Skip to main content
. 2011 Apr 20;100(8):1930–1939. doi: 10.1016/j.bpj.2011.02.046

Figure 1.

Figure 1

PHA-1-causing mutations in hENaC decrease channel activity. (A) Representative macroscopic Na+ currents from CHO cells expressing wild-type hENaC α-, β-, and γ-subunits (top) or subunits engineered to contain PHA-1-causing mutations (middle and bottom) coexpressed with the complementary wild-type subunits before and after addition of 10 μM amiloride (arrow). Whole-cell, macroscopic currents evoked with a voltage ramp (shown in inset) from 60 mV to −100 mV from a holding potential of 40 mV. For these experiments, the bath and pipette [Na+] were asymmetrical at 150 and 5 mM, respectively. (B) Summary graph of (amiloride-sensitive) current density at −80 mV (from voltage ramps) for voltage-clamped CHO cells, similar to that in panel A, expressing wild-type hENaC and hENaC harboring PHA-1-causing mutations in either the α- or β-subunit. The number of experiments for each group is indicated. Current was measured with voltage ramps. ∗ Significant (P < 0.05) decrease versus wild-type hENaC.