Study for the mechanism of N-cadherin endocytosis in synapse
| Project/Area Number |
15K18361
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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 | National Institute for Physiological Sciences |
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Principal Investigator |
NAGAOKA Tadahiro 生理学研究所, 生体機能調節研究領域, 特別協力研究員 (70634864)
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| Project Period (FY) |
2015-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2016: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2015: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
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| Keywords | カドヘリン / 平面内細胞極性因子 / Nカドヘリン / 細胞内平面極性 / シナプス |
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| Outline of Final Research Achievements |
Planar cell polarity protein Vangl2 regulates cell surface expression level of N-cadherin at synapse. To resolve this mechanism is major object of this project. PSD-95 is scaffold protein of post synapse and is shown that complementary localization with N-cadherin in normal neuron. PSD-95 is known as the binding partner of Vangl2 and Vangl2 may responsible for stabilization of PSD-95 localization at the synapse. Because PSD-95 puncta density was decreased and its signal was diffused in dendrite in Vangl2 knockdown neuron. Furthermore, merged localization of PSD-95 and N-cadherin was increased abnormally in Vangl2 knockdown neuron. Therefore we suggested that Vangl2 may regulate proper compartmentalization of PSD-95 and N-cadherin. We also investigate genetic interaction between Vangl2 and N-cadherin and that caused neural tube closure defect.
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Report
(3 results)
Research Products
(5 results)
