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. 2001 Apr;13(4):943–952. doi: 10.1105/tpc.13.4.943

Figure 5.

Figure 5.

Regulation of AKT3, AKT3/(p)KST1, KST1, and KST1/(p)AKT3 by Intracellular Protons.

(A) In the voltage range of +30 to −150 mV, voltage pulses from a holding voltage of −30 mV in steps of 20 mV for a duration of 2.5 sec demonstrate the inhibition of K+ fluxes through AKT3 in the presence of 10 mM acetate compared with control conditions (Inline graphic). Note the decrease of outward as well as inward K+ currents.

(B) K+ currents mediated by AKT3/(p)KST1 before and after addition of 10 mM acetate to the extracellular solution (Inline graphic). From the holding voltage of −20 mV, the membrane voltage was changed to −120 mV in 10-mV decrements.

(C) K+ currents through KST1 were elicited by 5-sec voltage pulses in the range of +20 to −150 mV (10-mV decrements) in the absence and in the presence of 10 mM acetate (n = 6).

(D) Activation of K+ inward currents through KST1/(p)AKT3 upon addition of 10 mM HAc. Current traces in response to voltages in the range from +30 to −130 mV (10-mV decrements) are shown (Inline graphic).

The solutions used for results shown in (A) to (D) were composed of 30 mM KCl, 1 mM CaCl2, 2 mM MgCl2, and 10 mM Mes/Tris, pH 5.6, as well as 10 mM NaCl or 10 mM Na-acetate, respectively. Steady state currents in the presence of sodium acetate were significantly different from those in sodium chloride in the voltage range from −80 to −130 mV (P < 0.05).