Molecular and structural basis of insulin resistance revealed by high precision nanometry
| Project/Area Number |
25713010
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| Research Category |
Grant-in-Aid for Young Scientists (A)
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| Allocation Type | Partial Multi-year Fund |
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| Research Field |
General physiology
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| Research Institution | Tohoku University |
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Principal Investigator |
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥24,570,000 (Direct Cost: ¥18,900,000、Indirect Cost: ¥5,670,000)
Fiscal Year 2015: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2014: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2013: ¥20,930,000 (Direct Cost: ¥16,100,000、Indirect Cost: ¥4,830,000)
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| Keywords | 糖輸送体 / ライブイメージング |
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| Outline of Final Research Achievements |
The aim of this study was to understand the molecular and structural basis of insulin resistance, a characteristic etiology of type 2 diabetes, by improving the GLUT4 nanometry and performing high-precision measurements of GLUT4 trafficking regulatory systems. To achieve this, we first established a new experimental and analytical system for performing GLUT4 nanometry, with which we successfully performed simultaneous high-precision imaging of single molecule behavior of two distinct trafficking molecules and observed single molecule behavior and subcellular structures simultaneously. Furthermore, we enabled GLUT4 nanometry in isolated mice skeletal myofibers, which have higher-order structures and functions than cell line cultures, used in previous studies do. Using skeletal myofibers, combined with a cell-based reconstitution model, we revealed GLUT4 trafficking systems and the molecular basis of exercise effects on skeletal muscles.
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Report
(4 results)
Research Products
(18 results)
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[Journal Article] Single quantum dot tracking reveals that an individual multivalent 2 HIV-1 Tat-protein transduction domain can activate machinery for 3 lateral transport and endocytosis2013
Author(s)
3.Yasuhiro Suzuki*, Chandra Nath Roy, Warunya Promjunyaku, Hiroyasu Hatakeyama, Kohsuke Gonda, Junji Imamura, Biju Vasudevan Pillai, Noriaki Ohuchi, Makoto Kanzaki , Hideo Higuchi, and Mitsuo Kaku
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Journal Title
Mol. Cell Biol.
Volume: 33
Issue: 15
Pages: 3039-3049
DOI
Related Report
Peer Reviewed / Open Access
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