Remodelling of Kir6. x after cardiac Tschemia and its functional consequence
| Project/Area Number |
10670041
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
General physiology
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| Research Institution | KYOTO UNIVERSITY |
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Principal Investigator |
TAKANO Makoto Kyoto University, Graduate School of Medicire, Research Associate, 医学研究科, 助手 (30236252)
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| Project Period (FY) |
1998 – 1999
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| Project Status |
Completed (Fiscal Year 1999)
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| Budget Amount *help |
¥3,800,000 (Direct Cost: ¥3,800,000)
Fiscal Year 1999: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 1998: ¥2,900,000 (Direct Cost: ¥2,900,000)
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| Keywords | Kir6.1 / Kir6.2 / SUR2A / KIR6.1 / KIR6.2 / SUR / ATP sensitive K^+ channel / patch clamp |
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| Research Abstract |
ATP-sensitive KィイD1+ィエD1 channels (KィイD2ATPィエD2) are hetromeric octmer composed of inwardly rectifying KィイD1+ィエD1 channels (Kir6. x) and sulfonylurea receptors (SURx). We have previously reported that amongst the above molecules, Kir6.1 was selectively up-regulated after cardiac ischemia. However, its functional consequences remain unclear. We therefore constucted a cDNA of Kir6.1-Kir6.2 tandem fusion protein (TDM), and coexpressed it with SUR2A in COS7 cells. TDM possessed an intermediate single channel conductance between Kir6.1 and Kir6.2 In the absence of intracellular MgィイD12+ィエD1, TDM and Kir6.2 showed identical ATP sensitivity, whereas in the presence of MgィイD12+ィエD1, the ATP sensitivity of TDM was significantly lower. Thereby, the cardioprotective role of TDM may be enhanced.
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Report
(3 results)
Research Products
(15 results)
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[Publications] Mukai,E.,Ishida,H.,Horie,M.,Noma,A.,Seino,Y.and Takano,M.: "The anti-arnythmic agent cibenzoline inhibits KATP channel by binding to Kir6.2" Biochemical Bio physical Research Communications. 251. 477-481 (1998)
