Gene interactions and pathways from curated databases and text-mining

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IL1A — JUN

Text-mined interactions from Literome

Dreikhausen et al., Eur J Immunol 2001 (MAP Kinase Signaling System) : The recombinant C3-like chimeric toxin, which consists of the C3 toxin of Clostridium limosum and the N-terminal part of Clostridium botulinum C2 toxin ( C2IN-C3 ) interacting with the C2II binding subunit to facilitate uptake into cells, and selectively inactivates Rho A by ADP-ribosylation, prevented IL-1 stimulated activation of Jun-NH2-terminal-kinases (JNK) and p38 mitogen-activated-protein kinases ( MAPK )
Garat et al., Cytokine 2003 : IL-1 activated all three mitogen activated protein ( MAP ) kinase family members : p38 MAP kinase, extracellular regulated kinases (ERK), and c-Jun amino-terminal kinases (JNK)
Kwon et al., Endocrinology 1996 : IL-1 induced protein synthesis of Fos and Jun was observed as early as 30 min, peaked between 3-5 h, and decreased by 8 h after IL-1 treatment ... The present study, however, indicates that IL-1 induced expression of Fos and Jun does not seem to participate in the regulation of iNOS and mRNA expression, because : 1 ) cycloheximide ( 1 microM ) completely inhibited Fos expression but had no inhibitory effect on iNOS mRNA levels ; and 2 ) tyrosine kinase inhibitors genistein and herbimycin A completely inhibited IL-1 induced iNOS expression but did not block c-fos and c-jun expression
Chambers et al., Exp Cell Res 2013 (Periodontitis) : IL-4 inhibition of IL-1 induced Matrix Metalloproteinase-3 (MMP-3) expression in human fibroblasts involves decreased AP-1 activation via negative crosstalk involving of Jun N-terminal Kinase (JNK) ... Here we show that IL-1 induced binding of transcription factor AP-1 to the MMP-3 promoter consists primarily of c-Jun, JunB, and c-Fos and that binding of c-Jun and c-Fos is inhibited by the combination of cytokines while binding of Jun B is not ... Here we show that IL-1 induced binding of transcription factor AP-1 to the MMP-3 promoter consists primarily of c-Jun, JunB, and c-Fos and that binding of c-Jun and c-Fos is inhibited by the combination of cytokines while binding of Jun B is not
Wu et al., J Neurochem 2004 (Translocation, Genetic) : In accordance with these findings, IL-1beta stimulated phosphorylation of p42/p44 MAPK, p38, and c-Jun N-terminal kinase (JNK) , which was attenuated by U0126, SB202190, or SP600125, respectively
Wolf et al., Clin Cancer Res 2001 (Carcinoma, Squamous Cell...) : In this study, we examined the role of IL-1alpha in the activation of NFkappaB and AP-1 , the expression of proangiogenic cytokine IL-8, and in the survival and proliferation of HNSCC cell lines
Chedid et al., J Immunol 1991 (Thymoma) : Activation of AP-1 by IL-1 and phorbol esters in T cells ... IL-1 and agents that elevate intracellular cAMP levels do not, by themselves, induce AP-1 activation, but they synergize with phorbol esters ... IL-1 and forskolin may enhance AP-1 function by different mechanisms, because forskolin enhanced gene expression without producing an increase in nuclear AP-1 DNA binding, whereas IL-1 increased AP-1 binding activity and gene expression ... These observations, in conjunction with the lack of a demonstrable effect of IL-1 on cAMP production in EL-4 cells, are consistent with the view that IL-1 enhances AP-1 activation by a pathway that does not directly involve cAMP and PKA ... However, the induction of AP-1 activity by IL-1 and phorbol esters is dependent upon the presence of PKA, as evidenced by the loss of AP-1 inducibility in cells transfected with a cDNA encoding protein kinase inhibitor, a specific inhibitor of PKA ... The effect of protein kinase inhibitor on AP-1 activation in response to IL-1 and tetradecanoyl-phorbol-13-acetate was reversed in the presence of the serine/threonine protein phosphatase inhibitor okadaic acid
