Amounts of GRK2 (blue), GRK3 (turquoise), β-arrestin1 (lime) and β-arrestin2 (green) recruited were determined by β-galactosidase complementation assay. Data are means ± SEM from at least n = 3 independent experiments performed in duplicates. Where error bars are not apparent, SEM was smaller than symbol size. Note for better comparison to GRK and arrestin receuitment, (a, c, e, g) depicted the same data set for DAMGO-induced and (b, d, f, h) for morphine-induced GIRK activation (gray). All data points were normalized to 10 µM DAMGO stimulation.

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