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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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

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.[1]

References

  1. Role of insulin receptor substrate-2 in interleukin-9-dependent proliferation. Demoulin, J.P., Grasso, L., Atkins, J.M., Stevens, M., Louahed, J., Levitt, R.C., Nicolaides, N.C., Renauld, J.C. FEBS Lett. (2000) [Pubmed]
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