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. 2011 May 24;6(5):e20123. doi: 10.1371/journal.pone.0020123

Figure 1. Inhibition of hTAS2R16, hTAS2R38, and hTAS2R43 by probenecid.

Figure 1

HEK-293T cells were transiently transfected with Gα16gust44 and the indicated TAS2R receptors in a 384-well microplate. 22 hours post-transfection, calcium influx was measured in cells challenged with the indicated ligands in the presence (closed triangles) or absence (open diamonds) of probenecid (1 mM; 1 hour pre-incubation). Probenecid treatment completely attenuated (A) salicin-dependent (3 mM) calcium influx by the hTAS2R16 receptor and (B) PTC- (100 µM) and (C) PROP-dependent (30 µM) calcium influx by the hTAS2R38 receptor. (D) Probenecid treatment similarly attenuated aloin-induced (3 mM) hTAS2R43 signaling. (E) Probenecid treatment did not inhibit saccharin induced signaling of hTAS2R31. (F) hTAS2R38 transfected cells challenged with probenecid or buffer alone (1 mM) did not result in calcium influx, but do flux with the PTC control.