Coexpression of Kv2.1 with Kv5.1 or Kv6.1 in Xenopus oocytes modulated channel gating, with Kv5.1 accelerating inactivation and Kv6.1 shifting steady-state activation.
Kv5.1 and Kv6.1 function as regulatory alpha-subunits that modulate Kv2.1 channel gating in distinct, physiologically relevant ways.
We have determined the effects of coexpression of Kv2.1 with electrically silent Kv5.1 or Kv6.1 alpha-subunits in Xenopus oocytes on channel gating. Kv2.1/5.1 selectively accelerated the rate ofinactivation at intermediate potentials (-30 to 0 mV), without affecting the rate at strong depolarization (0 to +40 mV), and markedly accelerated the rate of cumulative inactivation evoked by high-frequency trains of short pulses. Kv5.1 coexpression alsoslowed deactivation of Kv2.1. In contrast, Kv6.1 was much less effective in speeding inactivation at intermediate potentials, had a slowing effect on inactivation at strong depolarizations, and had no effect on cumulative inactivation. Kv6.1, however, had profound effects on activation, including a negative shift of the steady-state activation curve and marked slowing of deactivation tail currents. Support for the notion that the Kv5.1's effects stem from coassembly of alpha-subunits into heteromeric channels was obtained from biochemical evidence of protein-protein interaction and single-channel measurements that showed heterogeneity in unitary conductance. Our results show that Kv5.1 and Kv6.1 function as regulatory alpha-subunits that when coassembled with Kv2.1 can modulate gating in a physiologically relevant manner.
Kramer et al. (Mon,) reported a other. Coexpression of Kv2.1 with Kv5.1 or Kv6.1 alpha-subunits was evaluated on Channel gating (inactivation and activation rates). Coexpression of Kv2.1 with Kv5.1 or Kv6.1 in Xenopus oocytes modulated channel gating, with Kv5.1 accelerating inactivation and Kv6.1 shifting steady-state activation.