Table 1.

Effects of SVs on ligand binding and GIPR-mediated signal transduction in HEK293T cells coexpressing GIPR and individual SVs

	Ligand binding		cAMP accumulation			β-arr1 recruitment			β-arr2 recruitment
	pIC50 ± SEM	Span (%) ± SEM	pEC50 ± SEM	Emax (%) ± SEM	Δlog (τ/KA)	pEC50 ± SEM	Emax (%) ± SEM	Δlog (τ/KA)	pEC50 ± SEM	Emax (%) ± SEM	Δlog (τ/KA)
WT GIPR	7.91 ± 0.10	100.00 ± 4.87	10.54 ± 0.03	100.00 ± 0.88	0	7.94 ± 0.26	99.03 ± 6.83	0	7.68 ± 0.09	100.00 ± 3.83	0
GIPR+SV1	7.96 ± 0.11	46.52 ± 2.30***	9.89 ± 0.05***	100.01 ± 1.87	−0.33 ± 0.14	7.67 ± 0.44	88.87 ± 9.90	−0.37 ± 0.44	7.39 ± 0.12	66.15 ± 4.09**	−0.67 ± 0.17*
GIPR+SV2	7.82 ± 0.13	51.01 ± 3.26***	10.26 ± 0.05**	102.39 ± 1.44	0.12 ± 0.11	7.70 ± 0.39	96.31 ± 8.45	0.18 ± 0.43	7.36 ± 0.14	83.14 ± 5.53	−0.25 ± 0.12

cAMP accumulation, ligand binding and β-arrestin 1/2 recruitment assays were performed in HEK293T cells. Whole-cell binding assay was performed in CHO-K1 cells. All the measures were fitted to nonlinear regression three-parameter logistic curves. pEC₅₀ is the negative logarithm of the concentration of an agonist that gives a half of the maximum response. pIC₅₀ is the negative logarithm of the 50% inhibitory concentration in competitive radiolabeled ligand binding assay. E_max and span values are the percentage (%) of the maximum response in cells expressing GIPR only. LogR value (log τ/K_A, i.e., logarithm of the transduction ratio) is determined by nonlinear regression using the operational model equation. τ is the efficacy value of the agonist and was corrected by cell surface expression of the receptor. K_A is dissociation constant. Changes in transduction ratio (Δlog R) were calculated to determine the relative effectiveness of the SVs. Data shown are means ± SEM of at least three independent experiments. One-way ANOVA was used to determine statistical difference (*P < 0.05, **P < 0.01 and ***P < 0.001). β-arr1, β-arrestin 1; β-arr2, β-arrestin 2; WT, wild-type.