| Project/Area Number |
23590366
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Pathological medical chemistry
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| Research Institution | University of the Ryukyus |
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Principal Investigator |
KARIYA Ken-ichi 琉球大学, 医学(系)研究科(研究院), 教授 (40263371)
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| Co-Investigator(Kenkyū-buntansha) |
MARUYAMA Ichiro 沖縄科学技術大学院大学, 情報処理ユニット, 教授 (70426568)
YOSHIMI Naoki 琉球大学, 大学院医学研究科, 教授 (30166996)
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| Co-Investigator(Renkei-kenkyūsha) |
MATSUZAKI Goro 琉球大学, 大学院医学研究科, 教授 (30229455)
KAKEYAMA Masaki 東京大学, 大学院医学研究科, 助教 (30353535)
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| Project Period (FY) |
2011-04-28 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2013: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2012: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2011: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | Rap2 / ノックアウトマウス / 表現型 / ックアウトマウス |
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| Outline of Final Research Achievements |
Rap2 is a Ras-like small G protein. We found that it regulates mitogen-activated kinase kinase kinase kinases (MAP4Ks) upstream of JNK (Rap2-MAP4K system). The Rap2-regulated kinases include Nck-interacting kinase (NIK/HGK)，Traf2- and Nck-interacting kinase (TNIK), and Misshapen/NIKs-related kinase (MINK). The system affects synaptic structure/function of neurons. We have investigated in vivo functions of Rap2 by generating knockout mice. Knockout mice were not embryonic lethal, did not show major deformity, but some were sterile. The null mutation slightly shortened natural life span but did not appear tumorigenic. As expected from interaction of TNIK with a psychiatric disease protein DISC1, knockout mice showed various behavioral abnormalities, especially in interaction with other mice. Their hematopoietic system was generally normal but defective in some T cell subpopulations.
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