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Vol. 13, Issue 7, 2276-2288, July 2002
Abramson Family Cancer Research Institute, University of
Pennsylvania, Philadelphia, Pennsylvania 19104
In multicellular organisms, constituent cells depend on
extracellular signals for growth, proliferation, and survival. When cells are withdrawn from growth factors, they undergo apoptosis. Expression of constitutively active forms of the serine/threonine kinase Akt/PKB can prevent apoptosis upon growth factor withdrawal. Akt-mediated survival depends in part on the maintenance of glucose metabolism, suggesting that reduced glucose utilization contributes to
growth factor withdrawal-induced death. However, it is unclear how
restricting access to extracellular glucose alone would lead to the
metabolic collapse observed after growth factor withdrawal. We report
herein that growth factor withdrawal results in the loss of surface
transporters for not only glucose but also amino acids, low-density
lipoprotein, and iron. This coordinated decline in transporters
and receptors for extracellular molecules creates a catabolic state
characterized by atrophy and a decline in the mitochondrial membrane
potential. Activated forms of Akt maintained these transporters on the
cell surface in the absence of growth factor through an mTOR-dependent
mechanism. The mTOR inhibitor rapamycin diminished Akt-mediated
increases in cell size, mitochondrial membrane potential, and cell
survival. These results suggest that growth factors control cellular
growth and survival by regulating cellular access to extracellular
nutrients in part by modulating the activity of Akt and mTOR.
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S. Ahmad, A. Ahmad, M. Ghosh, C. C. Leslie, and C. W. White Extracellular ATP-mediated Signaling for Survival in Hyperoxia-induced Oxidative Stress J. Biol. Chem., April 16, 2004; 279(16): 16317 - 16325. [Abstract] [Full Text] [PDF]
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K. A. Frauwirth and C. B. Thompson Regulation of T Lymphocyte Metabolism J. Immunol., April 15, 2004; 172(8): 4661 - 4665. [Abstract] [Full Text] [PDF]
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 K. L. Hoehn, S. F. Hudachek, S. A. Summers, and G. L. Florant Seasonal, tissue-specific regulation of Akt/protein kinase B and glycogen synthase in hibernators Am J Physiol Regulatory Integrative Comp Physiol, March 1, 2004; 286(3): R498 - R504. [Abstract] [Full Text] [PDF]
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T. Schmelzle, T. Beck, D. E. Martin, and M. N. Hall Activation of the RAS/Cyclic AMP Pathway Suppresses a TOR Deficiency in Yeast Mol. Cell. Biol., January 1, 2004; 24(1): 338 - 351. [Abstract] [Full Text] [PDF]
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A. L. Edinger, C. M. Linardic, G. G. Chiang, C. B. Thompson, and R. T. Abraham Differential Effects of Rapamycin on Mammalian Target of Rapamycin Signaling Functions in Mammalian Cells Cancer Res., December 1, 2003; 63(23): 8451 - 8460. [Abstract] [Full Text] [PDF]
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I. Adini, I. Rabinovitz, J. F. Sun, G. C. Prendergast, and L. E. Benjamin RhoB controls Akt trafficking and stage-specific survival of endothelial cells during vascular development Genes & Dev., November 1, 2003; 17(21): 2721 - 2732. [Abstract] [Full Text] [PDF]
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 J. Faridi, J. Fawcett, L. Wang, and R. A. Roth Akt promotes increased mammalian cell size by stimulating protein synthesis and inhibiting protein degradation Am J Physiol Endocrinol Metab, November 1, 2003; 285(5): E964 - E972. [Abstract] [Full Text] [PDF]
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J. Debnath, S. J. Walker, and J. S. Brugge Akt activation disrupts mammary acinar architecture and enhances proliferation in an mTOR-dependent manner J. Cell Biol., October 27, 2003; 163(2): 315 - 326. [Abstract] [Full Text] [PDF]
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J. C. Rathmell, C. J. Fox, D. R. Plas, P. S. Hammerman, R. M. Cinalli, and C. B. Thompson Akt-Directed Glucose Metabolism Can Prevent Bax Conformation Change and Promote Growth Factor-Independent Survival Mol. Cell. Biol., October 15, 2003; 23(20): 7315 - 7328. [Abstract] [Full Text] [PDF]
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J. Bentley, D. Itchayanan, K. Barnes, E. McIntosh, X. Tang, C. P. Downes, G. D. Holman, A. D. Whetton, P. J. Owen-Lynch, and S. A. Baldwin Interleukin-3-mediated Cell Survival Signals Include Phosphatidylinositol 3-Kinase-dependent Translocation of the Glucose Transporter GLUT1 to the Cell Surface J. Biol. Chem., October 10, 2003; 278(41): 39337 - 39348. [Abstract] [Full Text] [PDF]
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C. J. Fox, P. S. Hammerman, R. M. Cinalli, S. R. Master, L. A. Chodosh, and C. B. Thompson The serine/threonine kinase Pim-2 is a transcriptionally regulated apoptotic inhibitor Genes & Dev., August 1, 2003; 17(15): 1841 - 1854. [Abstract] [Full Text] [PDF]
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T. B. Huber, B. Hartleben, J. Kim, M. Schmidts, B. Schermer, A. Keil, L. Egger, R. L. Lecha, C. Borner, H. Pavenstadt, et al. Nephrin and CD2AP Associate with Phosphoinositide 3-OH Kinase and Stimulate AKT-Dependent Signaling Mol. Cell. Biol., July 15, 2003; 23(14): 4917 - 4928. [Abstract] [Full Text] [PDF]
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C. Yu, M. Rahmani, Y. Dai, D. Conrad, G. Krystal, P. Dent, and S. Grant The Lethal Effects of Pharmacological Cyclin-dependent Kinase Inhibitors in Human Leukemia Cells Proceed through a Phosphatidylinositol 3-Kinase/Akt-dependent Process Cancer Res., April 15, 2003; 63(8): 1822 - 1833. [Abstract] [Full Text] [PDF]
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