Skip to main content
. Author manuscript; available in PMC: 2016 Aug 6.
Published in final edited form as: J Biomol Screen. 2014 Oct 31;20(3):341–349. doi: 10.1177/1087057114557233

Figure 2.

Figure 2

ERK/β-arrestin interaction signals in response to activation of endogenous GPCRs in U2OS cells. (A) Dose-response curves generated using the ERK/β-arrestin interaction assay in response to varying doses of GPCR agonists adrenaline, isoproterenol, dopamine, and S1P. Cells were stimulated with varying doses of GPCR agonists in serum-free DMEM for 90 min at 37°C. (B) Antagonists inhibit GPCR agonist-induced ERK/β-arrestin interaction signals. Cells were treated with varying doses of GPCR antagonists BD-1047, ICI118551, and Clozapine in serum-free DMEM for 15 min and then treated with 1 μM adrenaline, isoproterenol, and dopamine respectively for 90 min.