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UCSC Genome Browser Gene Interaction Graph
Gene interactions and pathways from curated databases and text-mining

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SMAD5 — TNF

Text-mined interactions from Literome

Verrecchia et al., J Biol Chem 2000 : Tumor necrosis factor-alpha inhibits transforming growth factor-beta /Smad signaling in human dermal fibroblasts via AP-1 activation ... In this report, we demonstrate that TNF-alpha prevents TGF-beta induced Smad-specific gene transactivation without inducing detectable levels of inhibitory Smad7 in human dermal fibroblasts ... Expression of antisense c-Jun mRNA prevents TNF-alpha inhibition of TGF-beta/Smad signaling whereas that of dominant negative Ikappa-B kinase-alpha or antisense Smad7 does not
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
Tzimas et al., Cell Signal 2006 : Overexpression of USP31 in HEK 293T cells inhibited TNFalpha , CD40, LMP1, TRAF2, TRAF6 and IKKbeta mediated NF-kappaB activation, but did not inhibit Smad mediated transcription activation
Li et al., J Bone Miner Res 2007 (Osteoporosis) : In vitro, TNFalpha suppresses BMP-2- and TGFbeta mediated Smad activation through induction of NF-kappaB ... In vitro, TNFalpha potently suppressed Smad signaling induced by TGFbeta and BMP-2, downregulated BMP-2 mediated Runx2 expression, and inhibited mineralization of osteoblasts
Yamaguchi et al., Int J Mol Med 2011 (Bone Resorption) : Furthermore, vitamin K2 prevented repression by tumor necrosis factor a (TNFa) of SMAD signaling induced by either transforming growth factor ß ( TGFß ) or bone morphogenetic protein-2 (BMP-2)
Tang et al., Stem Cells Dev 2013 (Lupus Erythematosus, Systemic) : TNF activated NF-?B pathway and inhibited the phosphorylation of Smad 1/5/8 and BMP-2 induced osteoblastic differentiation in BMMSCs from normal controls, while addition of pyrollidine dithiocarbamate ( PDTC ), an NF-?B inhibitor, to SLE-BMMSCs could partially reverse these effects