Figure 3.

3hi2one-G4 decreases GIRK4 current inhibition after PIP₂dephosphorylation by 5-ptaseOCRL in HEK cells.A, representative plot of GIRK4 current decrease (control, black open circle). B, representative plot of 3hi2one-G4 induced GIRK4 current decrease in response to optogenetic dephosphorylation by phosphatase 5-ptaseOCRL (20 μM 3hi2one-G4, mauve open circle). C, the decrease in current (%current remaining) is reduced when GIRK4 channels are studied in the presence of 3hi2one-G4. D, 5-ptaseOCRL-mediated decrease in GIRK4 current is characterized by monoexponential fits in the presence of 5-ptaseOCRL in the presence (mauve circles) and the absence of 3hi2one-G4 (black circles). E, 3hi2one-G4 increases the τ (tau) of current decrease, following activation of 5-ptaseOCRL. Data are currents recorded from HEK293T cells using patch clamp in the whole-cell mode and are shown as means ± SD for six to seven cells per group. Statistical significance was calculated using unpaired Student's t tests using GraphPad Prism (∗∗p < 0.005; ∗∗∗p < 0.0005). GIRK, G protein–sensitive inwardly rectifying potassium channel; HEK, human embryonic kidney cell line; 3hi2one, 3-[2-(3,4-dimethoxyphenyl)-2-oxoethyl]-3-hydroxy-1-(1-naphthylmethyl)-1,3-dihydro-2H-indol-2-one; PIP_2, phosphatidylinositol-4,5-bisphosphate.