Reference : Non-redundant signal transduction of interleukin-6-type cytokines. The adapter protei... |
Scientific journals : Article | |||
Life sciences : Biochemistry, biophysics & molecular biology | |||
http://hdl.handle.net/10993/6249 | |||
Non-redundant signal transduction of interleukin-6-type cytokines. The adapter protein Shc is specifically recruited to rhe oncostatin M receptor | |
English | |
Hermanns, H. M. [> >] | |
Radtke, S. [> >] | |
Schaper, F. [> >] | |
Heinrich, P. C. [> >] | |
Behrmann, Iris ![]() | |
2001 | |
Journal of Biological Chemistry | |
American Society for Biochemistry and Molecular Biology | |
275 | |
52 | |
40742-8 | |
Yes (verified by ORBilu) | |
International | |
0021-9258 | |
1083-351X | |
Baltimore | |
MD | |
[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. | |
http://hdl.handle.net/10993/6249 | |
10.1074/jbc.M005408200 |
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