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. 2012 Nov 16;288(1):181–191. doi: 10.1074/jbc.M112.382473

FIGURE 9.

FIGURE 9.

Attenuation of GHS-R1a-mediated signaling depends on specific 5-HT2C isoform co-expression. Cells co-expressing the GHS-R1a receptor and the 5-HT2C receptor or the partially edited isoform, 5-HT2C-VSV were treated with ghrl or MK0677 in a dose-response manner (300 to 3.7 nm, 3-fold serial dilution), following pretreatment with the GHS-R1a inverse agonist, peptide [d-Arg1,d-Phe5,d-Trp7,9,Leu11]-substance P (1 μm). A, no effect of 5-HT2C receptor blockade in cells solely expression the GHS-R1a receptor. B and C, RS102221 rescues GHS-R1a-induced calcium influx in GHS-R1/5-HT2C-expressing cells (B), but there was no change in GHS-R1a/5-HT2C-VSV-expressing cells (C). Intracellular calcium increase was depicted as a percentage of maximal calcium increase as elicited by control in each separate experiment (3% FBS in presence of SP-analog). The data represent the means ± S.E. of a representative experiment of three independent transductions with each concentration point performed in triplicate.