| Project/Area Number |
17570130
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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 |
Biophysics
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| Research Institution | Nagoya University |
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Principal Investigator |
TATSUMI Hitoshi Nagoya University, Graduate school of Medicine, Associate Professor (20171720)
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| Co-Investigator(Kenkyū-buntansha) |
SOKABE Masahiro Nagoya University, Graduate school of Medicine, Professor (10093428)
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| Project Period (FY) |
2005 – 2006
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| Project Status |
Completed (Fiscal Year 2006)
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| Budget Amount *help |
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2006: ¥1,700,000 (Direct Cost: ¥1,700,000)
Fiscal Year 2005: ¥1,800,000 (Direct Cost: ¥1,800,000)
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| Keywords | Mechano-sensor / actin / cofilin / single molecule / mechanical stimuli / molecular machinery / depolvmerization / cytoskeleton / ADF / 光ピンセット / 力学受容 / 張力 / 分子機構 |
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| Research Abstract |
Wide range of biological roles have been proposed for "force" in cell biology, including cell signal pathways for survival, development, wound healing, and growth. It is generally believed that force initiates signal transduction via stretch activated ion channels in the membrane, but recently it is suggested that force may also initiate signal transduction via changes in cytoskeletal-matrix linkages. Cells may use mechanisms other than ion channels to sense forces such as an actin filament. This study directly demonstrate that a single actin filament works as a mechano-sensor and regulates the enzymatic activity of cofilin by employing an in vitro reconstituted system ; we have prepared a single actin filament stretched with optical tweezers and applied cofilin to it in the presence or absence of mechanical tension in the filament. Surprisingly, it demonstrated that mechanical tension in the single actin filament prevented it from the severing by cofilin, providing a strong support for the model in which the actin filament acts as a tension-sensor and regulates the severing ability of cofilin in a tension-dependent manner. This is the first demonstration that tension in a certain protein regulates the susceptibility to the modulating proteins. We examined the molecular mechanism underlying this peculiar property of actin filament, and also demonstrate data that this mechanism works in living cells.
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