| Project/Area Number |
17K08298
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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 |
Biological pharmacy
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| Research Institution | Showa University (2019)
National Cardiovascular Center Research Institute (2017-2018) |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
渡邉 裕介 国立研究開発法人国立循環器病研究センター, 研究所, 室長 (20562333)
中川 修 国立研究開発法人国立循環器病研究センター, 研究所, 部長 (40283593)
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| Project Period (FY) |
2017-04-01 – 2020-03-31
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| Project Status |
Completed (Fiscal Year 2019)
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| Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2019: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2018: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2017: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | 血管新生 / 内皮細胞 / ALK1受容体 / SGK1 / 血管形成 / ALK1 / BMP |
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| Outline of Final Research Achievements |
Angiogenesis in the embryonic stage is strictly regulated by many kinds of signaling pathways. The ALK1 signaling pathway is one of the essential pathways in angiogenesis, and BMP9 is known as a ligand for the ALK1 receptor. In this study, we found Serum and glucocorticoid-regulated kinase 1 (SGK1) to be a novel downstream target of the ALK1 signaling pathway, which is essential for angiogenesis. and identified a BMP9 responsive enhancer region for SGK1 expression.
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| Academic Significance and Societal Importance of the Research Achievements |
ALK1遺伝子の変異は、難病に指定される遺伝性血管疾患のオスラー病の原因の一つとなる。ALK1シグナルは血管新生過程に必須であり、そのシグナル分子機構を解明することは遺伝性疾患のみならず癌や虚血性疾患の治療戦略の発見にもつながる可能性がある。今回、ALK1シグナルの構成因子を同定し、このことがALK1シグナルの分子機構解明の端緒になることが期待される。
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