| Project/Area Number |
20500324
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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 |
Nerve anatomy/Neuropathology
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| Research Institution | Nagasaki University |
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Principal Investigator |
YAMAGUCHI Naohiro Nagasaki University, 病院, 医員 (40432976)
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| Co-Investigator(Kenkyū-buntansha) |
UEZONO YASUHITO 国立がんセンター研究所, がん患者病態生理研究部, 部長 (20213340)
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| Project Period (FY) |
2008 – 2010
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| Project Status |
Completed (Fiscal Year 2010)
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| Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2010: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2009: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2008: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Keywords | 神経変性疾患 / プリオン / プリオン蛋白質(PrP) / Doppel(Dpl) / Shadoo(sho) / 神経変性死 / 代謝型グルタミン酸受容体 / mGluR1 / 細胞内Ca2+オーバーロード / 免疫沈降 / プリオン蛋白質PrP / 蛍光共鳴エネルギー移動(FRET) / 代謝型グルタミン酸受容体I型(mGluR1) |
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| Research Abstract |
In this study, We proved that the Prion protein(PrP) bind to the glutaminic acid receptor type I (mGluR1) which regulated the Ca2+ in nerve cells. So the function of PrP is to regulate the Ca2+ in the cell by interacting with mGluR1 receptor, and this suggests that neuronal degeneration is caused by the adjustment this mechanism's failure. The Purkinje cell death in the PrP knockout mouse (Ngsk Prnp-/-) and the neurodegeneration of prion disease might be caused by this mechanism. In addition, We cloned a new PrP intracting gene : plasmalemma vesicle associated protein (Plvap/PV-1) by expression cloning method using the cDNA library from mouse brain. Additionally we proved that Dpl which is homolog of PrP isn't influenced prion infection, and Shadoo which is another homolog of PrP may promote accumulation of PrPSc(abnormal type of Prion protein) in culture cell systems.
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