锚蛋白调节可兴奋细胞中 KATP 通道的膜运输和门控。
Ankyrin regulates KATP channel membrane trafficking and gating in excitable cells.
机构信息
Department of Internal Medicine, Division of Cardiovascular Medicine, University of Iowa Carver College of Medicine, Iowa City, IA, USA.
出版信息
Channels (Austin). 2010 Jan-Feb;4(1):55-7. doi: 10.4161/chan.4.1.10362. Epub 2010 Jan 16.
Abstract
K(ATP) channels play critical roles in many cellular functions by coupling cell metabolic status to electrical activity. First discovered in cardiomyocytes,(1) K(ATP) channels (comprised of Kir6.x and SUR subunits) have since been found in many other tissues, including pancreatic beta cells, skeletal muscle, smooth muscle, brain, pituitary and kidney. By linking cellular metabolic state with membrane potential, K(ATP) channels are able to regulate a number of cellular functions such as hormone secretion, vascular tone and excitability. Specifically, a reduction in metabolism causes a decrease in the ATP:ADP ratio, opening of K(ATP) channels, K(+) efflux, membrane hyperpolarization, and suppression of electrical activity. Conversely, increased cellular metabolism causes an increase in the ATP:ADP ratio that leads to closure of the K(ATP) channel, membrane depolarization, and stimulation of cell electrical activity.
摘要
K(ATP) 通道通过将细胞代谢状态与电活动偶联，在许多细胞功能中发挥关键作用。K(ATP) 通道最初在心肌细胞中被发现，（1）由 Kir6.x 和 SUR 亚基组成，此后在许多其他组织中也被发现，包括胰岛β细胞、骨骼肌、平滑肌、脑、垂体和肾脏。通过将细胞代谢状态与膜电位联系起来，K(ATP) 通道能够调节许多细胞功能，如激素分泌、血管张力和兴奋性。具体来说，代谢的减少会导致 ATP:ADP 比例的降低，从而打开 K(ATP) 通道，导致 K(+)外流，膜超极化，并抑制电活动。相反，细胞代谢的增加会导致 ATP:ADP 比例的增加，从而导致 K(ATP) 通道关闭，膜去极化，并刺激细胞电活动。
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