14-3-3θ is a Binding Partner of Rat Eag1 Potassium Channels
Figure 7
The effect of 14-3-3θ over-expression on rEag1 K+ currents.
(A) (Left panel) Representative K+ currents recorded from HEK293T cells expressing rEag1 in the absence or presence of 14-3-3θ. HEK293T cells were co-transfected with the cDNAs for rEag1 and myc-vector or myc-14-3-3θ in the molar ratio of 1∶5. The holding potential was −90 mV. The pulse protocol comprised 300-ms depolarizing test pulses ranging from −90 to +50 mV, with 10-mV increments. (Right panel) Normalized mean K+ current density (at +40 mV) of rEag1 channels in the absence or presence of myc-14-3-3θ. The numbers in the parentheses refer to the number of cells analyzed, and the asterisk denotes significant difference from the rEag1 control (*, t-test: p<0.05). (B) (Left panel) Representative K+ currents recorded from oocytes expressing rEag1 in the absence or presence of 14-3-3θ. The molar ratio for cRNA co-injection was 1∶5 and 1∶10 for 14-3-3θ and Kvβ1, respectively. The pulse protocol was identical to that described in (A). (Right panel) Normalized mean K+ current density (at +40 mV) of rEag1 channels in the absence or presence of 14-3-3θ. (C) Biophysical properties of rEag1 channels in the absence (open circles) or presence (filled diamonds) of 14-3-3θ. The voltage-dependant curves for steady-state activation (upper left panel), activation kinetics (upper right panel), deactivation kinetics (lower left panel), and non-superimposable Cole-Moore shift (lower right panel) were analyzed as described previously [17]. Data were collected from recordings performed in oocytes.