Tanabe et al., Journal of neuroinflammation 2011 : We previously reported that interleukin (IL)-1ß stimulates IL-6 synthesis from rat C6 glioma cells and that IL-1ß induces phosphorylation of inhibitory kappa B ( I?B ), p38 mitogen activated protein ( MAP ) kinase, stress activated protein kinase ( SAPK ) /c-Jun N-terminal kinase (JNK) , extracellular signal regulated kinase 1/2, and signal transducer and activator of transcription ( STAT ) 3
Chen et al., Oncogene 2006 (Multiple Myeloma) : We found that siRNA targeting the TRAF6 C-terminal ( siTRAF6C ) receptor interaction domain specifically reduced only TRAF6 protein expression, without affecting TRAF2 or 5 levels, and substantially interfered with IL-1 induced NF-kappaB and c-Jun/AP-1 activation
Li et al., Hepatology 2006 : In conclusion, IL-1 beta and CDCA inhibit HNF4 alpha but induce c-Jun , which in turn blocks HNF 4 alpha recruitment of PGC-1 alpha to the CYP7A1 chromatin and results in inhibition of CYP7A1 gene transcription
Lee et al., Eur J Immunol 1998 : ROI have been implicated in the activation of NF-kappaB as well as c-Jun N-terminal kinase (JNK) in response to IL-1 and TNF-alpha stimulation
Reddy et al., Biochem Biophys Res Commun 2004 (Carcinoma...) : CDelta27, however, had no effect on IL-1 dependent activation of the Jun N-terminal kinase (JNK) , indicating that distinct regions of IL-1R AcP mediate the activation of PI 3-kinase and JNK
Hung et al., Immunol Invest 2008 : In consistent with the results in primary chondrocytes, t-RA down-regulated IL-1 induced AP-1 DNA binding activity and transcriptional activity in a human fibroblast-like ( commercially labeled as chondrocyte ) cell line
Stulic et al., Cytokine 2007 : Effect of the alpha3beta1 integrin on the IL-1 stimulated activation of c-Jun N-terminal kinase (JNK) in CACO-2 cells ... Furthermore, suppressed levels of IL-1 induced c-Jun N-terminal kinase (JNK) phosphorylation and kinase activity were seen with the antibody treated cells
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
Das et al., Mol Cell Biochem 1995 (Adenocarcinoma...) : Likewise, some of the thiol modifying compounds inhibited AP-1 activation by TNF alpha or IL-1 , whereas others did not
Clarke et al., Mol Cell Proteomics 2013 (MAP Kinase Signaling System) : Mixed-effects modeling analysis of our data was vital for ascertaining that IL-1a and TGF-a treatment increased the activities of more pathways than IL-6 and TNF-a and that TGF-a and TNF-a increased p38 MAPK and c-Jun N-terminal kinase (JNK) phospho-protein levels in a synergistic manner
Mengshol et al., Arthritis Rheum 2000 (MAP Kinase Signaling System) : We found that IL-1 induction of MMP-13 requires p38 activity, c-Jun N-terminal kinase (JNK) activity and NF-kappaB translocation
Li et al., Proc Natl Acad Sci U S A 2001 : IL-1 induced NFkappa B and c-Jun N-terminal kinase (JNK) activation diverge at IL-1 receptor associated kinase (IRAK)
Albanito et al., Glia 2011 : c-Jun is essential for the induction of Il-1ß gene expression in in vitro activated Bergmann glial cells ... Moreover, LPS induced IL-1ß expression and inhibition of c-Jun N-terminal kinase (JNK) activity abolished both c-Jun phosphorylation and the increase of IL-1ß mRNA ... Notably, LPS failed to induce IL-1ß mRNA in neuronal/glial cerebellar cultures generated from conditional knockout mice lacking c-Jun expression in the CNS, indicating the essential role of c-Jun in astroglial-specific induction of IL-1ß
Morita et al., Ann Rheum Dis 1998 (Arthritis, Rheumatoid) : The expression of AP1 activity induced by IL1 was suppressed by treatment with antisense oligonucleotides
