| Project/Area Number |
15K07044
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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 |
Cell biology
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| Research Institution | Mukogawa Women's University |
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Principal Investigator |
Habu Toshiyuki 武庫川女子大学, 生活環境学部, 准教授 (70346071)
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| Co-Investigator(Renkei-kenkyūsha) |
KOIZUMI Akio 京都大学, 医学研究科, 教授 (50124574)
KOBAYASHI Hatasu 中部大学, 生命健康科学部, 准教授 (70542091)
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2017: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000)
Fiscal Year 2016: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2015: ¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
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| Keywords | モヤモヤ病 / オートファジー / 脂質代謝 / 酸素環境 / 低酸素環境 / 脂肪滴 / 血管内皮細胞 |
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| Outline of Final Research Achievements |
P.R4810K of RNF213 (mysterin: rs112735431), which is an AAA(+) ATPase, is the susceptibility polymorphism for moyamoya disease (MMD) in East Asians. However, the role of RNF213 R4810K in the etiology of MMD is unknown.To clarify the role of RNF213, RNF213 overexpressed in human culture cells was subjected to microscopic analysis. Using various mutated RNF213 overexpressing cells, morphological cahanges of autopagosomes were found and mobility of cells movement were largely different between wt of RNF213 and SNPs, mutants .RNF213 protein function in moyamoya disease was still unknown but from this analysis we concluded SNPs of this disease might affect the interaction of intermolecule RNF213 domain.
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