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

Jean Baptiste Demoulin, Luigi Grasso, John M. Atkins, Monique Stevens, Jamila Louahed, Roy C. Levitt, Nicholas C. Nicolaides, Jean Christophe Renauld

Research output: Contribution to journalArticlepeer-review

18 Scopus citations


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 languageEnglish (US)
Pages (from-to)200-204
Number of pages5
JournalFEBS letters
Issue number3
StatePublished - Oct 6 2000
Externally publishedYes


  • Apoptosis
  • Insulin receptor substrate
  • Interleukin-9
  • Proliferation
  • Protein kinase B

ASJC Scopus subject areas

  • Biochemistry
  • Biophysics
  • Molecular Biology


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