| Project/Area Number |
23592021
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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 |
Digestive surgery
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| Research Institution | Tokyo Women's Medical University |
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Principal Investigator |
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| Co-Investigator(Renkei-kenkyūsha) |
TSUCHIYA Ken 東京女子医科大学, 医学部, 臨床教授 (00246472)
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| Project Period (FY) |
2011-04-28 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2014: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2013: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2012: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2011: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
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| Keywords | mafA / mafB / siRNA / c-maf / 転写因子 / 細胞極性 / 膵細胞 / maf / 糖尿病 |
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| Outline of Final Research Achievements |
Gene profiling performed after in vivo modulation of mafs expression levels revealed up regulation of Nupr1 and Ddit3 and downregulation of Hsp8 in mafB siRNA-treated pancreas. Transfection of mafB siRNA to pancreatic cells (AsPc-1,BxPC3) prominently accelerated autophagy, as assessed by LC3 expression using immunosteining, regardless of small changes in cell cycling (BrdU uptake), cell senescence (beta Gal staining), and apoptosis (Tunnel assay). Regarding cell function, although no difference was observed during the steady state, cell proliferation under the stress condition, as assessed by cell scratch assay, was markedly diminished in mafB-suppressed cells. Addition of quercetin restored cell migration and proliferation. In addition, the restration of autophagy was accompanied by suppression of Nupr1 and ATF6 by quercetin treatment in mafB siRNA-treated cells.large mafs modulates biological cell activity such as autophagy or response to ER stress under disrupted glucose metabolism.
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