Reference : Non-redundant signal transduction of interleukin-6-type cytokines. The adapter protei...
Scientific journals : Article
Life sciences : Biochemistry, biophysics & molecular biology
Non-redundant signal transduction of interleukin-6-type cytokines. The adapter protein Shc is specifically recruited to rhe oncostatin M receptor
Hermanns, H. M. [> >]
Radtke, S. [> >]
Schaper, F. [> >]
Heinrich, P. C. [> >]
Behrmann, Iris mailto [University of Luxembourg > Faculty of Science, Technology and Communication (FSTC) > Life Science Research Unit >]
Journal of Biological Chemistry
American Society for Biochemistry and Molecular Biology
Yes (verified by ORBilu)
[en] Adaptor Proteins, Signal Transducing ; Peptides ; Promoter Regions (Genetics) ; Proteins ; Rats ; Receptors, Cytokine ; Receptors, Oncostatin M ; Signal Transduction ; Tyrosine ; Oncostatin M ; Mitogen-Activated Protein Kinases ; Lymphokines ; Adaptor Proteins, Vesicular Transport ; Animals ; COS Cells ; Dimerization ; GRB2 Adaptor Protein ; Growth Inhibitors ; Interleukin-6 ; Leukemia Inhibitory Factor ; alpha-Macroglobulins
[en] The common use of the cytokine receptor gp130 has served as an explanation for the extremely redundant biological activities exerted by interleukin (IL)-6-type cytokines. Indeed, hardly any differences in signal transduction initiated by these cytokines are known. In the present study, we demonstrate that oncostatin M (OSM), but not IL-6 or leukemia inhibitory factor, induces tyrosine phosphorylation of the Shc isoforms p52 and p66 and their association with Grb2. Concomitantly, OSM turns out to be a stronger activator of ERK1/2 MAPKs. Shc is recruited to the OSM receptor (OSMR), but not to gp130. Binding involves Tyr(861) of the OSMR, located within a consensus binding sequence for the Shc PTB domain. Moreover, Tyr(861) is essential for activation of ERK1/2 and for full activation of the alpha(2)-macroglobulin promoter, but not for an exclusively STAT-responsive promoter. This study therefore provides evidence for qualitative differential signaling mechanisms exerted by IL-6-type cytokines.

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