Skip to main content
. 2021 Jun 24;12:3938. doi: 10.1038/s41467-021-23756-y

Fig. 6. GM3 binds GHSR and modulates G protein activation.

Fig. 6

a FRET signal between C11 TopFluor GM3 (GM3*; 5 molar%) and Lumi-4 Tb attached to either C2556.27 or C3047.34 of GHSR in the absence of competing lipid or in the presence of 5% (molar ratio) unlabeled GM3, PIP2, or POPG. b Changes in MB emission λmax for the wild-type receptor and the PIP2-binding sites mutant assembled into nanodiscs containing 5% GM3, PIP2 or GM3 and PIP2 in equimolar amounts in the absence or presence of 10 µM ghrelin. Data are mean ± SD of three experiments. c–e GTP turnover for Gq and Gi2 catalyzed by wild-type GHSR (c, d) or its PIP2-binding sites mutant (e, f) in nanodiscs containing 5% GM3, PIP2 or GM3 and PIP2 in equimolar amounts, in the absence or presence of 10 µM ghrelin. The signal was normalized to that obtained for the G protein in the absence of receptor, and data are mean ± SD of five experiments. In all cases, statistical values were obtained by means of unpaired Student’s t test (*0.01 < p < 0.05, **0.001 < p < 0.01, ***0.0001 < p < 0.001, ****p < 0.0001). Source data are provided as a Source data file.