REGULATORY MECHANISM OF FUNCTION IN PHYSICAL EXERCISE BY A GROUP OF PROTEASES
| Project/Area Number |
21591899
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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 |
Orthopaedic surgery
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| Research Institution | Kobe International University |
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Principal Investigator |
KOBAYASHI Toshihiro 神戸国際大学, リハビリテーション学部・理学療法学科, 准教授 (40153621)
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| Co-Investigator(Kenkyū-buntansha) |
MITSUI Shinichi 群馬大学, 大学院・保健学研究科, 教授 (20295661)
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| Project Period (FY) |
2009 – 2011
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| Project Status |
Completed (Fiscal Year 2011)
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| Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2011: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2010: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2009: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Keywords | シナプス / セリンプロテアーゼ / プラスミノーゲンアクチベータ / プロテアーゼ / モトプシン / 脊髄運動ニューロン / 軸索再生 / 運動機能 / 運動障害 / 遺伝子欠損マウス / スピネシン |
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| Research Abstract |
The overexpression of serine protease inhibitor, protease nexin-1, in motor neurons in the anterior horn causes abnormal structure of neuromuscular junctions(NMJ). However, the deletion of either tissue plasminogen activator(tPA) or motopsin gene, which encodes a serine protease secreted by motor neurons in the anterior horn, shows no effect on motor function. This suggests that these proteases compensate dysfunction each other. We produced double knockout mice lacking both tPA and motopsin genes, to analyze the proteolytic function on the development of the neuromuscular junction. Double knockout mice appeared to move comparable to heterogenic mice and show normal morphology of acetylcholine receptors at the NMJ. Detailed analyses should be necessary to reveal proteolytic functions on the NMJ formation.
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Report
(4 results)
Research Products
(5 results)
