Project/Area Number |
21790856
|
Research Category |
Grant-in-Aid for Young Scientists (B)
|
Allocation Type | Single-year Grants |
Research Field |
Neurology
|
Research Institution | 財団法人東京都医学研究機構 (2010) National Center of Neurology and Psychiatry (2009) |
Principal Investigator |
HIGASHI Shinji 財団法人東京都医学研究機構, 東京都精神医学総合研究所, 研究員 (30365647)
|
Co-Investigator(Renkei-kenkyūsha) |
ISEKI Eu 順天堂大学, 医学部, 教授 (30203061)
MOORE Darren ローザンヌ工科大学, ブレインマインド研究所, 准教授
|
Project Period (FY) |
2009 – 2010
|
Project Status |
Completed (Fiscal Year 2010)
|
Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2010: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2009: ¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000)
|
Keywords | 神経分子病態学 / パーキンソン病 / 神経変性 / GIGYF2 / インスリンシグナル / Grb10 |
Research Abstract |
GIGYF2 has been reported as a candidate gene for PARK11-linked Parkinson's disease (PD). GIGYF2 was widely expressed, most highly in the pancreas and testis, and moderately in brain. GIGYF2 was present in Rab4-positive endosomes. Expression of GIGYF2 altered insulin-like growth factor-1 (IGF-1) receptor trafficking and enhanced IGF-1-induced ERK1/2 activation. We failed to find any differences in IGF-1-induced signaling between cells expressing wild-type and mutant GIGYF2 and observed only minimal expression of GIGYF2 in the nigrostriatal pathway, indicating no contribution of GIGYF2 to the pathogenesis of PD.
|