| Project/Area Number |
26670121
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
General pharmacology
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| Research Institution | Nagoya University |
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Principal Investigator |
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| Co-Investigator(Renkei-kenkyūsha) |
ITOH Norimichi 名古屋大学, 医学部附属病院, 特任助教 (30726310)
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| Project Period (FY) |
2014-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
Fiscal Year 2015: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2014: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | ＩＦＩＴＭ３ / アストロサイト / ＲａｂＧＤＩ / Ｆｓｔｌ１ / 神経発達障害 / 神経科学 / 脳神経疾患 / IFITM3 / RabGDI |
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| Outline of Final Research Achievements |
We have demonstrated that interferon-induced transmembrane protein 3 (IFITM3) in astrocytes plays a crucial role in neurodevelopmental impairment in polyIC-treated mouse model of perinatal neuroinflammation. In this study, RabGDI was identified as a novel binding protein of IFITM3. Furthermore, we observed that overexpression of IFITM3 in COS7 cells resulted in an increase in the size of intracellular vesicles, probably due to an increase in Rab5 activity through the interaction with RabDGI. These findings suggest that IFITM3 facilitates the formation of multi-vesicular body (MVB), by regulating Rab5 activity through the interaction with RabGDI.
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