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Science 7 April 1995:
Vol. 268. no. 5207, pp. 100 - 102
DOI: 10.1126/science.7701328
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Articles

Science, Vol 268, Issue 5207, 100-102
Copyright © 1995 by American Association for the Advancement of Science

articles

Ras-dependent induction of cellular responses by constitutively active phosphatidylinositol-3 kinase

Q Hu, A Klippel, AJ Muslin, WJ Fantl, and LT Williams

Cardiovascular Research Institute, University of California, San Francisco 94143-0130, USA.

Phosphatidylinositol (Pl)-3 kinase is one of many enzymes stimulated by growth factors. A constitutively activated mutant, p110, that functions independently of growth factor stimulation was constructed to determine the specific responses regulated by Pl-3 kinase. The p110 protein exhibited high specific activity as a Pl-3 kinase and as a protein kinase. Expression of p110 in NIH 3T3 cells induced transcription from the fos promoter. Co-expression of dominant negative Ras blocked this response. When expressed in Xenopus laevis oocytes, p110 increased the amount of guanosine 5'-triphosphate-bound Ras, caused activation of the Ras effector Raf-1, and induced Ras-dependent oocyte maturation. These findings show that Pl-3 kinase can stimulate diverse Ras-dependent cellular processes, including oocyte maturation and fos transcription.


