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MBC in Press, published online ahead of print July 14, 2004
Mol. Biol. Cell 10.1091/mbc.E04-04-0333

A more recent version of this article appeared on October 1, 2004
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Submitted on April 22, 2004
Revised on July 2, 2004
Accepted on July 6, 2004

Insulin Stimulation of GLUT4 Exocytosis, but Not Its Inhibition of Endocytosis, Is Dependent on RabGAP AS160

Anja Zeigerer*, Mary Kate McBrayer{dagger}, and Timothy E. McGraw*{dagger}{ddagger}

*Department of Biochemistry and {dagger}Training Program in Chemical Biology, Weill Medical College of Cornell University, New York, NY 10021

Monitoring Editor: Juan S. Bonifacino

Insulin maintains whole body blood glucose homeostasis, in part, by regulating the amount of the GLUT4 glucose transporter on the cell surface of fat and muscle cells. Insulin induces the redistribution of GLUT4 from intracellular compartments to the plasma membrane, by stimulating a large increase in exocytosis and a smaller inhibition of endocytosis. A considerable amount is known about the molecular events of insulin signaling and the complex itinerary of GLUT4 trafficking, but less is known about how insulin signaling is transmitted to GLUT4 trafficking. Here we show that the AS160 RabGAP, a substrate of Akt, is required for insulin stimulation of GLUT4 exocytosis. A dominant-inhibitory mutant of AS160 blocks insulin stimulation of exocytosis at a step prior to the fusion of GLUT4-containing vesicles with the plasma membrane. This mutant, however, does not block insulin-induced inhibition of GLUT4 endocytosis. These data support a model in which insulin signaling to the exocytosis machinery (AS160-dependent) is distinct from its signaling to the internalization machinery (AS160-independent).

{ddagger}Corresponding author. E-mail: temcgraw{at}med.cornell.edu






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