Role of insulin receptor substrate‐2 in interleukin‐9‐dependent proliferation

FEBS Letters

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