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      Function of PI3Kgamma in thymocyte development, T cell activation, and neutrophil migration.

      Science (New York, N.Y.)

      Animals, Antigens, CD, analysis, Apoptosis, Cell Line, Chemotactic Factors, pharmacology, Chemotaxis, Leukocyte, physiology, Heterotrimeric GTP-Binding Proteins, metabolism, Lymph Nodes, cytology, Lymphocyte Activation, Mice, Mice, Knockout, Mitogen-Activated Protein Kinases, Neutrophils, Peritonitis, immunology, Phosphatidylinositol 3-Kinases, Phosphatidylinositol Phosphates, Protein-Serine-Threonine Kinases, Proto-Oncogene Proteins, Proto-Oncogene Proteins c-akt, Respiratory Burst, Signal Transduction, Spleen, T-Lymphocytes, Thymus Gland

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          Abstract

          Phosphoinositide 3-kinases (PI3Ks) regulate fundamental cellular responses such as proliferation, apoptosis, cell motility, and adhesion. Viable gene-targeted mice lacking the p110 catalytic subunit of PI3Kgamma were generated. We show that PI3Kgamma controls thymocyte survival and activation of mature T cells but has no role in the development or function of B cells. PI3Kgamma-deficient neutrophils exhibited severe defects in migration and respiratory burst in response to heterotrimeric GTP-binding protein (G protein)-coupled receptor (GPCR) agonists and chemotactic agents. PI3Kgamma links GPCR stimulation to the formation of phosphatidylinositol 3,4,5-triphosphate and the activation of protein kinase B, ribosomal protein S6 kinase, and extracellular signal-regulated kinases 1 and 2. Thus, PI3Kgamma regulates thymocyte development, T cell activation, neutrophil migration, and the oxidative burst.

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          Journal
          10669416
          10.1126/science.287.5455.1040

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