Gene interactions and pathways from curated databases and text-mining

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IL6 — JUN

Pathways - manually collected, often from reviews:

Text-mined interactions from Literome

Franchimont et al., J Biol Chem 1999 : Platelet derived growth factor induces interleukin-6 transcription in osteoblasts through the activator protein-1 complex and activating transcription factor-2
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
Solís-Herruzo et al., J Biol Chem 1999 : Mobility shift assays demonstrated that IL-6 induced the DNA binding activity of AP1
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 )
Pinteaux et al., J Neurochem 2002 : Bacterial lipopolysaccharide (LPS) caused increased expression of IL-1RI, IL-1RII and IL-1RAcP mRNAs, induced the release of IL-1beta, IL-6 and prostaglandin-E2 ( PGE2 ), and activated nuclear factor kappaB (NF-kappaB) and the mitogen activated protein kinases ( MAPKs ) p38, and extracellular signal regulated protein kinase ( ERK1/2 ), but not c-Jun N-terminal kinase (JNK) in microglial cultures
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
Xiao et al., Cancer Biol Ther 2004 (Multiple Myeloma) : Among these regulatory sites, IL6-AP1 is the most important cis-regulatory site, and plays a vital role in the constitutive expression of IL-6 in IM9 cells
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
Hsieh et al., Carcinogenesis 2007 (Bone Neoplasms...) : Silibinin also inhibited interleukin-6 induced ERK 1/2 and c-Jun phosphorylation, and cell invasiveness
Gazi et al., Clin Chim Acta 2007 (Prostatic Neoplasms) : Taken together, our results suggest that sodium selenite not methylseleninic acid can inhibit IL-6 mediated AR activation by increased c-Jun in LNCaP cells
Rohrbach et al., Mol Med 2007 (Heart Failure) : Activation of AP-1 contributes to the beta-adrenoceptor mediated myocardial induction of interleukin-6
Vanden Bush et al., Eur J Immunol 2008 : The enhanced IL-6 production was dependent upon the activity of c-Jun kinase (JNK) and cFos
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
Shen et al., Curr Eye Res 2009 : Under high glucose conditions, interleukin-1beta significantly increased expression of c-Jun and decreased the expression of glutamine synthetase
Li et al., J Cell Biochem 2010 (MAP Kinase Signaling System) : We also observed that IL-6 and high glucose stimulated the expression of c-Jun , a key subunit of AP-1 known to be essential for MMP-1 transcription
Sierra et al., Microb Pathog 2010 (Gram-Negative Bacterial Infections) : Further, AexU prevented phosphorylation of c-Jun , JNK and IkappaBalpha and inhibited IL-6 and IL-8 secretion from HeLa cells
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
Zhang et al., Zhonghua Jie He He Hu Xi Za Zhi 2010 (Ventilator-Induced Lung Injury) : [ Expression of intercellular cell adhesion molecule-1, interleukin-10 and the activation of activator protein-1 in ventilator induced lung injury in rabbits ]
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
Herfs et al., Am J Respir Cell Mol Biol 2012 (Hyperplasia...) : Using immunohistological techniques, we showed a higher epithelial expression of TNF-a, IL-1ß, and IL-6 , as well as an activation of NF-?B and activator protein-1/mitogen activated protein kinase signaling pathways in the respiratory tract of smoking patients, compared with the normal ciliated epithelium of nonsmoking patients
Whitham et al., J Biol Chem 2012 : Contraction induced interleukin-6 gene transcription in skeletal muscle is regulated by c-Jun terminal kinase/activator protein-1
El Hajj et al., Endocrinology 2012 (Inflammation) : Furthermore, expression of IL-6 and IL-8 cytokines in patient fibroblasts was down-regulated by MAPK, p38MAPK, and Jun N-terminal kinase inhibitors
Byun et al., Biochem Biophys Res Commun 2012 (Inflammation) : In addition, EGCG treated DCs inhibited lipopolysaccharide (LPS) induced production of pro-inflammatory cytokines ( tumor necrosis factor [TNF ] -a, interleukin [ IL]-1ß, and IL-6 ) and activation of mitogen activated protein kinases ( MAPKs ), e.g., extracellular signal regulated kinase 1/2 ( ERK1/2 ), p38, c-Jun N-terminal kinase (JNK) , and nuclear factor ?B ( NF-?B ) p65 translocation through 67LR ... In addition, EGCG treated DCs inhibited lipopolysaccharide (LPS) induced production of pro-inflammatory cytokines ( tumor necrosis factor [TNF ] -a, interleukin [ IL]-1ß, and IL-6 ) and activation of mitogen activated protein kinases ( MAPKs ), e.g., extracellular signal regulated kinase 1/2 ( ERK1/2 ), p38, c-Jun N-terminal kinase (JNK) , and nuclear factor ?B ( NF-?B ) p65 translocation through 67LR
Zhang et al., Arch Biochem Biophys 2012 (MAP Kinase Signaling System...) : IL-6 significantly downregulated P4Ha1 expression in HASMCs through an RAF-MEK1/2-ERK1/2 mitogen activated protein kinase ( MAPK ) pathway, and c-Jun was involved in the process
Valles et al., Journal of translational medicine 2013 (Melanoma, Experimental...) : Corticosterone- and noradrenaline induced transcriptional up-regulation of IL-6 gene involves changes in the DNA binding activity of nuclear factor-?B, cAMP response element binding protein, activator protein-1 , and nuclear factor for IL-6
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 ... 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
Melamed et al., Cell Growth Differ 1993 (Leukemia, Myeloid, Acute) : Interleukin 6 induces DNA binding activity of AP1 in M1 myeloblastic cells but not in a growth resistant cell derivative ... The data correlate the IL-6 induced AP1 activity with the suppression of c-myc and growth inhibition
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
Schwenger et al., Proc Natl Acad Sci U S A 1997 : c-Jun N-terminal kinase activation induced by interleukin 1 or epidermal growth factor was less strongly inhibited by NaSal
Sansbury et al., Carcinogenesis 1997 (Thymoma) : Phorbol ester induced morphological changes, ERK activation, calcium dependent activation of the c-Jun N-terminal kinase (JNK) , interleukin-2 synthesis, and growth inhibition in sensitive but not resistant cells
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