| Project/Area Number |
16380229
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Applied molecular and cellular biology
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| Research Institution | Kyoto University |
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Principal Investigator |
KIOKA Noriyuki Kyoto University, Division of Applied life Sciences, Associate Professor (90234179)
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| Co-Investigator(Kenkyū-buntansha) |
YAMADA Masayasu Kyoin University, Division of Biosciences, Associate Professor (10243073)
UEDA Kazumitsu Kyoto University, Institute for Integrated Cell-Material Sriences(iCeMS), Professor (10151789)
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| Project Period (FY) |
2004 – 2007
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| Project Status |
Completed (Fiscal Year 2007)
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| Budget Amount *help |
¥16,290,000 (Direct Cost: ¥15,600,000、Indirect Cost: ¥690,000)
Fiscal Year 2007: ¥2,990,000 (Direct Cost: ¥2,300,000、Indirect Cost: ¥690,000)
Fiscal Year 2006: ¥4,200,000 (Direct Cost: ¥4,200,000)
Fiscal Year 2005: ¥4,200,000 (Direct Cost: ¥4,200,000)
Fiscal Year 2004: ¥4,900,000 (Direct Cost: ¥4,900,000)
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| Keywords | Cell Adhesion / Wound healing / Tumorigenesis / Migration / Signal transduction / がん / 再生医学 / ビネキシン / 細胞骨格 / 分化 / アクチン / 浸潤 / 足場依存性 |
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| Research Abstract |
Cell migration play important roles in various physiological and pathophysiological conditions, including wound healing, angiogenesis, and tumor invasion. Clarifying the mechanisms of cell migration can contribute to the development of new anti-cancer or anti-metastasis drugs. This research has investigated the function of a novel focal adhesion protein, vinexin, in wound healings, cell migration, and signal transduction,using vinexin-knock out mice and knockdown cells.
1) Wound healing-We found that gene disruption of vinexin induces the delayed wound healing of cutaneous injury. Knockdown of vinexin expression in cultured keratinocytes showed that vinexin regulate wound healing through regulating the activation and localization of EGRR
2) Anchorage-dependence of signaling-Mechanisms of regulating anchorage-independent activation of ERK by vinexin was examined. We found that vinexin inhibits the inactivation of ERK. We also showed that anchorage-dependent regulation of ERK activation depends on the inactivation process in part.
3) Roles in the regulation of cytoskeleton and spreading-Knockdown of vinexin expression in Highly invasive HT1080 cells showed that vinexin has roles in cell spreading through the control of a small G-protein activation. We also found that vinexin directly associates with WAVE2, a downstream factor of the small G protein, and regulates its phosphorylation and amount.
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