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首页> 外文期刊>American Journal of Physiology >Increased focal Kv4.2 channel expression at the plasma membrane is the result of actin depolymerization.
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Increased focal Kv4.2 channel expression at the plasma membrane is the result of actin depolymerization.

机译：在质膜上增加的焦点Kv4.2通道表达是肌动蛋白解聚的结果。

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摘要

Voltage-dependent potassium channel trafficking and localization are regulated by proteins of the cytoskeleton, but the mechanisms by which these occur are still unclear. Using human embryonic kidney (HEK) cells as a heterologous expression system, we tested the role of the actin cytoskeleton in modulating the function of Kv4.2 channels. Pretreatment (>or=1 h) of HEK cells with 5 microM cytochalasin D to disrupt the actin microfilaments greatly augmented whole cell Kv4.2 currents at potentials positive to -20 mV. However, no changes in the voltage dependence of activation and inactivation of macroscopic currents were observed to account for this increase. Similarly, single channel recordings failed to reveal any significant changes in the single channel conductance, open probability, and kinetics. However, the mean patch current was increased from 0.9 +/- 0.2 pA in control to 6.7 +/- 3.0 pA in the presence of cytochalasin D. Imaging experiments revealed a clear increase in the surface expression of thechannels and the appearance of "bright spot" features, suggesting that large numbers of channels were being grouped at specific sites. Our data provide clear evidence that increased numbers and altered distribution of Kv4.2 channels at the cell surface are primarily the result of reorganization of the actin cytoskeleton.
机译：电压依赖性钾离子通道的运输和定位受细胞骨架蛋白的调控，但这些机制的发生机制仍不清楚。使用人类胚胎肾脏（HEK）细胞作为异源表达系统，我们测试了肌动蛋白细胞骨架在调节Kv4.2通道功能中的作用。用5 microM细胞松弛素D预处理（>或= 1小时）HEK细胞以破坏肌动蛋白微丝，以-20 mV的正电位极大地增加了全细胞Kv4.2电流。但是，没有观察到宏观电流的激活和失活的电压依赖性变化来解释这种增加。同样，单通道录音无法揭示单通道电导，打开概率和动力学方面的任何重大变化。但是，在存在细胞松弛素D的情况下，平均贴片电流从对照组的0.9 +/- 0.2 pA增加到了6.7 +/- 3.0 pA。成像实验显示通道的表面表达和“亮点”的出现明显增加”功能，这表明在特定网站上已对大量渠道进行了分组。我们的数据提供了明确的证据，表明细胞表面Kv4.2通道数量的增加和分布的改变主要是肌动蛋白细胞骨架重组的结果。

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