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. 2010 Jan 4;107(4):1660–1665. doi: 10.1073/pnas.0907342107

Fig. 4.

Fig. 4.

RvD1 activates GPR32 and ALX receptors. (A) The β-arrestin system used to monitor receptor–ligand interaction (see text for details). (BD) Dose responses obtained with RvD1, LXA4, and compound (Compd) 43 with β-arrestin cells stably expressing GPR32. Results are mean ± SEM (n = 4–8). (E) RvE1 comparison with RvD1 with β-arrestin cells stably expressing the ChemR23 receptor; mean ± SEM (n = 4). (FH) Dose responses obtained with RvD1, LXA4, and compound 43 on β-arrestin cells stably expressing ALX; mean ± SEM (n = 4–7). (Insets in F and G) Concentration-dependent inhibition of ALX activation by RvD1 (F) and LXA4 (G) in the presence of escalating concentrations of antagonist t-Boc-Met-Leu-Phe; means from triplicates of two separate experiments. (RLU, relative luminescence unit).

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