Funakoshi-Tago et al., Eur J Biochem 2003 : We found that IL-1 mediated c-Src activation was required for AP-1 activation, but not for NF-kappa B activation and also revealed that c-Src induced AP-1 activation was enhanced synergistically by the coexpression of TNF receptor associated factor 6 (TRAF6) ... Taken together, our results demonstrate that c-Src and TRAF6 are key mediators of IL-1 induced AP-1 activation and provide evidence of cross talk between c-Src and TRAF6 molecules through PI3 kinase-Akt-JNK pathways
Zhang et al., J Ethnopharmacol 2012 : The present study tries to demonstrate differential role of YiGanKang Decoction in interleukin-1ß (IL-1ß) induction of the type I receptor ( IL-1RI ) and the activator protein 1 (AP-1) in rat hepatic stellate cell (HSC) ... The differences between IL-1RI expression after treatment for 10 and 60 min were significantly higher than the corresponding values in the control ( P < 0.01, P < 0.01, respectively ) ; After pretreatment with YiGanKang Decoction, IL-1RI expression induced by IL-1ß was not decrease obviously ; IL-1ß could activate AP-1 in rat HSCs ( P < 0.01 ) ... Meanwhile YiGanKang Decoction could inhibit activity of AP-1 induced by IL-1ß ( P < 0.01 ), and the inhibition rate was 42.71 % ... YiGanKang Decoction could not decrease IL-1RI expression, but it could inhibit activity of AP-1 in rat HSCs induced by IL-1ß
Ling et al., Cancer Cell 2012 (Carcinoma, Pancreatic Ductal...) : Our findings reveal that Kras ( G12D ) -activated AP-1 induces IL-1a , which, in turn, activates NF-?B and its target genes IL-1a and p62, to initiate IL-1a/p62 feedforward loops for inducing and sustaining NF-?B activity
Quinones et al., Biochem J 1994 (Carcinoma, Hepatocellular...) : Protein binding to this region and to the AP-1 site was modestly induced by IL-1 treatment
Ha et al., Int J Biol Macromol 2013 : In the mechanism of LGC, while extracellular signal regulated kinase ( ERK ) was important for the induction of TNF-a, IL-1ß and IL-8, the phosphorylation of C-Jun NH2-termianl kinase (JNK) contributed to the induction of TNF-a and IL-1ß to a greater degree
Brooks et al., Mol Immunol 1995 (Thymoma) : IL-1 synergistically enhances the stimulatory effect of TPA on AP-1 mediated gene expression in this cell line ... To elucidate the mechanism ( s ) by which IL-1 enhances AP-1 mediated gene expression, we examined the effect of IL-1 on the synthesis and turnover of Jun B, the member of the jun gene family that is present in AP-1 complexes in EL4 cells
Yu et al., J Biol Chem 2008 : Phosphorylation of Thr-178 and Thr-184 in the TAK1 T-loop is required for interleukin (IL)-1 mediated optimal NFkappaB and AP-1 activation as well as IL-6 gene expression ... Consistently, TAK1 mutant with alanine substitution of these two residues severely inhibits IL-1 induced NFkappaB and AP-1 activities, whereas TAK1 mutant with replacement of these two sites with acidic residues slightly enhances IL-1 induced NFkappaB and AP-1 activities compared with the TAK1 wild-type ... Reconstitution of TAK1-deficient mouse embryo fibroblast cells with wild-type TAK1 or a TAK1 mutant containing threonine 178 and 184 to alanine mutations revealed the importance of these two sites in IL-1 mediated IKK-NFkappaB and JNK-AP-1 activation as well as IL-1 induced IL-6 gene expression
Stalińska et al., J Physiol Pharmacol 2005 : We used human hepatoma ( HepG2 ) and human umbilical vein endothelial cells ( HUVEC ) as a model system : NF-kappaB and AP-1 were activated by the proinflammatory cytokine IL-1 in the absence or presence of 21 selected plant extracts and the effect was evaluated by the electrophoretic mobility shift assay ( EMSA ) ... The IL-1 induced AP-1 activation was diminished by extracts from Scandix australis, Amaranthus sp. and Artemisia alba more potently in HUVEC, while extracts from Urospermum picroides and Scandix pecten-veneris in HepG2 cells
