| Project/Area Number |
21790283
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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 | Kyushu University |
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Principal Investigator |
MIYANO Kei Kyushu University, 医学研究院, 学術研究員 (60444783)
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| Project Period (FY) |
2009 – 2010
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| Project Status |
Completed (Fiscal Year 2010)
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| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2010: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2009: ¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
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| Keywords | NADPHオキシダーゼ / 活性酸素 / Nox2 / gp91^<phox> / 膜タンパク質 / Nox2/gp91^<phox> / Rac / p67^<phox> |
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| Research Abstract |
The phagocyte NADPH oxidase, dormant in resting cells, is activated during phagocytosis to produce superoxide, a precursor of microbicidal oxidants. The catalytic core of the phagocyte oxidase is Nox2/gp91^<phox>, a membrane-spaning protein that forms a stable heterodimer with p22^<phox>. In this study, I found that both N- and C-terminal regions play a crucial role in Nox binding to p22^<phox>. Furthermore, I showed that a short region between the TPR and activation domains in p67^<phox> is crucial for activation of Nox2.
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