Gene interactions and pathways from curated databases and text-mining

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SOCS1 — TNF

Text-mined interactions from Literome

Chong et al., J Biol Chem 2002 (MAP Kinase Signaling System) : A further analysis revealed that SOCS-1 deficiency results in augmented TNF signaling via the p38 mitogen activated protein kinase pathway but not NFkappaB or c-Jun N-terminal kinase pathways ... Therefore, these findings provide evidence that physiological levels of SOCS-1 negatively regulate TNF signaling
Federici et al., J Immunol 2002 (Dermatitis, Allergic Contact...) : We show in this work that SOCS1, SOCS2, SOCS3, and cytokine-inducible SH2 containing protein mRNA were up-regulated by IFN-gamma in normal human keratinocytes, whereas only SOCS1 or SOCS1 and cytokine-inducible SH2 containing protein were induced by TNF-alpha or IL-4, respectively
Wesemann et al., J Immunol 2002 : Additionally, IFN-gamma induced TNF-alpha secretion, as well as STAT-1alpha and NF-kappaB activation, are inhibited in the presence of SOCS-1
Fasshauer et al., J Endocrinol 2004 (Insulin Resistance) : Furthermore, TNFalpha and GH caused sustained upregulation of SOCS-1 for up to 24 h, whereas stimulation by IL-6 was only transient, with SOCS-1 mRNA returning to basal levels 2 h after effector addition
Chong et al., J Immunol 2004 (Diabetes Mellitus, Type 1...) : Additionally, IFN-gamma induced class I MHC up-regulation and TNF- and IFN-gamma induced IL-15 expression by beta cells were inhibited by SOCS-1 , which correlated with suppressed 8.3 T cell proliferation in vitro
Kimura et al., Int Immunol 2004 : We also show that the activations of Jaks and caspases by TNF-alpha are suppressed by SOCS-1
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
González-León et al., J Endotoxin Res 2006 : Nitric oxide induces SOCS-1 expression in human monocytes in a TNF-alpha dependent manner
Prêle et al., J Immunol 2008 : This study has used an adenoviral transfection system to determine the role of SOCS1 in the regulation of TNF-alpha production by activated human monocytes ... However, SOCS1 suppressed the sustained production of TNF-alpha by primary human monocytes and synovial fluid macrophages ex vivo
Oh et al., Oncogene 2009 : In Jurkat T cells and mouse splenocytes, we have found that SOCS1 is induced in response to tumor necrosis factor-alpha or H ( 2 ) O ( 2 ), concomitant with the activation of Jaks which act as important mediators of reactive oxygen species ( ROS ) -induced apoptosis upstream of p38 mitogen activated protein kinase
John et al., J Orthop Res 2010 : TNFalpha stimulation augmented SOCS1 , whereas SOCS3 expression in tenocytes was also induced by IL-6
Woodward et al., Immunology 2010 : We investigated whether the early induction of SOCS1 by IL-4 was responsible for the suppression of LPS induced tumour necrosis factor (TNF)-alpha production by IL-4 ... These data suggest that SOCS1 is not involved in the suppression of LPS induced TNF-alpha production by IL-4
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