TRAF6 Mediates Smad-Independent Activation of JNK and p38 by TGF-β
Copyright policy )TRAF6 Mediates Smad-Independent Activation of JNK and p38 by TGF-β
In many physiological and disease processes, TGF-beta usurps branches of MAP kinase pathways in conjunction with Smads to induce apoptosis and epithelial-to-mesenchymal transition, but the detailed mechanism of how a MAP kinase cascade is activated by TGF-beta receptors is not clear. We report here that TRAF6 is specifically required for the Smad-independent activation of JNK and p38, and its carboxyl TRAF homology domain physically interacts with TGF-beta receptors. TGF-beta induces K63-linked ubiquitination of TRAF6 and promotes association between TRAF6 and TAK1. Our results indicate that TGF-beta activates JNK and p38 through a mechanism similar to that operating in the interleukin-1beta/Toll-like receptor pathway.
- National Cancer Institute United States
- Center for Cancer Research United States
- National Institute of Health Pakistan
TNF Receptor-Associated Factor 6, Lysine, JNK Mitogen-Activated Protein Kinases, Ubiquitination, Apoptosis, Smad Proteins, Cell Biology, MAP Kinase Kinase Kinases, p38 Mitogen-Activated Protein Kinases, Epithelium, Cell Line, Enzyme Activation, Mesoderm, Mice, Transforming Growth Factor beta, Animals, Humans, Molecular Biology, Receptors, Transforming Growth Factor beta, Protein Binding, Signal Transduction
TNF Receptor-Associated Factor 6, Lysine, JNK Mitogen-Activated Protein Kinases, Ubiquitination, Apoptosis, Smad Proteins, Cell Biology, MAP Kinase Kinase Kinases, p38 Mitogen-Activated Protein Kinases, Epithelium, Cell Line, Enzyme Activation, Mesoderm, Mice, Transforming Growth Factor beta, Animals, Humans, Molecular Biology, Receptors, Transforming Growth Factor beta, Protein Binding, Signal Transduction
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