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. 2017 Sep 9;6(9):e006465. doi: 10.1161/JAHA.117.006465

Figure 5.

Figure 5

Wildtype (WT) and mutant KCNK3 dimers respond to pharmacological modulation. A, WT KCNK3 dimer (top) is activated by ONO‐RS‐082 (ONO) 10 μmol/L (red trace) and inhibited by ML365 10 μmol/L (blue trace), in current recordings from voltage clamp experiments. Control (predrug, pH 7.4) traces are shown in black. Bar graphs show fold change in current at −50 mV for the WT KCNK3 dimer, after ONO (red, n=4 cells) or ML365 (blue, n=7 cells) application. B, WT−V221L KCNK3 heterodimer (top) is activated by ONO 10 μmol/L (red trace), and inhibited by ML365 10 μmol/L (blue trace), and heterodimer channel activity was confirmed by channel activation at extracellular pH 10.4 (gray dotted traces). Control (predrug, pH 7.4) traces are shown in black. Bar graphs show fold change in current at −50 mV for the WT−V221L heterodimer, after ONO (red, n=5 cells) or ML365 (blue, n=3 cells) application. Bar graphs display mean±SEM. *P<0.05 by the paired Student t test.