| Project/Area Number |
13557011
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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 | 展開研究 |
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| Research Field |
General medical chemistry
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| Research Institution | The University of Tokushima |
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Principal Investigator |
EBINA Yousuke The University of Tokushima, Institute for Enzyme Research, Professor, 分子酵素学研究センター, 教授 (00112227)
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| Co-Investigator(Kenkyū-buntansha) |
YUASA Tomoyuki The University of Tokushima, Institute for Enzyme Research, Research Associate, 分子酵素学研究センター, 助手 (50304556)
OBATA Toshiyuki The University of Tokushima, Institute for Enzyme Research, Research Associate, 分子酵素学研究センター, 助手 (40325296)
KISHI Kazuhiro The University of Tokushima, Institute for Enzyme Research, Associate Professor, 分子酵素学研究センター, 助教授 (70284320)
ASAHI Yoshihiko Otsuka Pharmaceutical Co., Ltd., Tokushima Institute, 栄養研究所, 研究員
TANIGUCHI Hisaaki The University of Tokushima, Institute for Enzyme Research, Professor, 分子酵素学研究センター, 教授 (10257636)
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| Project Period (FY) |
2001 – 2003
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| Project Status |
Completed (Fiscal Year 2003)
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| Budget Amount *help |
¥13,900,000 (Direct Cost: ¥13,900,000)
Fiscal Year 2003: ¥3,400,000 (Direct Cost: ¥3,400,000)
Fiscal Year 2002: ¥4,700,000 (Direct Cost: ¥4,700,000)
Fiscal Year 2001: ¥5,800,000 (Direct Cost: ¥5,800,000)
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| Keywords | Insulin signalling / protein phosphorylation / proteome / drug / インスリン作用 / 糖尿病薬 / Akt / プロテオミクス / 経口糖尿病薬 |
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| Research Abstract |
Evidence suggesting that polygenetic factors contribute to the pathogenesis of non-insulin-dependent diabetes mellitus (NIDDM) is accumulating, but the nature of the genetic defect is unknown. The common form of NIDDM is a heterogeneous disorder in which at least two major defects contribute to the pathophysiology of the phenotype : insulin deficiency and insulin resistance. Insulin stimulates the disposal of blood glucose into skeletal muscles and adipose tissues by the translocation of glucose transporter type4 (GLUT4) from intracellular pools to the plasma membrane, and consequently the concentration of blood glucose levels decreases rapidly in vivo. Failure of this action of insulin seems to be one of the major causes of Type2 diabetes. Phosphatidylinositol 3-kinase (PI 3-kinase) and AKT play a pivotal role in the stimulation of glucose transport by insulin, but detailed mechanisms are unknown
Dur aim is to elucidate the new signalling factors after Akt and to develop the drug to stimulate the insulin signalling. we analyzed the proteins which bind to the PH domain of Akt2 using proteome analysis and found some factors which may participate the insulin signalling
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