Fig. 4

Slc7a5 shifts the voltage-dependence of Kv1.2 activation. a Indicated combinations of Kv1.2, Slc7a5, and Slc3a2 were transfected in ltk- mouse fibroblasts. Cells were hyperpolarized to −120 mV for 30 s prior to recording, leading to disinhibition of Kv1.2 currents. Conductance-voltage relationships were measured as described in Fig. 1. Conductance-voltage relationships were generated from the tail current amplitudes and fit with a Boltzmann function (Kv1.2 V_1/2 = −11 ± 3, k = 11 ± 3 mV, n = 5; Kv1.2 + Slc7a5 V_1/2 = −58 ± 3, k = 10 ± 2 mV, n = 16; Kv1.2 + Slc3a2 V_1/2 = −11 ± 10, k = 10 ± 3 mV, n = 10; and Kv1.2 + Slc7a5 + Slc3a2 V_1/2 = −16 ± 3 mV, k = 11 ± 2 mV, n = 9). b Representative traces of the activation curves measured in a, with the pulse to −20 mV highlighted. c HEK cells were transfected with equal amounts of the indicated combinations of Kv1.2, Slc7a5, and Kvβ1.3. Conductance-voltage relationships were generated as in a (Kv1.2 V_1/2 = −16 ± 3, k = 9 ± 4 mV; Kv1.2 + Kvβ V_1/2 = −22 ± 4, k = 9 ± 2 mV; Kv1.2 + Slc7a5 V_1/2 = −60 ± 1, k = 9 ± 1 mV; and Kv1.2 + Slc7a5 + Kvβ V_1/2 = −56 ± 3 mV, k = 9 ± 3 mV). d Current density at +10 mV was measured at the beginning and of a pulse train with a −120 mV holding potential (identical to Fig. 3; Kv1.2 + Kvβ n = 7; Kv1.2 + Kvβ + Slc7a5 n = 11). e Representative traces illustrating N-type inactivation conferred by Kvβ in the presence and absence of Slc7a5 (100 ms step from −80 mV to +60 mV)