Mendes et al., Nitric Oxide 2002 : Finally, the p42/44MAPK inhibitor, PD 98059, prevented IL-1 induced AP-1 activation in a concentration that did not inhibit iNOS expression
Zhu et al., Atherosclerosis 1999 : IL-1 alpha at this dose ( which activates NF-kappa B, but not AP-1 ) also enhanced LDL activated AP-1 binding
Nguyen et al., J Interferon Cytokine Res 2003 : Chemical inhibitors or dominant negative forms of signaling components required to activate NF-kappa B, ATF, or AP-1 in response to IL-1 do not affect the phosphorylation of Stat1 on serine
Sakoda et al., J Dent Res 2006 : Dominant negative Rac1 severely inhibited interleukin-1alpha induced NF-kappaB and AP-1 promoter activity
Granet et al., Cytokine 2004 : IL-1 and TNF-alpha induced egr-1 and all AP-1 member expression, except fosB and junD
Mohan et al., Endocrinology 2007 : In contrast, IL-1beta increased both AP-1 and NF-kappaB DNA binding at 1 h only
Arts et al., Arterioscler Thromb Vasc Biol 1999 (Carcinoma, Hepatocellular...) : In line with these findings, IL-1alpha poorly induced c-Jun homodimer binding to the PAI-1 TRE in gel mobility-shift assays
Kim et al., Comp Immunol Microbiol Infect Dis 2011 (Staphylococcal Infections) : Staphylococcus aureus induces IL-1ß expression through the activation of MAP kinases and AP-1 , CRE and NF-?B transcription factors in the bovine mammary gland epithelial cells
Lee et al., J Biol Chem 1994 : In addition, both TPA and IL-1 alpha caused increases not only in the phosphorylation of c-Jun and c-Fos protein but also in the transactivating activity of AP-1 nuclear transcription factor
Florin et al., Oncogene 2004 : After skin injury, the release of IL-1 from keratinocytes induces the activity of the AP-1 subunits c-Jun and JunB in fibroblasts leading to a global change in gene expression
Sawai et al., Med Sci Monit 2005 (Pancreatic Neoplasms) : EMSA confirmed that IL-1alpha increased DNA binding activity of AP-1 and NF-kappaB
Oda et al., J Immunol 2002 : These results show that the inhibition of IL-1alpha mediated MCP-1 production by alprazolam is mainly due to inhibition of c-Rel/p65 and c-Rel/p50 binding to the MCP-1 promoter region, since alprazolam did not affect the IL-1alpha mediated activation of NF-kappaB ( p50/p65 ) or AP-1 ( c-Jun/c-Fos ) binding to the IL-8 promoter region
Cirillo et al., Mol Cell Biol 1999 : The analysis of two distinct mitogen activated protein kinase pathways shows that stress activated protein kinase-Jun N-terminal kinase activation, resulting in the phosphorylation of ATF-2, c-Jun, and JunD, is required not only for the IL-1- but also for the TPA dependent induction, while the extracellular signal related kinase 1 ( ERK-1 ) and ERK-2 activation is involved in the TPA- but not in the IL-1 dependent stimulation of the uPA enhancer
Simões et al., Journal of neuroinflammation 2012 (MAP Kinase Signaling System) : The effect of SCH58261 on the IL-1ß induced phosphorylation of the mitogen activated protein kinases ( MAPKs ) c-Jun N-terminal kinase (JNK) and p38 was evaluated by western blotting and immunocytochemistry
Wang et al., Chin Med J (Engl) 2006 : UVB irradiated human keratinocytes and interleukin-1alpha indirectly increase MAP kinase/AP-1 activation and MMP-1 production in UVA irradiated dermal fibroblasts ... IL-1alpha increased MAP kinase activity and c-Jun mRNA expression, IL-1alpha also increased c-Fos mRNA expression
Hsu et al., J Agric Food Chem 2006 : In essence, we found that c-Jun N-terminal kinase (JNK) and p38 mitogen activated protein kinase ( p38 ), but not extracellular signal regulated kinase ( ERK ), play an important role in the regulation of IL-1 gene expression in RASP stimulated J774A.1 cells
