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
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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
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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