| Project/Area Number |
21790281
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
General medical chemistry
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| Research Institution | Kumamoto University (2010)
Kyushu University (2009) |
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Principal Investigator |
HAMADA Koichi Kumamoto University, エイズ学研究センター, 特定事業研究員 (00343070)
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| Project Period (FY) |
2009 – 2010
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| Project Status |
Completed (Fiscal Year 2010)
|
| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2010: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2009: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | 細胞増殖 / 細胞死 / セリンプロテアーゼ / 炎症 / 胎生致死 / 遺伝子改変マウス / プロテアーゼ |
|---|
| Research Abstract |
Innate immune responses are vital for pathogen defense but can result in septic shock when excessive. A key mediator of septic shock is TNFα, which is shed into intercellular spaces after cleavage from the plasma membrane by the protease TACE. Here we report that the rhomboid family member RHBDF2 interacts with TACE and regulates TNFαshedding in vitro and in vivo. Our study has identified RHBDF2 as a novel regulator of innate immunity that may be an important target for modulating sepsis and pathogen defense.
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