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IL18 — JUN

Pathways - manually collected, often from reviews:

• OpenBEL Selventa BEL large corpus: JUN → IL18 (increases) Chandrasekar et al., J Biol Chem 2006*
  Evidence: ELISA of nuclear proteins revealed a significant increase in c-Fos, Fra-1, and c-Jun and, to smaller extent, in FosB and JunB. Fra-2 and JunD levels were not modulated by IL-18 (Fig. 7B).
• OpenBEL Selventa BEL large corpus: JUN → IL18 (increases, IL18 Activity) Chandrasekar et al., J Biol Chem 2006*
  Evidence: The results in Fig. 7D show that antisense ODN targeting of c-Fos, c-Jun, and Fra-1 significantly attenuated MMP9 transcription. In contrast, ectopic expression of c-Fos, c-Jun, and Fra-1 inducedMMP9transcription (Fig. 7E).

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
Guo et al., Immunopharmacology 2000 : Antisense IRAK-1 oligonucleotide blocks activation of NF-kappa B and AP-1 induced by IL-18 ... Interleukin-1 receptor associated kinase-1 ( IRAK-1 ) has recently been shown to be involved in IL-18 stimulated activation of NF-kappaB and AP-1 ... The purpose of this study is to investigate the effects of preventing IRAK-1 expression by antisense IRAK-1 oligodeoxynucleotide ( ODN ) on IL-18 stimulated activation of NF-kappaB and AP-1 ... As a result, antisense IRAK-1 ODN attenuated IL-18 induced activation of NF-kappaB and AP-1 as measured by sandwich ELISA in a concentration ( 1-8 microg ml(-1) ) - and time ( 5-24 h ) -dependent fashion
Greene et al., J Immunol 2000 (Sarcoidosis, Pulmonary) : We examined the effects of IL-18 on AP1 and NF-kappaB in Jurkat T cells in vitro
Nakahira et al., J Immunol 2002 : Synergy of IL-12 and IL-18 for IFN-gamma gene expression : IL-12 induced STAT4 contributes to IFN-gamma promoter activation by up-regulating the binding activity of IL-18 induced activator protein 1 ... An increase in c-Jun, a component of AP-1, in the nuclear compartment was elicited by stimulation with either IL-12 or IL-18, but accumulation of serine phosphorylated c-Jun was induced only by IL-18 capable of activating c-Jun N-terminal kinase
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
Morel et al., J Biol Chem 2002 (Arthritis, Rheumatoid...) : Electrophoretic mobility shift assay showed that activator protein-1 (AP-1) is activated by IL-18 through ERK and Src but not through PI3-kinase
Cho et al., Biochem Biophys Res Commun 2002 : The enhanced IL-18 production by UVB irradiation requires ROI and AP-1 signaling in human keratinocyte cell line ( HaCaT ) ... Furthermore, inhibitors of UVB induced AP-1 activity, such as PD98059, blocked enhanced IL-18 production, indicating that AP-1 activation is required for UVB induced IL-18 production
Sugimoto et al., Eur J Immunol 2003 : IL-18 , but not IL-12, induced activator protein-1 (AP-1) responsible for high levels of IFN-gamma promoter activation
Chandrasekar et al., J Biol Chem 2005 : Src kinase inhibitors PP1 and PP2, phosphatidylinositol 3-kinase (PI3K) inhibitors wortmannin and LY294002, Akt inhibitor, the c-Jun N-terminal kinase (JNK) inhibitor SP600125, antisense JNK and dominant negative MyD88, interleukin-1 receptor associated kinase ( IRAK)-1, IRAK4, and phosphatidylinositol 3-kinase expression all attenuated IL-18 mediated AP-1 binding and reporter activity, CXCL16 promoter-reporter activity, and CXCL16 expression
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
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
Venkatesan et al., J Mol Cell Cardiol 2010 : We show for the first time that EMMPRIN stimulates the activation of NF-kappaB, AP-1 , CREB, and ATF-2 in cardiomyocytes, and induces IL-18 expression via Rac1 dependent PI3K/Akt/IKK/NF-kappaB and MKK7/JNK/AP-1 signaling
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 ]
Valente et al., J Mol Cell Cardiol 2012 (Cardiomegaly...) : Here we report that Ang-II induced CIKS mRNA and protein expression, CIKS binding to IKK and JNK perhaps functioning as a scaffold protein, CIKS dependent IKK/NF-?B and JNK/AP-1 activation, p65 and c-Jun phosphorylation and nuclear translocation, NF-?B- and AP-1 dependent IL-18 and MMP-9 induction, and hypertrophy of adult cardiomyocytes isolated from WT, but not CIKS-null mice
Valente et al., Am J Physiol Heart Circ Physiol 2012 (Hyperplasia) : ANG II-induced superoxide generation, NF-?B and AP-1 activation, and IL-18 and MMP-9 induction were all markedly attenuated by losartan, diphenyleneiodonium chloride ( DPI ), and Nox1 knockdown ... Similar to ANG II, addition of IL-18 also induced superoxide generation, activated NF-?B and AP-1 , and stimulated SMC migration and proliferation, in part via Nox1, and both ANG II and IL-18 induced NOX1 transcription in an AP-1 dependent manner
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
Valente et al., Cell Signal 2013 : IL-18 induced Nox1 dependent ROS generation, TRAF3IP2 expression, and IKK/NF-?B and JNK/AP-1 activation
Valente et al., Cell Signal 2013 : Silencing TRAF3IP2 using a phosphorothioated, 2'-O-methyl modified, cholesterol tagged TRAF3IP2 siRNA duplex markedly attenuated IL-18 induced NF-?B and AP-1 activation and CF migration
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
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
Adachi et al., Immunity 1998 : Furthermore, IL-18 induced activation of NF-kappaB and c-Jun N-terminal kinase (JNK) is blocked in MyD88-/- Th1 developing cells