FEBS Letters | |
Role of insulin receptor substrate‐2 in interleukin‐9‐dependent proliferation | |
Levitt, Roy C.2  Atkins, John M.2  Louahed, Jamila1  Renauld, Jean-Christophe1  Grasso, Luigi2  Nicolaides, Nicholas C.2  Demoulin, Jean-Baptiste1  Stevens, Monique1  | |
[1] Ludwig Institute for Cancer Research and Experimental Medicine Unit, Université Catholique de Louvain, 74 avenue Hippocrate, 1200 Brussels, Belgium;Magainin Institute of Molecular Medicine, Magainin Pharmaceuticals Inc., 5110 Campus drive, Plymouth Meeting, PA 19462, USA | |
关键词: Interleukin-9; Proliferation; Apoptosis; Insulin receptor substrate; Protein kinase B; IL; interleukin; IL-9R; interleukin-9 receptor; JAK; janus kinase; STAT; signal transducer and activator transcription factor; IRS; insulin receptor substrate; PI 3-K; phosphatidylinositol-3 kinase; PKB; protein kinase B; | |
DOI : 10.1016/S0014-5793(00)02059-7 | |
学科分类:生物化学/生物物理 | |
来源: John Wiley & Sons Ltd. | |
【 摘 要 】
Interleukin-9 (IL-9) stimulation results in JAK, STAT and IRS1/2 phosphorylation. The role of IRS adaptor proteins in IL-9 signaling is not clear. We show that IL-9 induces IRS2 phosphorylation and association with phosphatidylinositol-3 kinase (PI 3-K) p85 subunit in TS1 cells and BaF/9R cells, which proliferate upon IL-9 stimulation. We observed a PI 3-K-dependent phosphorylation of protein kinase B (PKB) in TS1 cells, but not in BaF/9R, nor in other IL-9-dependent cell lines. Finally, 32D cells that were transfected with the IL-9 receptor but lack IRS expression survived in the presence of IL-9. Ectopic IRS1 expression allowed for IL-9-induced proliferation, in the absence of significant PKB phosphorylation.
【 授权许可】
Unknown
【 预 览 】
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