| First Author | Hirsch E | Year | 2000 |
| Journal | Science | Volume | 287 |
| Issue | 5455 | Pages | 1049-53 |
| PubMed ID | 10669418 | Mgi Jnum | J:60349 |
| Mgi Id | MGI:1353195 | Doi | 10.1126/science.287.5455.1049 |
| Citation | Hirsch E, et al. (2000) Central role for G protein-coupled phosphoinositide 3-kinase gamma in inflammation [see comments]. Science 287(5455):1049-53 |
| abstractText | 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. |
