Hidetoshi Hayashi

TL;DR: A novel function for MAD-related proteins as intracellular antagonists of the type I kinase domain of TGFβ family receptors is defined as blocking the association, phosphorylation, and activation of Smad2.

TL;DR: The results indicate that TRB3 is a novel target of CHOP/ATF4 and downregulates its own induction by repression of CHop/atF4 functions, and that it is involved in CHOP‐dependent cell death during ER stress.

TL;DR: Results indicate that receptor-dependent phosphorylation of Smad2 on serines 465 and 467 is required in mammalian cells to permit association with Smad4 and to propagate TGF-β signals.

TL;DR: It is shown that the co-activator p300/CBP bound and acetylated Smad3 as well as Smad2 in vivo, and that the acetylation was stimulated by TGF-β.

TL;DR: TAK1-mediated activation of NF-κB required the transient formation of a signaling complex that included tumor necrosis factor receptor–associated factor 6 (TRAF6), MEKK3, and TAK1, which was required for the production of sufficient cytokines.