Investigation of new signal transduction and cell function of ADAM-type hemorrhagic toxin
| Project/Area Number |
22590061
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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 |
Biological pharmacy
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| Research Institution | Nagoya University |
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Principal Investigator |
ARAKI Satohiko 名古屋大学, 大学院・理学研究科, 講師 (80242808)
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| Co-Investigator(Kenkyū-buntansha) |
SAWADA Hitoshi 名古屋大学, 大学院・理学研究科, 教授 (60158946)
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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 |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2012: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2011: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2010: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | 細胞生物学 / 毒素 / 血管内皮細胞 / ヘビ毒素 / プロテアーゼ / 細胞死 / ADAM / 細胞骨格 / 出血 |
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| Research Abstract |
ADAM-type hemorrhagic toxins induce cell fragmentation on vascular endothelial cells. A signaling molecule was identified as the responsible factor regulating the cell fragmentation, and shown to perform on various cell types. It suggests one of regulating mechanism of cell morphology is clarified.
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Report
(4 results)
Research Products
(11 results)
