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Papers In Press, published online ahead of print February 28, 2005
Biochemistry and Molecular Biology, University of Oklahoma Health Sciences Center, Oklahoma City, OK 73190
Corresponding Author: ann-olson{at}ouhsc.edu
The actin cytoskeleton has been shown to be required for insulin-dependent GLUT4 translocation, however, the role that the actin network plays is unknown. Work from other laboratories has suggested that actin may play a role in formation of an active signaling complex, and others suggest that actin may be required for movement of vesicles to the plasma membrane surface. To distinguish between these possibilities, we examined the ability of myr-AKT, a constitutively active form of AKT that signals GLUT4 translocation to the plasma membrane in the absence of insulin, to signal translocation of an HA-GLUT4-GFP reporter protein in the presence or absence of an intact cytoskeleton in 3T3-L1 adipocytes. Expression of myr-Akt signaled the redistribution of the GLUT4 reporter protein to the cell surface in the absence or presence of 10 µM Latrunculin B, a concentration sufficient to completely inhibit insulin-dependent redistribution of the GLUT4 reporter to the cell surface. These data suggest that the actin network plays a primary role in organization of the insulin-signaling complex. To further support this conclusion, we measured the activation of known signaling proteins using a saturating concentration of insulin in cells pretreated without or with 10 µM Latrunculin B. We found that Latrunculin treatment did not effect insulin-dependent tyrosine phosphorylation of the insulin receptor beta-subunit and IRS-1 but completely inhibited activation of AKT enzymatic activity. Phosphorylation of Akt/PKB at S473 and T308 were inhibited by Latrunculin B treatment, indicating that the defect in signaling lies prior to Akt activation. In summary, our data support the hypothesis that the actin network plays a role in organization of the insulin-signaling complex, but is not required for vesicle trafficking and/or fusion.
J. Biol. Chem, 10.1074/jbc.M409806200
Submitted on August 26, 2004
Revised on February 23, 2005
Accepted on February 28, 2005
Expression of a constitutively active Akt/PKB signals GLUT4 translocation in the absence of an intact actin cytoskeleton
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