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FOS — IL6
Pathways - manually collected, often from reviews:
Text-mined interactions from Literome
Seppänen et al., Oncol Res 1998
(Adenocarcinoma...) :
In the present study, we have investigated the
effects of interferons-alpha (IFN-alpha) and -gamma ( IFN-gamma ),
interleukin-10 (IL-10) and -13 ( IL-13 ), transforming growth factor-beta1 ( TGF-beta1 ), granulocyte-macrophage colony stimulating factor ( GM-CSF ), and tumor necrosis factor-alpha (TNF-alpha) on cell proliferation and induction of transcription factors
AP-1 and NF-kappaB in UM-EC-3 human endometrial adenocarcinoma cells and UT-OC-5 ovarian carcinoma cells in vitro
Jeon et al., Immunopharmacology 2000
:
Treatment of DEX to RAW 264.7 cells
induced a dose related inhibition of NF-kappaB/Rel and
AP-1 in chloramphenicol acetyltransferase activity, while neither
NF-IL6 nor CREB/ATF activation was affected by DEX
Hungness et al., Shock 2000
:
The effect of IL-1beta on AP-1 activity in the enterocyte and the potential
role of
AP-1 in enterocyte
IL-6 production are not known ... Stimulation of these cells with IL-1beta gave rise to results supporting the
role of
AP-1 in the regulation of
IL-6 production ... These results suggest that the AP-1 family of transcription factors is activated by IL-1beta in human enterocytes and that
AP-1 may at least in part
regulate IL-6 production in these cells
Beetz et al., Int J Radiat Biol 2000
:
NF-kappaB and
AP-1 are
responsible for inducibility of the
IL-6 promoter by ionizing radiation in HeLa cells
Georganas et al., J Immunol 2000
(Arthritis, Rheumatoid) :
Inhibition of
c-Jun/AP-1 had no effect on the production of either
IL-6 or IL-8
Schuringa et al., Cytokine 2001
:
In immunoprecipitation experiments, a direct association of STAT3 with c-Jun and
c-Fos was observed in
response to
IL-6
Mann et al., J Biol Chem 2002
:
CD40 induces
interleukin-6 gene transcription in dendritic cells :
regulation by TRAF2,
AP-1 , NF-kappa B, AND CBF1
Liacini et al., Matrix Biol 2002
(Osteoarthritis, Hip) :
Inhibition of
interleukin-1 stimulated MAP kinases,
activating protein-1 (AP-1) and nuclear factor kappa B (NF-kappa B) transcription factors down-regulates matrix metalloproteinase gene expression in articular chondrocytes
Viedt et al., J Am Soc Nephrol 2002
(Nephritis) :
In the present experiments, NF-kappaB and
AP-1 were
involved in the MCP-1 mediated induction of
IL-6 , as demonstrated by cis element double stranded ( decoy ) oligonucleotides ( ODN )
Huang et al., Am J Respir Cell Mol Biol 2003
:
Curcumin, an inhibitor of
AP-1 , also
reduced BK-induced
IL-6 expression
Park et al., Oncogene 2003
(Prostatic Neoplasms) :
TGF-beta1 activated c-Jun phosphorylation, and IL-6 induction by TGF-beta1 was severely impeded by DN-c-Jun and DN-JNK or AP-1 inhibitor curcumin, showing that the
JNK-c-Jun-AP-1 signaling
plays a pivotal role in TGF-beta1 stimulation of
IL-6 ... It was also found that the Ras-Raf-MEK1 cascade is activated by TGF-beta1 and participates in the TGF-beta1 induction of
IL-6 in an
AP-1 dependent manner
An et al., Blood 2004
:
RNA interference experiments confirmed that LANA activates the AP1 RE, stimulates binding of a
c-Jun-Fos heterodimer to the AP1 RE, and
induces expression of
IL-6
Yamauchi et al., Fertil Steril 2004
(Endometriosis) :
These findings demonstrate that NF-kappaB and
AP-1 activation is
critical for TNF-alpha induced
IL-6 expression in endometriotic stromal cells
Lu et al., Mol Biol Cell 2005
(Helicobacter Infections) :
Luciferase reporter gene assays and electrophoretic mobility shift assays showed that full
IL-6 transcription
required binding sites for nuclear factor-kappaB (NF-kappaB), cAMP response element ( CRE ), CCAAT/enhancer binding protein (C/EBP), and
activator protein (AP)-1
Xie et al., J Virol 2005
(Herpesviridae Infections...) :
KSHV activation of
AP-1 leads to the transcriptional induction of
interleukin 6 (IL-6) , which is inhibited by inhibitors or dominant negative constructs of MAPK pathways
Wang et al., Nat Immunol 2006
:
Tumor necrosis factor receptor associated factor 6 ( TRAF6 ) is critical for mediating Toll-like receptor ( TLR )
-interleukin 1 receptor (IL-1R) signaling and subsequent
activation of NF-kappaB and
AP-1 , transcriptional activators of innate immunity
Rohrbach et al., Mol Med 2007
