TRAF6 Mediates Smad-Independent Activation of JNK and p38 by TGF-β

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Abstract

In many physiological and disease processes, TGF-β 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-β 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-β receptors. TGF-β induces K63-linked ubiquitination of TRAF6 and promotes association between TRAF6 and TAK1. Our results indicate that TGF-β activates JNK and p38 through a mechanism similar to that operating in the interleukin-1β/Toll-like receptor pathway. © 2008 Elsevier Inc. All rights reserved.

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Yamashita, M., Fatyol, K., Jin, C., Wang, X., Liu, Z., & Zhang, Y. E. (2008). TRAF6 Mediates Smad-Independent Activation of JNK and p38 by TGF-β. Molecular Cell, 31(6), 918–924. https://doi.org/10.1016/j.molcel.2008.09.002

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