| Project/Area Number |
25461137
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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 |
Cardiovascular medicine
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| Research Institution | Aichi Medical University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
中川 修 京都大学, 医学(系)研究科(研究院), その他 (40283593)
坂部 正英 奈良県立医科大学, 医学部, 助教 (00525983)
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2015: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2014: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2013: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | 血管新生 / 血管内皮細胞 / VEGFシグナル / G蛋白 / G-protein / VEGF signal / Endothelial cells / シグナル伝達 / G蛋白活性調節因子 / VEGF / 細胞間シグナル |
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| Outline of Final Research Achievements |
In multicellular organisms, communication between the cells is taken with a variety of signal molecules. Its collapse causes cell dysfunction, eventually leading to a variety of disease. Here, we conducted a study about how to control the blood vessel formation, including angiogenesis, by regulating the cell-to-cell signaling with a new trimeric G-protein -binding protein, AGS8. When expression of AGS8 molecules in vascular endothelial cells was suppressed, basic functions of the endothelial cells (cell growth, movement, lumen formation) was inhibited. Further detailed analysis finally suggested that AGS8 is a new regulatory molecules of VEGF signaling, mainly via acting an appropriate VEGF receptor localization by transporting it from cytosol to cell membrane.
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