| Project/Area Number |
26460356
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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 |
General medical chemistry
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| Research Institution | Nagoya City University (2016)
University of Tsukuba (2014-2015) |
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Principal Investigator |
OISHI Hisashi 名古屋市立大学, 大学院医学研究科, 教授 (30375513)
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| Co-Investigator(Kenkyū-buntansha) |
高橋 智 筑波大学, 医学医療系, 教授 (50271896)
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2016: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2015: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2014: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | インスリン / 大Maf転写因子 / 膵内分泌細胞 / 糖尿病 / 大Maf群転写因子 |
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| Outline of Final Research Achievements |
In this study, the functional similarity and difference of large Maf transcription factors has been elucidated in endocrine pancreas. The phenotypic comparison among MafA(-/-), β-cell specific MafB(-/-), and MafA(-/-);MafB(+/-) mice revealed that: (1) MafA gene was important for the maturation of β-cell function but not for β-cell development, (2)conversely, MafB gene was important for the normal β-cell development, and β-cell specific MafB(-/-) mice in adult showed no obvious abnormality including fasting blood glucose levels and glucose stimulated insulin secretion.
In addition, in order to apply diabetic treatment of large Maf genes, MafA or MafB gene together with other β-cell related genes were transferred in to mouse liver. The result demonstrated MafA is capable to induce more effective β-like cell induction than MafB.
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