| Project/Area Number |
25870070
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Tumor biology
General physiology
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| Research Institution | Tohoku University |
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Principal Investigator |
KOBAYASHI Miho 東北大学, 加齢医学研究所, 助教 (50630539)
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| Project Period (FY) |
2013-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2014: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2013: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | 血管新生 / Vasohibin-1 / VEGF / シグナル伝達 / 抗血管新生 / 受容体探索 |
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| Outline of Final Research Achievements |
Major target of anti-cancer therapy is VEGF, but its therapeutic approach gave several issues such as a switching to other angiogenic factors from VEGF, and causes vessel disorder in other normal tissue. Vasohibin-1 (VASH1) is a VEGF- or FGF2-inducible anti-angiogenic factor that plays a role of negative feedback regulator on angiogenesis by broad angiogenic factors. VASH1 potently induces increase in detyrosination of α-tubulin in endothelial cells (ECs). This study revealed that VASH1 simultaneously induced Glu-tubulin increment, inhibition of VEGF-signaling, VEGF-inducible ECs migration and network formation. Co-expression of TTL (tubulin tyrosine ligase), normalized the level of Glu-tubulin, and abrogated the VASH1-induced suppression both of VEGF-signaling and VEGF-induced angiogenesis. Thus, I propose that VASH1 induces inhibition of VEGF-signaling and angiogenesis through the bias of a tubulin tyrosination/detyrosinatin cycle.
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