First Author | Sasaki T | Year | 2000 |
Journal | Science | Volume | 287 |
Issue | 5455 | Pages | 1040-6 |
PubMed ID | 10669416 | Mgi Jnum | J:60347 |
Mgi Id | MGI:1353193 | Doi | 10.1126/science.287.5455.1040 |
Citation | Sasaki T, et al. (2000) Function of PI3Kgamma in thymocyte development, T cell activation, and neutrophil migration [see comments]. Science 287(5455):1040-6 |
abstractText | 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. |