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Mitochondrial K(ATP) channels: probing molecular identity and pharmacology.

作者信息

Terzic A, Dzeja P P, Holmuhamedov E L

出版信息

J Mol Cell Cardiol. 2000 Nov;32(11):1911-5. doi: 10.1006/jmcc.2000.1256.

DOI:10.1006/jmcc.2000.1256
PMID:11040097
Abstract
摘要

相似文献

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Mitochondrial K(ATP) channels: probing molecular identity and pharmacology.线粒体ATP敏感性钾通道:探索分子特性与药理学
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Testosterone induces cytoprotection by activating ATP-sensitive K+ channels in the cardiac mitochondrial inner membrane.睾酮通过激活心脏线粒体内膜上的ATP敏感性钾通道诱导细胞保护作用。
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Effects of inhibitors and activators of ATP-regulated K+ channel on mitochondrial potassium uniport.ATP调节钾通道抑制剂和激活剂对线粒体单向钾转运的影响。
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Ion conduction pore is conserved among potassium channels.离子传导孔在钾通道中是保守的。
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Selective inhibition of inward rectifier K+ channels (Kir2.1 or Kir2.2) abolishes protection by ischemic preconditioning in rabbit ventricular cardiomyocytes.选择性抑制内向整流钾通道(Kir2.1或Kir2.2)可消除兔心室心肌细胞中缺血预处理的保护作用。
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Kir6.1 is the principal pore-forming subunit of astrocyte but not neuronal plasma membrane K-ATP channels.Kir6.1是星形胶质细胞质膜而非神经元质膜K-ATP通道的主要孔形成亚基。
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Adenylate kinase phosphotransfer communicates cellular energetic signals to ATP-sensitive potassium channels.腺苷酸激酶磷酸转移将细胞能量信号传递给ATP敏感性钾通道。
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Multiplicity of effectors of the cardioprotective agent, diazoxide.心脏保护剂二氮嗪的多种效应物。
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Human K(ATP) channelopathies: diseases of metabolic homeostasis.人类 K(ATP)通道病:代谢稳态的疾病。
Pflugers Arch. 2010 Jul;460(2):295-306. doi: 10.1007/s00424-009-0771-y. Epub 2009 Dec 24.
3
Adenine nucleotide translocase mediates the K(ATP)-channel-openers-induced proton and potassium flux to the mitochondrial matrix.
腺嘌呤核苷酸转位酶介导钾离子ATP通道开放剂诱导的质子和钾离子向线粒体基质的通量。
J Bioenerg Biomembr. 2003 Apr;35(2):141-8. doi: 10.1023/a:1023746103401.
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Diazoxide and pinacidil uncouple pyruvate-malate-induced mitochondrial respiration.二氮嗪和平尼地尔可使丙酮酸-苹果酸诱导的线粒体呼吸解偶联。
J Bioenerg Biomembr. 2002 Feb;34(1):49-53. doi: 10.1023/a:1013870704002.
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Restoration of Ca2+-inhibited oxidative phosphorylation in cardiac mitochondria by mitochondrial Ca2+ unloading.
Mol Cell Biochem. 2001 Apr;220(1-2):135-40. doi: 10.1023/a:1010894427373.