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Probing the regulation of TASK potassium channels by PI(45)P2 with switchable phosphoinositide phosphatases

机译:用可转换的磷酸肌醇磷酸酶探索PI(45)P2对TASK钾通道的调节

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摘要

Non-technical summaryThe electrical activity of nerve cells is produced by the flux of ions through specialized membrane proteins called ion channels. Some ion channels can be regulated by the signalling lipid PIP2, a component of the channels’ membrane environment. Here we examine the relevance of PIP2 for the regulation of one specific channel type, termed TASK. Many chemical transmitters in the brain change neural activity by shutting off TASK channels and it has been suggested that this results from reduction of PIP2. By using novel techniques to alter the concentration of PIP2 in living cells, we find that the activity of TASK is independent of PIP2. Besides demonstrating that another signalling mechanism must control the activity of nerve cells via TASK inhibition, we delineate a general approach for clarifying the relevance of PIP2 in many cell types and organs.
机译:非技术总结神经细胞的电活动是由离子流经称为离子通道的专门膜蛋白产生的。某些离子通道可以由信号脂质PIP2调节,该脂质是通道膜环境的组成部分。在这里,我们研究了PIP2与一种称为TASK的特定频道类型的调节的相关性。大脑中的许多化学递质会通过关闭TASK通道来改变神经活动,并且有人认为这是PIP2减少的结果。通过使用新技术来改变活细胞中PIP2的浓度,我们发现TASK的活性独立于PIP2。除了证明另一种信号传导机制必须通过TASK抑制来控制神经细胞的活性外,我们还提出了一种通用的方法来阐明PIP2在许多细胞类型和器官中的相关性。

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