The analysis of a GLUT4 binding ANK structure protein, which may facilitate insulin induced-glucose uptake.
| Project/Area Number |
17590935
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Metabolomics
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| Research Institution | Yamaguchi University |
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Principal Investigator |
OKUYA Shigeru Yamaguchi University, Graduate School of Medicine, Associate Professor, 大学院医学系研究科, 助教授 (20214083)
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| Co-Investigator(Kenkyū-buntansha) |
MATSUBARA Atsushi Yamaguchi University, University Hospital, Assistant Professor, 医学部附属病院, 講師 (40311815)
TSURU Masatoshi Yamaguchi University, University Hospital, Research Associate, 医学部附属病院, 助手 (20379960)
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| Project Period (FY) |
2005 – 2006
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| Project Status |
Completed (Fiscal Year 2006)
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| Budget Amount *help |
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2006: ¥1,600,000 (Direct Cost: ¥1,600,000)
Fiscal Year 2005: ¥1,900,000 (Direct Cost: ¥1,900,000)
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| Keywords | GLUT4 / translocation / recycling / adaptor protein / ANK structure / glucose uptake / insulin / adipocyte |
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| Research Abstract |
Purpose
It has been supposed that a protein binding to GLUT4 could play an important role during the recycling of GLUT4 vesicle and insulin-induced GLUT4 translocation. We assumed the existence of GLUT4 "adaptor protein" in adipocytes, and we have identified a novel GLUT4 binding protein "p61" that has ANK structure and presumed phosphorylated sites, and analyzed its function.
Methods
Anit-p61 antibody: After antiserum was made with guinea pig immunity, affinity purification was performed. Influence of p61 knockdown on glucose transport activity: p61 was knocked down by introducing shRNA into 3T3-L1 adipocytes, and then insulin-induced GLUT4 translocation and glucose uptake were examined. Intracellular localization: After the fixation and immunostaining 3T3-L1 adipocytes were observed with a confocal microscope, and the intracellular localization of p61 and the GLUT4 was examined.
Results
In the basal state, p61 existed in the 3T3-L1 adipocyte cytoplasm as well as GLUT4, and the partial co-localization was suggested. Both the insulin-dependent GLUT4 translocation and glucose uptake were suppressed by p61 knockdown. On the other hand, an obvious change in the p61 localization was not recognized under the insulin stimulation.
Conclusion
It is not probable that the p61 localization in the adipocyte was changed in insulin-dependent manner. It is suggested that a novel ANK structure protein p61 facilitates GLUT4 translocation, and then activates insulin-induced glucose uptake.
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Report
(3 results)
Research Products
(6 results)
