Molecular mechanism of neural tube formation by the small GTPase R-Ras
| Project/Area Number |
16H06163
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| Research Category |
Grant-in-Aid for Young Scientists (A)
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| Allocation Type | Single-year Grants |
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| Research Field |
Functional biochemistry
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| Research Institution | Musashino University |
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Principal Investigator |
Ohata Shinya 武蔵野大学, 薬学部, 講師 (00442939)
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| Project Period (FY) |
2016-04-01 – 2019-03-31
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| Project Status |
Completed (Fiscal Year 2019)
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| Budget Amount *help |
¥24,050,000 (Direct Cost: ¥18,500,000、Indirect Cost: ¥5,550,000)
Fiscal Year 2018: ¥7,800,000 (Direct Cost: ¥6,000,000、Indirect Cost: ¥1,800,000)
Fiscal Year 2017: ¥7,800,000 (Direct Cost: ¥6,000,000、Indirect Cost: ¥1,800,000)
Fiscal Year 2016: ¥8,450,000 (Direct Cost: ¥6,500,000、Indirect Cost: ¥1,950,000)
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| Keywords | 神経管形成不全 / R-Ras / 低分子量Gタンパク質 / 神経管 / PCP / Ras / 平面細胞極性 / 低分子領Gタンパク質 / 発生・分化 / 神経科学 / 脳・神経 / 薬学 |
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| Outline of Final Research Achievements |
Neural tube dysplasia, such as spina bifida, is a relatively common neurological disorder. Understanding the pathogenesis of the disease at the molecular level is expected to lead to the development of diagnostic techniques and treatment methods. Cells change their morphology and gene expression status in response to various extracellular stimuli, and this is called signal transduction. In this study, we investigated the molecular mechanism of signal transduction that regulates neural tube formation by focusing on the G protein, which is responsible for turning on and off signal transduction. We found that one of the G proteins, called R-Ras, may regulate neural tube formation in response to the ON/OFF of information transmission through Vangl2, which is involved in the development of neural tube dysplasia.
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| Academic Significance and Societal Importance of the Research Achievements |
神経管の形成は、細胞の非対称性（極性）を制御する分子に変異が起こることによって生じることが知られています。これらの分子がどのように外界からのシグナルに応じて機能するのかは不明でした。本研究では、細胞内のシグナル伝達のON/OFFを切り替えるR-Rasという分子が、細胞極性分子と相互作用することによって神経管形成を担うことを明らかにしました。本研究は、神経管形成不全の診断・予防法開発に貢献することが期待されます。
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Report
(4 results)
Research Products
(9 results)
