Regulation of expression of K+ channel by degradation
| Project/Area Number |
22590218
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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 | Kansai Medical University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
MATSUDA Hiroko 関西医科大学, 医学部, 教授 (10181736)
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| Project Period (FY) |
2010 – 2012
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| Project Status |
Completed (Fiscal Year 2012)
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| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2012: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2011: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000)
Fiscal Year 2010: ¥3,120,000 (Direct Cost: ¥2,400,000、Indirect Cost: ¥720,000)
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| Keywords | 内向き整流性 K+チャネル / 分解 / ホメオスタティック制御 / Kir2.1 / SNAPタグ / 蛍光タイマー / K+チャネル / 蛍光タンパク / 内向き整流性K+チャネル / タンパク分解 |
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| Research Abstract |
We examined the regulation of degradation of strongly inwardly rectifying potassium channel (Kir2.1), using new techniques of fluorescent proteins, i.e., SNAP-tag and fluorescent timer (FT). We found the half-life of Kir2.1 changes depending on the expression level, namely current level. Patch-clamp recording showed that the cultivation under the blockade of the channel increased the whole cell conductance of Kir2.1. These results suggest the homeostatic degradation of Kir2.1 in the 293T cells, and the usefulness of fluorescence-based methods for examining the degradation of ion channels.
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Report
(4 results)
Research Products
(13 results)
