Mol Cell Biol. 1994 July; 14(7): 4902-4911
Phosphatidylinositol 3-kinase activation is required for insulin stimulation of pp70 S6 kinase, DNA synthesis, and glucose transporter translocation.
B Cheatham,
C J Vlahos,
L Cheatham,
L Wang,
J Blenis and
C R Kahn
Joslin Diabetes Center, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts 02215.
ABSTRACT
Phosphatidylinositol 3-kinase (PI 3-kinase) is stimulated by insulin and a variety of growth factors, but its exact role in signal transduction remains unclear. We have used a novel, highly specific inhibitor of PT 3-kinase to dissect the role of this enzyme in insulin action. Treatment of intact 3T3-L1 adipocytes with LY294002 produced a dose-dependent inhibition of insulin-stimulated PI 3-kinase (50% inhibitory concentration, 6 microM) with > 95% reduction in the levels of phosphatidylinositol-3,4,5-trisphosphate without changes in the levels of phosphatidylinositol-4-monophosphate or its derivatives. In parallel, there was a complete inhibition of insulin-stimulated phosphorylation and activation of pp70 S6 kinase. Inhibition of PI 3-kinase also effectively blocked insulin- and serum-stimulated DNA synthesis and insulin-stimulated glucose uptake by inhibiting translocation of GLUT 4 glucose transporters to the plasma membrane. By contrast, LY294002 had no effect on insulin stimulation of mitogen-activated protein kinase or pp90 S6 kinase. Thus, activation of PI 3-kinase plays a critical role in mammalian cells and is required for activation of pp70 S6 kinase and DNA synthesis and certain forms of intracellular vesicular trafficking but not mitogen-activated protein kinase or pp90 S6 kinase activation. These data suggest that PI 3-kinase is not only an important component but also a point of divergence in the insulin signaling network.
Mol Cell Biol. 1994 July; 14(7): 4902-4911
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Anthony, J. C., Reiter, A. K., Anthony, T. G., Crozier, S. J., Lang, C. H., MacLean, D. A., Kimball, S. R., Jefferson, L. S.
(2002). Orally Administered Leucine Enhances Protein Synthesis in Skeletal Muscle of Diabetic Rats in the Absence of Increases in 4E-BP1 or S6K1 Phosphorylation. Diabetes
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Lingohr, M. K., Dickson, L. M., McCuaig, J. F., Hugl, S. R., Twardzik, D. R., Rhodes, C. J.
(2002). Activation of IRS-2--Mediated Signal Transduction by IGF-1, but not TGF-{alpha} or EGF, Augments Pancreatic {beta}-Cell Proliferation. Diabetes
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Butler, M., McKay, R. A., Popoff, I. J., Gaarde, W. A., Witchell, D., Murray, S. F., Dean, N. M., Bhanot, S., Monia, B. P.
(2002). Specific Inhibition of PTEN Expression Reverses Hyperglycemia in Diabetic Mice. Diabetes
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Hunt, D. G., Ding, Z., Ivy, J. L.
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Ueki, K., Fruman, D. A., Brachmann, S. M., Tseng, Y.-H., Cantley, L. C., Kahn, C. R.
(2002). Molecular Balance between the Regulatory and Catalytic Subunits of Phosphoinositide 3-Kinase Regulates Cell Signaling and Survival. Mol. Cell. Biol.
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Kim, Y.-B., Ciaraldi, T. P., Kong, A., Kim, D., Chu, N., Mohideen, P., Mudaliar, S., Henry, R. R., Kahn, B. B.
(2002). Troglitazone but not Metformin Restores Insulin-Stimulated Phosphoinositide 3-Kinase Activity and Increases p110{beta} Protein Levels in Skeletal Muscle of Type 2 Diabetic Subjects. Diabetes
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Davidson, R. T., Arias, E. B., Cartee, G. D.
(2002). Calorie restriction increases muscle insulin action but not IRS-1-, IRS-2-, or phosphotyrosine-PI 3-kinase. Am. J. Physiol. Endocrinol. Metab.
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Jiang, Z. Y., Chawla, A., Bose, A., Way, M., Czech, M. P.
(2002). A Phosphatidylinositol 3-Kinase-independent Insulin Signaling Pathway to N-WASP/Arp2/3/F-actin Required for GLUT4 Glucose Transporter Recycling. J. Biol. Chem.
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Kralik, S. F., Liu, P., Leffler, B. J., Elmendorf, J. S.
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Eto, K., Yamashita, T., Tsubamoto, Y., Terauchi, Y., Hirose, K., Kubota, N., Yamashita, S., Taka, J., Satoh, S., Sekihara, H., Tobe, K., Iino, M., Noda, M., Kimura, S., Kadowaki, T.
(2002). Phosphatidylinositol 3-Kinase Suppresses Glucose-Stimulated Insulin Secretion by Affecting Post-Cytosolic [Ca2+] Elevation Signals. Diabetes
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Tack, I., Elliot, S. J., Potier, M., Rivera, A., Striker, G. E., Striker, L. J.
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Park, J. G., Bose, A., Leszyk, J., Czech, M. P.
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Navarro, M., Valentinis, B., Belletti, B., Romano, G., Reiss, K., Baserga, R.
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Nadler, S. T., Stoehr, J. P., Rabaglia, M. E., Schueler, K. L., Birnbaum, M. J., Attie, A. D.
(2001). Normal Akt/PKB with reduced PI3K activation in insulin-resistant mice. Am. J. Physiol. Endocrinol. Metab.
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Somwar, R., Niu, W., Kim, D. Y., Sweeney, G., Randhawa, V. K., Huang, C., Ramlal, T., Klip, A.
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Foster, L. J., Li, D., Randhawa, V. K., Klip, A.
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Teruel, T., Hernandez, R., Lorenzo, M.
(2001). Ceramide Mediates Insulin Resistance by Tumor Necrosis Factor-{alpha} in Brown Adipocytes by Maintaining Akt in an Inactive Dephosphorylated State. Diabetes
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Podsypanina, K., Lee, R. T., Politis, C., Hennessy, I., Crane, A., Puc, J., Neshat, M., Wang, H., Yang, L., Gibbons, J., Frost, P., Dreisbach, V., Blenis, J., Gaciong, Z., Fisher, P., Sawyers, C., Hedrick-Ellenson, L., Parsons, R.
(2001). An inhibitor of mTOR reduces neoplasia and normalizes p70/S6 kinase activity in Pten+/- mice. Proc. Natl. Acad. Sci. USA
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Bose, A., Cherniack, A. D., Langille, S. E., Nicoloro, S. M. C., Buxton, J. M., Park, J. G., Chawla, A., Czech, M. P.
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Ono, H., Katagiri, H., Funaki, M., Anai, M., Inukai, K., Fukushima, Y., Sakoda, H., Ogihara, T., Onishi, Y., Fujishiro, M., Kikuchi, M., Oka, Y., Asano, T.
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Dunaif, A., Wu, X., Lee, A., Diamanti-Kandarakis, E.
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Bogan, J. S., McKee, A. E., Lodish, H. F.
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