(Heart Failure) :
Activation of
AP-1 contributes to the beta-adrenoceptor mediated myocardial induction of
interleukin-6
Jang et al., Proc Natl Acad Sci U S A 2008
(Encephalitis) :
Taken together, these data suggest luteolin
inhibits LPS induced
IL-6 production in the brain by inhibiting the JNK signaling pathway and activation of
AP-1 in microglia
Kogut et al., Innate Immun 2008
:
Flagellin and lipopolysaccharide up-regulation of
IL-6 and CXCLi2 gene expression in chicken heterophils is
mediated by ERK1/2 dependent activation of
AP-1 and NF-kappaB signaling pathways
Kirchmeyer et al., Arthritis Res Ther 2008
(MAP Kinase Signaling System) :
Among RAR and RXR agonists, only ATRA
inhibited IL-1 induced
IL-6 expression in rat synovial fibroblasts by inhibiting ERK1/2 pathway and subsequent activation of
AP-1 and NF-IL-6 independently of RAR
Wang et al., Int Immunopharmacol 2009
(Disease Models, Animal...) :
3 h after resuscitation, pulmonary capillary leakage and wet/dry weight ratio, levels of tumor necrosis factor (TNF)-alpha,
interleukin (IL)-6 , malondialdehyde ( MDA ), oxidized and reduced glutathione ( GSH and GSSG ), myeloperoxidase (MPO) activity, nuclear factor (NF)-kappaB,
activator protein (AP)-1 activation , and lung microscopic and ultrastructural histological changes were measured
Wang et al., Inflammation 2009
(Inflammation...) :
Three hour after resuscitation, bacterial translocation ( BT ), intestinal permeability, ileal levels of tumor necrosis factor (TNF)-alpha,
interleukin (IL)-6 , malondialdehyde ( MDA ), oxidized and reduced glutathione ( GSH and GSSG ), myeloperoxidase (MPO) activity, nuclear factor (NF)-kappaB,
activator protein (AP)-1 activation , and ileal microscopic and ultrastructural histological changes were measured
Lin et al., J Cell Physiol 2011
(MAP Kinase Signaling System) :
Our data demonstrate that PGN induced
IL-6 expression is
mediated by
AP-1 activation through the TLR2 and JNK/c-Jun pathways in microglia
Fan et al., J Cell Physiol 2011
:
AP-1 , NF-IL-6, and NF-?B cis-elements are
required for gAd induced
IL-6 transcription
Welc et al., Am J Physiol Cell Physiol 2013
(Fever) :
These studies demonstrate that
IL-6 regulation in hyperthermia is directly
controlled by HSF-1 and
AP-1 signaling and that the IL-6 response in C2C12 myotubes is sensitive to categories of protein stress that reflect accumulation of damaged or unfolded proteins
Klampfer et al., Mol Cell Biol 1994
:
Consistent with this possibility, IL-1 and TNF-alpha markedly increase the binding of Fos and Jun to the
AP-1 site, and
NF-IL6 activates the native TSG-6 promoter
Quentmeier et al., Leuk Res 1994
:
Alternatively, these data support the notion that neither
AP-1 nor the c-myc protein are
involved in the MDHM induced increase in IL-1 beta,
IL-6 or TNF alpha mRNA levels
Sung et al., J Biol Chem 1993
:
Stimulation of
interleukin-1 gene transcription may be
caused by the stimulation of transcription factor activities, including those of
AP-1 , by these protein phosphatase inhibitors
Hattori et al., Am J Physiol 1993
(Acute-Phase Reaction...) :
In addition,
IL-6 , tumor necrosis factor-alpha, and IL-1 beta, cytokine regulators of the acute phase response,
stimulated expression of an
AP-1 responsive reporter gene introduced by DNA mediated transfection into adult rat hepatocytes in primary culture
Tuyt et al., Br J Haematol 1996
:
Since AP-1 has been suggested as negative regulator of the IL-6 gene expression, it is conceivable that, after priming with IL-3, the reduced DNA binding activity of
AP-1 , in conjunction with the increased DNA binding of NF-IL6, might
result in a synergistic effect on
IL-6 mRNA expression, when compared to stimulation with LPS alone
Swiergiel et al., Brain Res Bull 1996
:
The role of cerebral noradrenergic systems in the
Fos response to
interleukin-1
Chang et al., Brain Res 1996
:
FOS expression
induced by
interleukin-1 or acute morphine treatment in the rat hypothalamus is attenuated by chronic exposure to morphine
Callahan et al., J Neuroimmunol 1997
:
IL-6 also
induced immunolabeled
Fos in the anterior pituitary gland, however, it did not induce Fos expression in CRF neurons of PVN
Wang et al., Surgery 1998
(Carcinoma, Hepatocellular) :
IL-6 increased c-jun mRNA, c-Jun protein, and
AP-1 binding activity but did not affect either junD or junB expression