Gene interactions and pathways from curated databases and text-mining

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IL6 — SMAD3

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
Park et al., Oncogene 2003 (Prostatic Neoplasms) : TGF-beta1 induced IL-6 gene expression was strongly inhibited by DN-Smad2 but not by DN-Smad3 while it was further activated by wild-type Smad2 transfection
Feinberg et al., J Biol Chem 2004 (Arteriosclerosis...) : Adenoviral overexpression of Smad3 potently repressed inducible expression of endogenous iNOS and IL-6
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
Xiao et al., J Immunol 2008 (Autoimmune Diseases) : Retinoic acid increases Foxp3+ regulatory T cells and inhibits development of Th17 cells by enhancing TGF-beta-driven Smad3 signaling and inhibiting IL-6 and IL-23 receptor expression ... Herein we show that RA enhances TGF-beta signaling by increasing the expression and phosphorylation of Smad3 , and this results in increased Foxp3 expression even in the presence of IL-6 or IL-21
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