Figure 5
The mutation in site Y disturbed the action of Cl− as PAM on mfT1R2a/mfT1R3. (A–C) Dose‒response curves of stable cell lines expressing (A) mfT1R2a K265A/mfT1R3, (B) mfT1R2a K265E/mfT1R3, or (C) mfT1R2a K295P/mfT1R3 to L-Gln, with G16gust44. Data are shown as the mean ± SEM (n = 3–4 independent experiments performed in duplicate or triplicate). Cross marks in the graph represent EC50 values. VEH: responses against the buffer. (D) Schematic illustration of the mechanism by which Cl− acts as PAM on mfT1R2a/mfT1R3. The labels “upper lobe” and “lower lobe” indicate the upper and lower lobes within the Venus flytrap domain of mfT1R2a. (E) Amino acid sequence alignment of seven T1Rs from medaka fish, zebrafish, and humans; rat mGluR4; and human CaSR at site Y.
