| Project/Area Number |
25830049
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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 |
Neurochemistry/Neuropharmacology
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| Research Institution | Nagoya University |
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Principal Investigator |
NAKAMUTA Shinichi 名古屋大学, 医学(系)研究科(研究院), 助教 (20647474)
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| Project Period (FY) |
2013-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2014: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2013: ¥3,120,000 (Direct Cost: ¥2,400,000、Indirect Cost: ¥720,000)
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| Keywords | 神経細胞 / 軸索 / 樹状突起 / 細胞接着 / 細胞外因子 / CaMKs / 軸索形成 / 神経栄養因子 / 接着因子 / TAG-1 |
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| Outline of Final Research Achievements |
Neurons are highly polarized cells that have structurally distinct processes―the axons and dendrites― that differentiate from common immature neurites. Various extracellular and intracellular signals contribute to axon specification; however, the specific intracellular pathways whereby particular extracellular stimuli lead to axon specification remain to be delineated. From our research, we found that the TAG-1-mediated cell-to-cell interaction between the unpolarized multipolar cells and the pioneering axons regulates the polarization of multipolar cells partly through Rac1. Recently, we identified the Rho guanine nucleotide exchange factor H1 (GEF-H1/ARHGEF2) as one of the CaMKs substrates in hippocampal neurons. GEF-H1 can be sequestered in an inactive state on polymerized microtubules. We identified the GEF-H1 phosphorylation site in the N-terminal region. GEF-H1 N-terminal region regulate its binding towards microtubules, thereby regulating the GEF activity.
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