| Project/Area Number |
24700357
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Nerve anatomy/Neuropathology
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| Research Institution | Keio University |
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Principal Investigator |
Honda Takao 慶應義塾大学, 医学部, 助教 (30365225)
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| Project Period (FY) |
2012-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2014: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2013: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2012: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | Reelin / Dab1 / reeler / yotari / NLS / NES / 核細胞質間シャトリング / 樹状突起形成 / 樹状突起 / reelin / dab1 |
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| Outline of Final Research Achievements |
As we have found that Dab1 is involved in dendrite formation and is subject to nucleocytoplamic shuttling, we hypothesized that Dab1 might regulate the dendrite formation through the regulation of gene expression. To examine this hypothesis, we expressed a candidate gene to dab1-knockdonwed neurons, and found that a candidate gene could partially rescue the abnormal dendrite formation. Because of no significant difference in Dab1 protein amount in reeler, we next examined whether the candidate molecule could enhance a putative dendrite formation signal by Dab1-signaling pathway. Dissociated neurons with or without knockdown plasmids against the candidate molecule were treated with Reelin, and Dab1 tyrosine phosphorylation, a plausible target of the candidate molecule, was compared. However, we could not detect a significant difference of the level, suggesting that the dendrite formation rescue effects by the candidate molecule might be caused by other regulation mechanism.
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