Intracellular transport of DISC1/Neuregulin-1 and schizophrenia
Project/Area Number |
23700443
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Research Category |
Grant-in-Aid for Young Scientists (B)
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Allocation Type | Multi-year Fund |
Research Field |
Neurochemistry/Neuropharmacology
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Research Institution | Nagoya University |
Principal Investigator |
MORI Daisuke 名古屋大学, 医学系研究科, COE 特任講師 (00381997)
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Project Period (FY) |
2011 – 2012
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Project Status |
Completed (Fiscal Year 2012)
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Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2012: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2011: ¥3,380,000 (Direct Cost: ¥2,600,000、Indirect Cost: ¥780,000)
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Keywords | 分子 / 細胞 / 神経生物学 / 統合失調症 / DISC1 / ニューレグリン / Neuregulin-1 |
Research Abstract |
We hypothesized that DISC1 would be involved in vesicular transport of various proteins and mRNAs which maintain neuronal function. Previously, we have identified direct interaction of DISC1 and Neuregulin-1, which is a ligand of ErbB3 and ErbB4. To understand the sense of their association, we have attempted to analyze their common interacting proteins. As a result of the comprehensive screenings, we have identified AP family proteins, which have essential roles for intracellular vesicle trafficking. Moreover, we have established a new experimental system that enables us to quantify the secretion of processed Neuregulin-1 by immunoblotting. We found that the processed Neuregulin-1 was decreased in cultured hippocampal neuron from DISC1-deficient mice. 交付決定額
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Report
(3 results)
Research Products
(4 results)
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[Journal Article] Behavioral alterations associated with targeted disruption of exons 2 and 3 of the Disc1 gene in the mouse2011
Author(s)
K Kuroda, S Yamada, M Tanaka, M Iizuka, H Yano, D Mori, D Tsuboi, T Nishioka, T Namba, Y Iizuka, S Kubota, T Nagai, D Ibi, R Wang, A Enomoto, M Isotani-Sakakibara, N Asai, K Kimura, H Kiyonari, T Abe, A Mizoguchi,M Sokabe, M Takahashi, K Yamada, K Kaibuchi
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Journal Title
Human molecular genetics
Volume: 20
Issue: 23
Pages: 4666-4683
DOI
Related Report
Peer Reviewed
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