Cation transport in mitochondria - The potassium cycle
Cation transport in mitochondria - The potassium cycle
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DOI：
10.1016/0005-2728(96)00061-8
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发表时间：
1996-07-18
影响因子：
4.3
通讯作者：
Garlid, KD
中科院分区：
文献类型：
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作者：
Garlid, KD
线粒体中存在独立的、高度调控的K+内流和外排途径，这强烈表明线粒体体积在体内受到调控。体积，反过来，已被证明调节电子传递链的活性。因此，线粒体K+循环似乎在调节细胞生物能量学（包括脂肪酸的代谢命运）中起着关键的信号作用。与此作用一致的是，该通道被长链酰基辅酶a酯抑制，并被GTP激活，这些配体与面对细胞质的位点相互作用。这些工作表明，来自线粒体和质膜的K-ATP通道受到相同的生化和药理学配体的调节。我们假设线粒体K- atp通道和质膜上的K- atp通道一样，是异多聚体，由一个调节性磺酰脲受体（mitoSUR）和一个向内整流的K+通道（mitoKIR）组成。
The existence in mitochondria of separate, highly regulated pathways for K+ influx and efflux strongly implies that mitochondrial volume is subject to regulation in vivo. Volume, in turn, has been shown to regulate activity of the electron transport chain. Thus, the mitochondrial K+ cycle appears to play a key signalling role in regulating cellular bioenergetics, including the metabolic fate of fatty acids. Consistent with this role, the channel is inhibited by long-chain acyl-CoA esters and activated by GTP, and these Ligands interact with sites that face the cytosol. The work to be summarized shows that K-ATP channels from mitochondria and plasma membranes are regulated by the same biochemical and pharmacological ligands. We hypothesize that the mitochondrial K-ATP channel, like its counterparts in the plasma membrane, is heteromultimeric, consisting of a regulatory sulfonylurea receptor (mitoSUR) and an inward-rectifying K+ channel (mitoKIR).