Structure and function of mitochondrial ATP-sensitive K^+ channel.

线粒体 ATP 敏感 K^ 通道的结构和功能。

基本信息

  • 批准号:
    11670080
  • 负责人:
  • 金额:
    $ 2.43万
  • 依托单位:
  • 依托单位国家:
    日本
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
  • 财政年份:
    1999
  • 资助国家:
    日本
  • 起止时间:
    1999 至 2000
  • 项目状态:
    已结题

项目摘要

ATP-sensitive K^+ (K_<ATP>) channels open and close depending on ATP concentration in the cytoplasm, and control excitability of the cells. We have previously shown that K_<ATP> channel of pancreatic β-cell comprises SUR1, a member of ABC protein, and Kir6.2, a member of inward rectifier K channels. In heart and skeletal muscles, and blood vessels, K_<ATP> channels of similar properties comprise SUR2A/B and Kir6.x, regulating muscle contraction during hypoxia or ischemia.Although similar K_<ATP> channel is expressed in mitochondria, and regulating energy metabolism, its constituting molecules are unknown.Using the patch-clamp technique, we recorded ion channel activity from the mitochondrial inner membrane of Jurkat cells. K^+ ion selective channels with conductance of 55 pS were observed, of which activity being suppressed by 2 mM ATP.These properties and burst kinetics are similar to the channel comprising Kir6.1 molecule. In other to study if Kir6.1 molecules are induced during hypo … More xia, A7r5 cells, derived from blood vessel were cultured in medium containing Co^<2+> ions, mimicking hypoxic conditions. Western blotting using anti Kir6.1 antibody revealed that Kir6.1 protein became expressed in 3-4 days after an addition of the ions. However, no activity of channels comprising activity Kir6.1 was observed in the plasma membrane of heart of blood vessel muscles. Following these results, a possibility that Kir6.1 molecule induced in ischemia composes mitochondrial K_<ATP> channel is currently investigated.In other series of experiments effects of protein kinase A mediated phosphorylation of K_<ATP> channels comprising SUR1 and Kir6.2 were studied. We found both subunits are phosphorylated and channel properties are modulated in a different manner.Finally, effects of anti-diabetic reagents, troglitazone, pioglitazone, and KAD-1229, were studied on reconstituted K_<ATP> channels. The studies are helpful in understanding structure-function relationship of K_<ATP> channels in the plasma membrane as well as mitochondria. Less
ATP敏感性K^+(K_<ATP>)通道依赖于细胞质中ATP浓度的变化而开放和关闭,并控制细胞的兴奋性。胰腺<ATP>β细胞钾通道由ABC蛋白SUR 1和内向整流钾通道Kir6.2组成。在心肌、骨骼肌和血管中,<ATP>具有相似特性的K_通道包括SUR 2A/B和Kir6.x,它们在缺氧或缺血时调节肌肉收缩,虽然类似的K_<ATP>通道在线粒体中表达,并调节能量代谢,但其组成分子尚不清楚。结果表明,K^+离子选择性通道的电导率为55 pS,其活性可被2 mM ATP抑制,这些特性和爆发动力学与Kir6.1分子组成的通道相似。在另一项研究中,如果Kir6.1分子在低血糖期间被诱导, ...更多信息 将来源于血管的A7 r5细胞在含有Co^2+离子的培养基中培养,模拟缺氧条件。用抗Kir6.1抗体进行的Western blotting显示,Kir6.1蛋白在加入离子后3-4天开始表达。然而,在血管肌肉的心脏的质膜中没有观察到包含活性Kir6.1的通道的活性。在此基础上,进一步探讨了缺血诱导的Kir6.1分子参与线粒体K_通道的可能性<ATP>,并进一步研究了蛋白激酶A(PKA)介导的K_2通道磷酸化的作用<ATP>。最后,研究了抗糖尿病药物曲格列酮、吡格列酮和KAD-1229对重构钾通道的影响<ATP>。这些研究有助于理解质膜和线粒体K通道的结构与功能关系<ATP>。少

项目成果

期刊论文数量(15)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
Sunaga,Y. 他: "Troglitazone but not poiglitazone affects ATP-sensitive K+ channel activity."Eur.J.Pharmacol.. 381. 71-76 (1999)
Sunaga, Y. 等人:“曲格列酮影响 ATP 敏感的 K+ 通道活性,但聚格列酮不影响。”Eur.J.Pharmacol.. 381. 71-76 (1999)
  • DOI:
  • 发表时间:
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  • 影响因子:
    0
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  • 通讯作者:
J. Kawaki, T. Gonoi 他: "Unresponsiveness to glibenclamide during chronic treatment induced by reduction of ATP-sensitive K^+ channel activity"Diabetes. 48. 2001-2006 (1999)
J. Kawaki、T. Gonoi 等人:“由于 ATP 敏感性 K^+ 通道活性降低而导致慢性治疗期间对格列本脲无反应”,糖尿病。 48. 2001-2006 (1999)
  • DOI:
  • 发表时间:
  • 期刊:
  • 影响因子:
    0
  • 作者:
  • 通讯作者:
Sunaga Y, et al.: "Troglitazone but not poiglitazone affects ATP-sensitive K^+ channel activity."Eur.J.Pharmacol.. 381. 71-76 (1999)
Sunaga Y 等人:“曲格列酮而不是聚格列酮影响 ATP 敏感的 Kk 通道活性。”Eur.J.Pharmacol.. 381. 71-76 (1999)
  • DOI:
  • 发表时间:
  • 期刊:
  • 影响因子:
    0
  • 作者:
  • 通讯作者:
T.Gonoi, S.Seino 他: "Structure and function of ATP-sensitive K^+ channels. in Handbook of Experimental pharmacology "Pharmacology of Ioninc Channel Function: Activators and Inhibitors" (Edt. Endo, M.)"Springer-Verlag (Berlin). 25 (2000)
T.Gonoi,S.Seino 等人:“ATP 敏感 K^+ 通道的结构和功能。实验药理学手册“离子通道功能的药理学:激活剂和抑制剂”(Edt. Endo,M.)”Springer -出版社(柏林)25(2000)。
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    0
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GONOI Tohru其他文献

GONOI Tohru的其他文献

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{{ truncateString('GONOI Tohru', 18)}}的其他基金

Search for new virulence factors in Aspergillus fumigatus: Molecular biological analysis of carbohydrate recognition proteins
寻找烟曲霉新的毒力因子:碳水化合物识别蛋白的分子生物学分析
  • 批准号:
    24659479
  • 财政年份:
    2012
  • 资助金额:
    $ 2.43万
  • 项目类别:
    Grant-in-Aid for Challenging Exploratory Research
Search and collection of pathogenic fungi and actinomycetes in areas with high incidents of AIDS patients.
艾滋病高发地区病原真菌和放线菌的查找和采集。
  • 批准号:
    21406003
  • 财政年份:
    2009
  • 资助金额:
    $ 2.43万
  • 项目类别:
    Grant-in-Aid for Scientific Research (B)
CLONING OF T-TYPE CALCIUM CHANNEL GENE
T型钙通道基因的克隆
  • 批准号:
    04670108
  • 财政年份:
    1992
  • 资助金额:
    $ 2.43万
  • 项目类别:
    Grant-in-Aid for General Scientific Research (C)

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