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R-Ras Signals through Specific Integrin {alpha} Cytoplasmic Domains to Promote Migration and Invasion of Breast Epithelial Cells.
P. J. Keely, E. V. Rusyn, A. D. Cox, and L. V. Parise (1999)
J. Cell Biol. 145, 1077-1088
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Changes in the Balance of Phosphoinositide 3-Kinase/Protein Kinase B (Akt) and the Mitogen-activated Protein Kinases (ERK/p38MAPK) Determine a Phenotype of Visceral and Vascular Smooth Muscle Cells.
K. Hayashi, M. Takahashi, K. Kimura, W. Nishida, H. Saga, and K. Sobue (1999)
J. Cell Biol. 145, 727-740
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Membrane-targeted Phosphatidylinositol 3-Kinase Mimics Insulin Actions and Induces a State of Cellular Insulin Resistance.
K. Egawa, P. M. Sharma, N. Nakashima, Y. Huang, E. Huver, G. R. Boss, and J. M. Olefsky (1999)
J. Biol. Chem. 274, 14306-14314
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A Novel Pathway for Tumor Necrosis Factor-alpha and Ceramide Signaling Involving Sequential Activation of Tyrosine Kinase, p21ras, and Phosphatidylinositol 3-Kinase.
A. N. Hanna, E. Y. W. Chan, J. Xu, J. C. Stone, and D. N. Brindley (1999)
J. Biol. Chem. 274, 12722-12729
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Dedifferentiation of adenocarcinomas by activation of phosphatidylinositol 3-kinase.
M. Kobayashi, S. Nagata, T. Iwasaki, K. Yanagihara, I. Saitoh, Y. Karouji, S. Ihara, and Y. Fukui (1999)
PNAS 96, 4874-4879
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A Novel SH2-Containing Phosphatidylinositol 3,4,5-Trisphosphate 5-Phosphatase (SHIP2) Is Constitutively Tyrosine Phosphorylated and Associated With src Homologous and Collagen Gene (SHC) in Chronic Myelogenous Leukemia Progenitor Cells.
D. Wisniewski, A. Strife, S. Swendeman, H. Erdjument-Bromage, S. Geromanos, W. M. Kavanaugh, P. Tempst, and B. Clarkson (1999)
Blood 93, 2707-2720
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p70 S6 Kinase Is Regulated by Protein Kinase Czeta and Participates in a Phosphoinositide 3-Kinase-Regulated Signalling Complex.
A. Romanelli, K. A. Martin, A. Toker, and J. Blenis (1999)
Mol. Cell. Biol. 19, 2921-2928
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Bradykinin-stimulated protein synthesis by myocytes is dependent on the MAP kinase pathway and p70S6K.
R. H. Ritchie, J. D. Marsh, and R. J. Schiebinger (1999)
Am J Physiol Heart Circ Physiol 276, H1393-H1398
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Transcriptional Activation of the Glucose Transporter GLUT1 in Ventricular Cardiac Myocytes by Hypertrophic Agonists.
C. Montessuit and A. Thorburn (1999)
J. Biol. Chem. 274, 9006-9012
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The Gab1 PH Domain Is Required for Localization of Gab1 at Sites of Cell-Cell Contact and Epithelial Morphogenesis Downstream from the Met Receptor Tyrosine Kinase.
C. R. Maroun, M. Holgado-Madruga, I. Royal, M. A. Naujokas, T. M. Fournier, A. J. Wong, and M. Park (1999)
Mol. Cell. Biol. 19, 1784-1799
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The Multisubstrate Docking Site of the MET Receptor Is Dispensable for MET-mediated RAS Signaling and Cell Scattering.
D. Tulasne, R. Paumelle, K. M. Weidner, B. Vandenbunder, and V. Fafeur (1999)
Mol. Biol. Cell 10, 551-565
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Activation of Stress-activated Protein Kinase/c-Jun NH2-terminal Kinase and p38 Kinase in Calphostin C-induced Apoptosis Requires Caspase-3-like Proteases but Is Dispensable for Cell Death.
I. Ozaki, E. Tani, H. Ikemoto, H. Kitagawa, and H. Fujikawa (1999)
J. Biol. Chem. 274, 5310-5317
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The Lck SH3 Domain Is Required for Activation of the Mitogen-activated Protein Kinase Pathway but Not the Initiation of T-cell Antigen Receptor Signaling.
M. F. Denny, H. C. Kaufman, A. C. Chan, and D. B. Straus (1999)
J. Biol. Chem. 274, 5146-5152
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Evidence That a Phosphatidylinositol 3,4,5-Trisphosphate-binding Protein Can Function in Nucleus.
K. Tanaka, K. Horiguchi, T. Yoshida, M. Takeda, H. Fujisawa, K. Takeuchi, M. Umeda, S. Kato, S. Ihara, S. Nagata, et al. (1999)
J. Biol. Chem. 274, 3919-3922
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An SH2 Domain-Containing 5' Inositolphosphatase Inhibits Insulin-Induced GLUT4 Translocation and Growth Factor-Induced Actin Filament Rearrangement.
P. Vollenweider, M. Clodi, S. S. Martin, T. Imamura, W. M. Kavanaugh, and J. M. Olefsky (1999)
Mol. Cell. Biol. 19, 1081-1091
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Cyclin D1 Expression Mediated by Phosphatidylinositol 3-Kinase through mTOR-p70S6K-Independent Signaling in Growth Factor-Stimulated NIH 3T3 Fibroblasts.
N. Takuwa, Y. Fukui, and Y. Takuwa (1999)
Mol. Cell. Biol. 19, 1346-1358
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Contrasting Signaling Pathways of {alpha}1A- and {alpha}1B-Adrenergic Receptor Subtype Activation of Phosphatidylinositol 3-Kinase and Ras in Transfected NIH3T3 Cells.
Z.-W. Hu, X.-Y. Shi, R. Z. Lin, and B. B. Hoffman (1999)
Mol. Endocrinol. 13, 3-14
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Raf-1 Is Involved in the Regulation of the Interaction between Guanine Nucleotide Exchange Factor and Ha-Ras. EVIDENCES FOR A FUNCTION OF Raf-1 AND PHOSPHATIDYLINOSITOL 3-KINASE UPSTREAM TO Ras.
C. Giglione and A. Parmeggiani (1998)
J. Biol. Chem. 273, 34737-34744
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Insulin Receptor Substrate 2 And Shc Play Different Roles In Insulin-like Growth Factor I Signaling.
B. Kim, H.-L. Cheng, B. Margolis, and E. L. Feldman (1998)
J. Biol. Chem. 273, 34543-34550
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Differential Regulation of Insulin Receptor Substrate-2 and Mitogen-Activated Protein Kinase Tyrosine Phosphorylation by Phosphatidylinositol 3-Kinase Inhibitors in SH-SY5Y Human Neuroblastoma Cells.
B. Kim, P. S. Leventhal, M. F. White, and E. L. Feldman (1998)
Endocrinology 139, 4881-4889
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Effects of General Receptor for Phosphoinositides 1 on Insulin and Insulin-Like Growth Factor I-Induced Cytoskeletal Rearrangement, Glucose Transporter-4 Translocation, and Deoxyribonucleic Acid Synthesis.
M. Clodi, P. Vollenweider, J. Klarlund, N. Nakashima, S. Martin, M. P. Czech, and J. M. Olefsky (1998)
Endocrinology 139, 4984-4990
   Abstract »    Full Text »    PDF »


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