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IL6 — SMAD4

Text-mined interactions from Literome

Verrecchia et al., J Biol Chem 2003 : We demonstrate that, in a cellular context devoid of JNK activity ( i.e. jnk ( -/- ) fibroblasts ), interleukin-1 and tumor necrosis factor-alpha (TNF-alpha) did not inhibit the formation of SMAD-DNA complexes and the resulting SMAD-driven transcription in response to TGF-beta
Zhang et al., J Biol Chem 2005 : These results indicate that IL-6 increased trafficking of TGF-beta1 receptors to non-lipid raft associated pools results in augmented TGF-beta1 Smad signaling
Lee et al., J Biol Chem 2010 : At the intracellular level, both Smad and p38 signaling pathways are required for the induction of IL-6
Ciuclan et al., Am J Respir Crit Care Med 2011 (Acute Disease...) : Molecular analysis showed a dysregulated transforming growth factor-ß/bone morphogenetic protein/Smad axis in SU5416- and/or hypoxia treated mice as well as augmented induction of IL-6 and Hif-1a levels
Ma et al., PloS one 2012 (Fibrosis) : Macrophage stimulated cardiac fibroblast production of IL-6 is essential for TGF ß/Smad activation and cardiac fibrosis induced by angiotensin II
Yamada et al., Eur J Cancer 2013 (Biliary Tract Neoplasms) : Smad4 functioned in this process in a dominant manner, and inhibition by SMAD4 siRNA reduced IL-6 and TGF-ß1 expression, blocked invasion, and reversed EMT and chemoresistance in cells exposed to rh IL-6 and TGF-ß1 and in gemcitabine-resistant cells