Journal
MOLECULAR CELL
Volume 31, Issue 6, Pages 918-924Publisher
CELL PRESS
DOI: 10.1016/j.molcel.2008.09.002
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Funding
- Intramural NIH HHS [Z01 BC010419-08] Funding Source: Medline
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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 TRAFIS 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 TAKII. Our results indicate that TGF-beta activates JNK and p38 through a mechanism similar to that operating in the interleukin-1 beta/Tolllike receptor pathway.
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