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SOCS3 — TNF

Text-mined interactions from Literome

Colson et al., Endocrinology 2000 : Although IL-1/beta and TNFalpha alone induced only weakly the expression of SOCS-3 and CIS, these cytokines strongly potentiated the induction of these two SOCS by GH ... Considering the ability of these SOCS to inhibit the JAK-STAT pathway induced by GH, these results suggest that the overexpression of SOCS-3 and CIS mRNAs induced by IL-1beta and TNFalpha or by endotoxin in vivo may play a role in the GH resistance induced by sepsis
Berlato et al., J Immunol 2002 (MAP Kinase Signaling System) : Herein, we show that stable transfection of SOCS-3 into the mouse macrophage cell line J774 resulted in an inhibition of NO, TNF-alpha , IL-6, and GM-CSF secretion in response to LPS at levels similar to those exerted by IL-10 in LPS stimulated wild-type J774 ... Constitutive SOCS-3 expression also down-regulated the mRNA expression of inducible NO synthase and IL-6 and impaired the production of TNF-alpha , mainly at a post-transcriptional level
Bode et al., J Immunol 2003 : Recently, it has been demonstrated that TNF-alpha and LPS induce the expression of suppressor of cytokine signaling 3 ( SOCS3 ) and inhibit IL-6 induced STAT3 activation in macrophages
Williams et al., J Immunol 2004 : Overexpression of STAT3 DN completely inhibited IL-10 induced suppressor of cytokine signaling 3 , tissue inhibitor of MMP-1, TNF receptor expression, and the recently identified IL-10-inducible genes, T cell protein tyrosine phosphatase and signaling lymphocyte activation molecule
Fasshauer et al., J Endocrinol 2004 (Insulin Resistance) : Recently, it was demonstrated that induction of suppressor of cytokine signaling (SOCS)-3 by TNFalpha and GH is an important mechanism by which these cytokines impair insulin sensitivity
Cassatella et al., Eur J Immunol 2005 : In this study, we show that modulation by IL-10 of LPS induced TNF-alpha , CXCL8/IL-8 and IL-1 receptor antagonist (IL-1ra) mRNA accumulation in neutrophils already expressing a functional IL-10R and antigenic SOCS-3 ( i.e. in `` 4-h cultured '' neutrophils ) occurs with kinetics that are similar to those observed in `` time 0 '' neutrophils, depends on de novo protein synthesis, but does not require SOCS-1, SOCS-3 , heme oxygenase and Bcl-3 induction
He et al., Biochem Biophys Res Commun 2006 : On the contrary, tumor necrosis factor (TNF) alpha and insulin, which very weakly induce SOCS-3 expression, have profound effects on IRS-1 degradation
Prêle et al., Immunology 2006 : Physiological levels of SOCS3 detected in IL-10 exposed human monocytes had no effect on LPS induced TNF-alpha production
Rigby et al., Oncogene 2007 (Colonic Neoplasms...) : In vitro, SOCS3 overexpression reduced proliferation, IL-6 mediated STAT3 activation and tumor necrosis factor (TNF) alpha mediated NF-kappaB activation
Ehlting et al., J Immunol 2007 (MAP Kinase Signaling System) : Regulation of suppressor of cytokine signaling 3 ( SOCS3 ) mRNA stability by TNF-alpha involves activation of the MKK6/p38MAPK/MK2 cascade ... In this study, we investigate SOCS3 expression initiated by the proinflammatory cytokine TNF-alpha ... In contrast to IL-6, TNF-alpha increases SOCS3 expression by stabilizing SOCS3 mRNA ... However, data from TTP-deficient cells suggest that TTP does not play an irreplaceable role in the regulation of SOCS3 mRNA stability by TNF-alpha ... In summary, these data indicate that TNF-alpha regulates SOCS3 expression on the level of mRNA stability via activation of the MKK6/p38 ( MAPK ) cascade and that the activation of MK2, a downstream target of p38 ( MAPK ), is important for the regulation of SOCS3 expression
Gupta et al., Exp Mol Pathol 2011 (Disease Models, Animal...) : Western blot data revealed significantly high SOCS-3 expression in PCASMCs in the presence of either TNF-a or IGF-1 ( 5-6 fold ) alone ... However, in the presence of both TNF-a and IGF-1 the SOCS-3 expression was significantly decreased ( 4-5 fold )
Dai et al., J Cell Biochem 2013 : Kallikrein binding protein inhibits LPS induced TNF-a by upregulating SOCS3 expression ... RNA interference assay and luciferase assay showed that SOCS3 was responsible for the down-regulation of TNF-a by KBP, rather than NF-?B subunit p65 and ß-catenin
Dhar et al., Am J Physiol Heart Circ Physiol 2013 : Downregulation of SOCS3 in the presence of both TNF-a and IGF-1 in hCASMCs is due to SOCS3 promoter hypermethylation involving STAT3-NFkBp65 interaction
Park et al., J Allergy Clin Immunol 2013 (Nasal Polyps...) : Nasal epithelial cell culture was used to elucidate the effect of IL-4, IL-5, IL-6, IL-10, IL-13, IFN-?, TNF-a , and TGF-ß1 on SOCS1 and SOCS3 expression in sinus mucosa ... SOCS1 was induced by IL-4, IL-13, IFN-?, and TNF-a , while SOCS3 expression was upregulated by IL-6, IL-13, IFN-?, and TNF-a
Carow et al., PLoS Pathog 2013 : Instead, SOCS3 expression in infected macrophages and DCs prevented the IL-6 mediated inhibition of TNF and IL-12 secretion and contributed to a timely CD4+ cell dependent IFN-? expression in vivo