徳島大学 教育・研究者情報データベース(EDB)

1. 徳島大学.疾患酵素学研究センター(2007年4月1日〜2016年3月31日/->組織[徳島大学.先端酵素学研究所.次世代酵素学研究領域])

1. 湯浅 智之([徳島大学.大学院医歯薬学研究部.医学域.連携研究部門(医学域).寄附講座系(医学域).実践地域診療・医科学])

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2. 内山 圭司([徳島大学.先端酵素学研究所.重点研究部門])

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3. (英) Yuko OGURA

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4. 木村 昌史

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5. (英) Kiyoshi TESHIGAWARA

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6. 保坂 利男

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7. (英) Yoshinori TANAKA

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8. 小畑 利之

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9. (英) Hiroyuki SANO

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10. 岸 和弘

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11. 蛯名 洋介

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(英) The Rab GTPase-Activating Protein AS160 as a Common Regulator of Insulin- and Gαq-Mediated Intracellular GLUT4 Vesicle Distribution

(英) Akt substrate of 160kDa (AS160) is a Rab GTPase activating protein (GAP) and was recently identified as a component of the insulin signaling pathway of glucose transporter type 4 (GLUT4) translocation. We and others, previously reported that the activation of Galphaq protein-coupled receptors (GalphaqPCRs) also stimulated GLUT4 translocation and glucose uptake in several cell lines. Here, we report that the activation of GalphaqPCRs also promoted phosphorylation of AS160 by the 5'-AMP activated protein kinase (AMPK). The suppression of AS160 phosphorylation by the siRNA mediated AMPKalpha1 subunit knockdown promoted GLUT4 vesicle retention in intracellular compartments. This suppression did not affect the ratio of non-induced cell surface GLUT4 to Galphaq-induced it. Rat 3Y1 cells lacking AS160 did not show insulin-induced GLUT4 translocation. The cells stably expressing GLUT4 revealed GLUT4 vesicles that were mainly localized in the perinuclear region and less frequently on the cell surface. After expression of exogenous AS160, GLUT4 on the cell surface decreased and GLUT4 vesicles were redistributed throughout the cytoplasm. Although PMA-induced or sodium fluoride-induced GLUT4 translocation was significantly increased in these cells, insulin did not affect GLUT4 translocation. These results suggest that AS160 is a common regulator of insulin- and GalphaqPCR activation-mediated GLUT4 distribution in the cells.

1. (英) 3T3-L1 Cells
2. (英) AMP-Activated Protein Kinases
3. (英) Animals
4. (英) CHO Cells
5. (英) Cricetinae
6. (英) Cricetulus
7. (英) GTP-Binding Protein alpha Subunits, Gq-G11
8. (英) GTPase-Activating Proteins
9. (英) Glucose Transporter Type 4
10. (英) Humans
11. (英) Insulin
12. (英) Mice
13. (英) Rats

1. (英) Article.Affiliation: Division of Molecular Genetics, Institute for Enzyme Research, The University of Tokushima, Kuramotocho, Tokushima, Japan.

2. (英) Article.PublicationTypeList.PublicationType: Journal Article

3. (英) Article.PublicationTypeList.PublicationType: Research Support, Non-U.S. Gov't