التفاصيل البيبلوغرافية
العنوان: |
EFR3 and phosphatidylinositol 4-kinase IIIα regulate insulin-stimulated glucose transport and GLUT4 dispersal in 3T3-L1 adipocytes. |
المؤلفون: |
Koester, Anna M., Geiser, Angéline, Laidlaw, Kamilla M. E., Morris, Silke, Cutiongco, Marie F. A., Stirrat, Laura, Gadegaard, Nikolaj, Boles, Eckhard, Black, Hannah L., Bryant, Nia J., Gould, Gwyn W. |
المصدر: |
Bioscience Reports; Jul2022, Vol. 42 Issue 7, p1-13, 13p |
مصطلحات موضوعية: |
FAT cells, GLUCOSE, GLUCOSE transporters, SCAFFOLD proteins, INSULIN receptors, CELL membranes, INSULIN, GLUCOSE-regulated proteins |
مستخلص: |
Insulin stimulates glucose transport in muscle and adipocytes. This is achieved by regulated delivery of intracellular glucose transporter (GLUT4)-containing vesicles to the plasmamembrane where they dock and fuse, resulting in increased cell surface GLUT4 levels. Recent work identified a potential further regulatory step, in which insulin increases the dispersal of GLUT4 in the plasmamembrane away from the sites of vesicle fusion. EFR3 is a scaffold protein that facilitates localization of phosphatidylinositol 4-kinase type IIIα to the cell surface. Here we show that knockdown of EFR3 or phosphatidylinositol 4-kinase type IIIα impairs insulin-stimulated glucose transport in adipocytes. Using direct stochastic reconstruction microscopy, we also show that EFR3 knockdown impairs insulin stimulated GLUT4 dispersal in the plasma membrane. We propose that EFR3 plays a previously unidentified role in controlling insulin-stimulated glucose transport by facilitating dispersal of GLUT4 within the plasma membrane. [ABSTRACT FROM AUTHOR] |
|
Copyright of Bioscience Reports is the property of Portland Press Ltd. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.) |
قاعدة البيانات: |
Complementary Index |