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. 2021 Jul 7;126(2):532–539. doi: 10.1152/jn.00257.2021

Figure 2.

Figure 2.

A PKC activator suppresses wild-type Kv3.1 currents, but not those of the A513V Kv3.1 mutant. A: representative voltage-clamp traces for wild-type Kv3.1 expressed in CHO cells before and after treatment with 100 nM TPA. Currents were evoked from a holding potential of −70 mV to test potentials between −80 and +70 mV. B: current-voltage relationship for CHO cells expressing wild-type Kv3.1 gene treated with 100 nM TPA. Currents were normalized by cell capacitance. C: immunoblots for phospho-S503 Kv3.1 in CHO cells expressing wild-type Kv3.1 and treated with either carrier solution DMSO alone, 100 nM TPA for 30 min, or pretreated with PKC inhibitor, 1 µM GF109203X for 30 min before exposure to 100 nM TPA with inhibitor for 30 min. D: quantification of phospho-S503 Kv3.1 levels in the three conditions. One-way ANOVA Turkey’s multiple-comparison test was performed. *P < 0.05. Values are means ± SE; n = 4, 4, 4 independent experiments. E–G: as for A–C but for CHO cells expressing 513V Kv3.1. H: quantification of phospho-S503 Kv3.1 levels in 513V Kv3.1 cells for the three conditions. One-way ANOVA Turkey’s multiple-comparison test was performed. Values are means ± SE; n = 4, 4, 4 independent experiments. CHO, Chinese hamster ovary; PKC, protein kinase C; TPA, 12-O-tetradecanoylphorbol-13-acetate.