Activated Phosphatidylinositol 3-Kinase Is Sufficient to Mediate Actin Rearrangement and GLUT4 Translocation in 3T3-L1 Adipocytes
Open Access
- 1 July 1996
- journal article
- Published by Elsevier BV
- Vol. 271 (30), 17605-17608
- https://doi.org/10.1074/jbc.271.30.17605
Abstract
No abstract availableThis publication has 11 references indexed in Scilit:
- Insulin-mediated Targeting of Phosphatidylinositol 3-Kinase to GLUT4-containing VesiclesPublished by Elsevier BV ,1996
- The GTP-binding protein Rac does not couple PI 3-kinase to insulin-stimulated glucose transport in adipocytesCurrent Biology, 1995
- Insulin-stimulated GLUT4 Translocation Is Mediated by a Divergent Intracellular Signaling PathwayPublished by Elsevier BV ,1995
- Role of IRS-2 in insulin and cytokine signallingNature, 1995
- Ras-Dependent Induction of Cellular Responses by Constitutively Active Phosphatidylinositol-3 KinaseScience, 1995
- Phosphoinositide 3-Kinase as an Upstream Regulator of the Small GTP-Binding Protein Rac in the Insulin Signaling of Membrane RufflingBiochemical and Biophysical Research Communications, 1995
- Genistein Inhibits Insulin-Stimulated Glucose Transport and Decreases Immunocytochemical Labeling of GLUT4 Carboxyl-Terminus without Affecting Translocation of GLUT4 in Isolated Rat Adipocytes: Additional Evidence of GLUT4 Activation by InsulinArchives of Biochemistry and Biophysics, 1993
- The small GTP-binding protein rac regulates growth factor-induced membrane rufflingCell, 1992
- Intracellular targeting of the insulin-regulatable glucose transporter (GLUT4) is isoform specific and independent of cell type.The Journal of cell biology, 1991
- Evidence that insulin causes translocation of glucose transport activity to the plasma membrane from an intracellular storage site.Proceedings of the National Academy of Sciences of the United States of America, 1980