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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