Voltage‐dependent inactivation of the human K+ channel KvLQT1 is eliminated by association with minimal K+ channel (minK) subunits
M Tristani‐Firouzi, MC Sanguinetti - The Journal of physiology, 1998 - Wiley Online Library
The Journal of physiology, 1998•Wiley Online Library
1 The time course and voltage dependence of inactivation of KvLQT1 channels expressed in
Xenopus oocytes were studied using two‐microelectrode voltage‐clamp techniques. 2 Tail
current analysis was used to characterize the kinetics of channel inactivation and
deactivation. The time constant for recovery from channel inactivation was voltage
dependent and varied from 30±2 ms at− 90 mV to 36±1 ms at− 30 mV. The time constant for
deactivation varied from 186±21 to 986±43 ms over the same voltage range. 3 Inactivation …
Xenopus oocytes were studied using two‐microelectrode voltage‐clamp techniques. 2 Tail
current analysis was used to characterize the kinetics of channel inactivation and
deactivation. The time constant for recovery from channel inactivation was voltage
dependent and varied from 30±2 ms at− 90 mV to 36±1 ms at− 30 mV. The time constant for
deactivation varied from 186±21 to 986±43 ms over the same voltage range. 3 Inactivation …
- 1The time course and voltage dependence of inactivation of KvLQT1 channels expressed in Xenopus oocytes were studied using two‐microelectrode voltage‐clamp techniques.
- 2Tail current analysis was used to characterize the kinetics of channel inactivation and deactivation. The time constant for recovery from channel inactivation was voltage dependent and varied from 30 ± 2 ms at −90 mV to 36 ± 1 ms at −30 mV. The time constant for deactivation varied from 186 ± 21 to 986 ± 43 ms over the same voltage range.
- 3Inactivation of KvLQT1 channels was incomplete, reducing fully activated current by 35 % at +40 mV. Inactivation of KvLQT1 channels was half‐maximal at −18 ± 2 mV.
- 4The onset of KvLQT1 channel inactivation during a single depolarization to +20 mV was exponential (τ= 130 ± 10 ms), and developed after a delay of ≈75 ms. In contrast, when inactivation was reinduced following transient recovery of channels to the open state(s), the onset of inactivation was immediate and 10 times faster. These findings suggest multiple open states, and a sequential gating model for KvLQT1 channel activation and inactivation (C1⇌ Cn⇌ O1⇌ O2⇌ I).
- 5Delayed rectifier K+ (IKs) channels formed by heteromultimeric coassembly of KvLQT1 and minimal K+ channel (minK) subunits did not inactivate. Thus, minK subunits eliminate, or greatly slow, the gating associated with channel inactivation when coassembled with KvLQT1.
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