| Project/Area Number |
24790192
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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 |
General anatomy (including Histology/Embryology)
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| Research Institution | Nagoya University |
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Principal Investigator |
INUTSUKA Ayumu 名古屋大学, 環境医学研究所, 研究員 (30584776)
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| Co-Investigator(Renkei-kenkyūsha) |
KISHI Masashi 新潟大学, 医歯学総合研究科, 准教授 (60573938)
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| Project Period (FY) |
2012-04-01 – 2014-03-31
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2013: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2012: ¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000)
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| Keywords | 神経突起 / 形態形成 / Ser/Thrキナーゼ / 細胞骨格 / キナーゼ / ゴルジ染色 |
|---|
| Research Abstract |
Neurite branching is a critical determinant of nervous system function, but the intracellular molecular mechanisms which regulate neurite branching remain poorly understood. To investigate the function of kinases in the regulation of neurite branching, we undertook qPCR screening and identified a kinase (BrancK) that is strongly enriched in brain. We found that elevation of BrancK activity in primary hippocampal neurons increased neurite number and promoted neurite branching, while these effects were not induced by kinase-dead mutant of BrancK. Consistent with these findings, neurons of BrancK KO mice show reduced dendritic arborization in both the CNS and PNS. We also indentified binding proteins by yeast two-hybrid system. Our findings suggest that BrancK play an important role in regulating neurite branching in vivo.
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