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. 2021 Oct 25;9:749607. doi: 10.3389/fcell.2021.749607

FIGURE 1.

FIGURE 1

Structural localization of R190Q and E288G on the wild-type GIPR and the molecular pharmacological phenotype of the variants. (A) Structural illustration of the wild-type GIPR and the position of the GIPR variants, R190Q and E288G. (B) Dose-response curve in cAMP accumulation of wild-type GIPR, R190Q, E288G and double mutant. (C) Dose-response curves of the homologous competition binding data with [125I]GIP and unlabeled GIP at 4°C for 3 h of wildtype GIPR, R190Q, E288G and double mutant. (D) Corresponding Bmax values. (E) Dose-response curve of β-arrestin 2 recruitment of wild-type GIPR, R190Q, E288G and double mutant. (F) Internalization of SNAP-GIPR, SNAP-R190Q and SNAP-E288G over time following stimulation with 1 μM GIP vs. baseline. (G) Receptor cell surface expression levels of SNAP-GIPR, SNAP-R190Q, SNAP-E288G, and FRT (empty-SNAP-vector). Data represent the mean ± SEM of minimum n = 3. Independent experiments are performed in either duplicate or triplicates. Statistical significance was assessed using an ordinary one-way ANOVA for receptor cell surface expression (*p < 0.05; **p < 0.01; as compared to wild-type response).