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Central role for G protein-coupled phosphoinositide 3-kinase gamma in inflammation.

Science (New York, N.Y.) | Feb 11, 2000

http://www.ncbi.nlm.nih.gov/pubmed/10669418

Phosphoinositide 3-kinase (PI3K) activity is crucial for leukocyte function, but the roles of the four receptor-activated isoforms are unclear. Mice lacking heterotrimeric guanine nucleotide-binding protein (G protein)-coupled PI3Kgamma were viable and had fully differentiated neutrophils and macrophages. Chemoattractant-stimulated PI3Kgamma-/- neutrophils did not produce phosphatidylinositol 3,4,5-trisphosphate, did not activate protein kinase B, and displayed impaired respiratory burst and motility. Peritoneal PI3Kgamma-null macrophages showed a reduced migration toward a wide range of chemotactic stimuli and a severely defective accumulation in a septic peritonitis model. These results demonstrate that PI3Kgamma is a crucial signaling molecule required for macrophage accumulation in inflammation.

Pubmed ID: 10669418 RIS Download

Mesh terms: Animals | Chemotactic Factors | Chemotaxis | Chemotaxis, Leukocyte | Enzyme Activation | Gene Targeting | Heterotrimeric GTP-Binding Proteins | Isoenzymes | Macrophages, Peritoneal | Mice | Mice, Inbred C57BL | Mice, Knockout | Neutrophils | Peritonitis | Phosphatidylinositol 3-Kinases | Phosphatidylinositol Phosphates | Protein-Serine-Threonine Kinases | Proto-Oncogene Proteins | Proto-Oncogene Proteins c-akt | Respiratory Burst | Signal Transduction

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Associated grants

  • Agency: Telethon, Id: E.0635

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