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

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

Authors

  • Hirsch E
  • Katanaev VL
  • Garlanda C
  • Azzolino O
  • Pirola L
  • Silengo L
  • Sozzani S
  • Mantovani A
  • Altruda F
  • Wymann MP

Journal

Science (New York, N.Y.)

Publication Data

February 11, 2000

Associated Grants

  • Agency: Telethon, Id: E.0635

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