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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