| Literature DB >> 18922473 |
Motozo Yamashita1, Karoly Fatyol, Chaoyang Jin, Xiangchun Wang, Zhenggang Liu, Ying E Zhang.
Abstract
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.Entities:
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Year: 2008 PMID： 18922473 PMCID： PMC2621323 DOI： 10.1016/j.molcel.2008.09.002
Source DB: PubMed Journal: Mol Cell ISSN： 1097-2765 Impact factor: 17.970