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- Publisher Website: 10.1126/science.287.5455.1040
- Scopus: eid_2-s2.0-0034635264
- PMID: 10669416
- WOS: WOS:000085245400048
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Article: Function of PI3Kγ in thymocyte development, T cell activation, and neutrophil migration
Title | Function of PI3Kγ in thymocyte development, T cell activation, and neutrophil migration |
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Authors | |
Issue Date | 2000 |
Citation | Science, 2000, v. 287, n. 5455, p. 1040-4046 How to Cite? |
Abstract | Phosphoinositide 3-kinase (PI3Ks) regulate fundamental cellular responses such as proliferation, apoptosis, cell motility, and adhesion. Viable gene-targeted mice lacking the p110 catalytic subunit of PI3Kγ were generated. We show that PI3Kγ controls thymocyte survival and activation of mature T cells but has no role in the development or function of B cells. PI3Kγ-deficient neutrophils exhibited severe defects in migration and respiratory burst in response to heterotrimeric GTP-binding protein (G protein)-coupled receptor (GPCR) agonist and chemotactic agents. PI3Kγ 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 signa-regulated kinases 1 and 2. Thus, PI3Kγ regulates thymocyte development, T cell activation, neutrophil migration, and the oxidative burst. |
Persistent Identifier | http://hdl.handle.net/10722/291539 |
ISSN | 2023 Impact Factor: 44.7 2023 SCImago Journal Rankings: 11.902 |
ISI Accession Number ID |
DC Field | Value | Language |
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dc.contributor.author | Sasaki, Takehiko | - |
dc.contributor.author | Irie-Sasaki, Junko | - |
dc.contributor.author | Jones, Russell G. | - |
dc.contributor.author | Oliveira-Dos-Santos, Antonio J. | - |
dc.contributor.author | Stanford, William L. | - |
dc.contributor.author | Bolon, Brad | - |
dc.contributor.author | Wakeham, Andrew | - |
dc.contributor.author | Itie, Annick | - |
dc.contributor.author | Bouchard, Dennis | - |
dc.contributor.author | Kozieradzki, Ivona | - |
dc.contributor.author | Joza, Nicholas | - |
dc.contributor.author | Mak, Tak W. | - |
dc.contributor.author | Ohashi, Pamela S. | - |
dc.contributor.author | Suzuki, Akira | - |
dc.contributor.author | Penninger, Josef M. | - |
dc.date.accessioned | 2020-11-17T14:54:35Z | - |
dc.date.available | 2020-11-17T14:54:35Z | - |
dc.date.issued | 2000 | - |
dc.identifier.citation | Science, 2000, v. 287, n. 5455, p. 1040-4046 | - |
dc.identifier.issn | 0036-8075 | - |
dc.identifier.uri | http://hdl.handle.net/10722/291539 | - |
dc.description.abstract | Phosphoinositide 3-kinase (PI3Ks) regulate fundamental cellular responses such as proliferation, apoptosis, cell motility, and adhesion. Viable gene-targeted mice lacking the p110 catalytic subunit of PI3Kγ were generated. We show that PI3Kγ controls thymocyte survival and activation of mature T cells but has no role in the development or function of B cells. PI3Kγ-deficient neutrophils exhibited severe defects in migration and respiratory burst in response to heterotrimeric GTP-binding protein (G protein)-coupled receptor (GPCR) agonist and chemotactic agents. PI3Kγ 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 signa-regulated kinases 1 and 2. Thus, PI3Kγ regulates thymocyte development, T cell activation, neutrophil migration, and the oxidative burst. | - |
dc.language | eng | - |
dc.relation.ispartof | Science | - |
dc.title | Function of PI3Kγ in thymocyte development, T cell activation, and neutrophil migration | - |
dc.type | Article | - |
dc.description.nature | link_to_subscribed_fulltext | - |
dc.identifier.doi | 10.1126/science.287.5455.1040 | - |
dc.identifier.pmid | 10669416 | - |
dc.identifier.scopus | eid_2-s2.0-0034635264 | - |
dc.identifier.volume | 287 | - |
dc.identifier.issue | 5455 | - |
dc.identifier.spage | 1040 | - |
dc.identifier.epage | 4046 | - |
dc.identifier.isi | WOS:000085245400048 | - |
dc.identifier.issnl | 0036-8075 | - |