Project/Area Number |
19500330
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Neurochemistry/Neuropharmacology
|
Research Institution | Tokai University |
Principal Investigator |
HADANO Shinji (2008-2009) Tokai University, 医学部, 准教授 (60281375)
國田 竜太 (2007) Tokai University, 医学部, 奨励研究員 (90449124)
|
Co-Investigator(Kenkyū-buntansha) |
秦野 伸二 東海大学, 医学部, 准教授 (60281375)
|
Project Period (FY) |
2007 – 2009
|
Project Status |
Completed (Fiscal Year 2009)
|
Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2009: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2008: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2007: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
|
Keywords | 分子 / 細胞 / 神経生物学 / 脳神経疾患 / シグナル伝逹 / 生体膜輸送 / 蛋白質 / 神経科学 / シグナル伝達 / 運動ニューロン疾患 / ALS2 / マクロピノサイトーシス / Rab5 / Rac1 / 筋委縮性側索硬化症 / エフェクター |
Research Abstract |
Amyotrophic lateral sclerosis (ALS) is a heterogeneous group of progressive neurodegenerative disorders characterized by a selective loss of motor neurons in the cerebral cortex, brainstem, and spinal cord. Currently, the mechanism for the selective degeneration of motor neurons is unclear. We focus on the newly-identified ALS causative gene product, called ALS2, and investigate the molecular function of ALS2 and its activators. We here identified Rac1 as a novel ALS2 activator, and revealed that ALS2 plays a role in macropinocytosis and endosome fusion in cells. Our study will contribute to,define the molecular mechanisms underlying the neuronal dysfunction and degeneration in ALS.
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