Science Signaling Podcast for 9 May 2017: Trafficking of BK channel subunits in arterial myocytes.
Science Signaling Podcast for 9 May 2017: Trafficking of BK channel subunits in arterial myocytes.
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2017 年 5 月 9 日科学信号播客：动脉肌细胞中 BK 通道亚基的运输。
DOI：
10.1126/scisignal.aan4849
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发表时间：
2017
影响因子：
7.3
通讯作者：
VanHook,AnnalisaM
中科院分区：
文献类型：
--
作者：
Jaggar,JonathanH;VanHook,AnnalisaM
This Podcast features a conversation with Jonathan Jaggar, senior author of a Research Article that appears in the 9 May 2017 issue ofScience Signaling, about trafficking of big potassium (BK) channel subunits in arterial myocytes.动脉肌细胞膜的去极化导致细胞内钙的升高，刺激细胞收缩，从而导致血管收缩。膜去极化还会激活 BK 通道，使钾流出细胞，从而使膜重新极化并促进血管舒张。莱奥特等人。发现这种负反馈机制的一个关键方面是将调节性 β1 BK 通道亚基运输到质膜。 Membrane depolarization caused the β1 subunit to translocate to the plasma membrane, where it associated with the pore-forming α subunit to increase the calcium sensitivity of the channel.这些发现将调节亚基的运输确定为多亚基离子通道的调节模式。收听播客
This Podcast features a conversation with Jonathan Jaggar, senior author of a Research Article that appears in the 9 May 2017 issue ofScience Signaling, about trafficking of big potassium (BK) channel subunits in arterial myocytes. Depolarization of the arterial myocyte membrane causes a rise in intracellular calcium that stimulates the cell to contract, which leads to vasoconstriction. Membrane depolarization also activates BK channels, which allow potassium to flow out of the cell, thus repolarizing the membrane and promoting vasodilation. Leoet al. found that a critical aspect of this negative feedback mechanism was the trafficking of the regulatory β1 BK channel subunit to the plasma membrane. Membrane depolarization caused the β1 subunit to translocate to the plasma membrane, where it associated with the pore-forming α subunit to increase the calcium sensitivity of the channel. These findings identify trafficking of regulatory subunits as a mode of regulation for multisubunit ion channels.Listen to Podcast