Abstract
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. (C) 2000 Federation of European Biochemical Societies.
Original language | English (US) |
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Pages (from-to) | 200-204 |
Number of pages | 5 |
Journal | FEBS letters |
Volume | 482 |
Issue number | 3 |
DOIs | |
State | Published - Oct 6 2000 |
Keywords
- Apoptosis
- Insulin receptor substrate
- Interleukin-9
- Proliferation
- Protein kinase B
ASJC Scopus subject areas
- Biochemistry
- Biophysics
- Molecular Biology