Hwang et al., J Biol Chem 2005 : Consistent with its ability to induce phosphorylation of c-Jun, IL-1beta caused transient activation of AP-1 , which is necessary for IL-1beta induced dedifferentiation
Hua et al., J Neuroimmunol 2002 : Electrophoretic mobility shift assay ( EMSA ) showed that IL-1 induced NF-kappaB and AP-1 DNA complex formation in astrocytes, and that SB203580 inhibited AP-1 complex formation
Reddy et al., Proc Soc Exp Biol Med 1998 : These data reveal that collagenase gene expression can be regulated by the impairment of IL-1 stimulated NF-kappaB, STAT3, and AP-1 activities, and can highlight a possible molecular mechanism for the anti-inflammatory effects of glucocorticoids
Han et al., J Pharmacol Exp Ther 1999 (Arthritis, Rheumatoid...) : IL-1 stimulated AP-1 binding was also inhibited by 25 microM SB 203580 in RA FLS
Tseng et al., PloS one 2013 : On the other hand, IL-1ß induced c-Jun and c-Fos mRNA expression, c-Jun phosphorylation, and AP-1 promoter activity ... Pretreatment with U0126 or SP600125 inhibited IL-1ß induced AP-1 and NF-?B promoter activity, but not NF-?B translocation from the cytosol into the nucleus
Funakoshi et al., Int Immunopharmacol 2001 : While IL-1 induced-AP-1 activation was moderate, both LY294002 and SB203580 suppressed IL-1 induced AP-1 activation ... These observations were prominent particularly in the TRAF6 transfection system, in which overexpression of wild type TRAF6 augmented the IL-1 mediated NF-kappa B and AP-1 activation, while dominant negative TRAF6 construct ( delta TRAF6 ) suppressed these activation ... Namely, LY294002 inhibited TRAF6 mediated IL-1 induced NF-kappa B and AP-1 activation markedly, while SB203580 inhibited TRAF6 induced AP-1 activation but not NF-kappa B activation ... Above results indicated that both PI3-kinase and p38 MAP kinase are differentially involved in IL-1 induced NF-kappa B and AP-1 activation
Werman et al., Proc Natl Acad Sci U S A 2004 (Inflammation) : Under conditions of IL-1 receptor blockade, intracellular overexpression of the precursor and propiece forms of IL-1alpha were sufficient to activate NF-kappaB and AP-1
Pang et al., Journal of neuroinflammation 2012 (MAP Kinase Signaling System) : Telmisartan did not modify IL-1ß induced ERK1/2 and p38 mitogen activated protein kinase ( MAPK ) phosphorylation or nuclear factor-?B activation but significantly decreased IL-1ß induced c-Jun N-terminal kinase (JNK) and c-Jun activation
Clerk et al., J Mol Cell Cardiol 1999 (MAP Kinase Signaling System) : However, IL-1 beta induced a greater increase in c-Jun protein
Mendes et al., Cell Biol Toxicol 2003 (Inflammation) : This study aimed at elucidating the role of ROS, particularly H2O2, in mediating IL-1 induced activation of the transcription factor activator protein-1 (AP-1) in primary cultures of articular chondrocytes ... The AP-1 complexes, induced by either IL-1 or H2O2, contained c-Fos/c-Jun and c-Fos/JunD heterodimers, but IL-1 activated AP-1 with a kinetics slower than that observed with H2O2 ... These results indicate that H2O2 is a major mediator of IL-1 induced AP-1 activation in articular chondrocytes and that inhibition of ROS production is an effective strategy to block this IL-1 induced response
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
Hui et al., Arthritis Rheum 1998 : Further, IL-1 induced AP-1 activation and AP-1 binding were inhibited by paclitaxel
Liacini et al., Matrix Biol 2002 (Osteoarthritis, Hip) : These results suggest the involvement of MAPKs, AP-1 and NF-kappa B transcription factors in the IL-1 induction of MMPs in chondrocytes
Wan et al., Cell Signal 2001 : In vitro kinase assay using GST-c-Jun as a substrate revealed that pretreatment of PD153035 completely inhibited UV- and IL-1 induced c-Jun kinase activity in cultured keratinocytes
Choi et al., Food Chem Toxicol 2010 (Sarcoma) : Moreover, IL-1beta induced activator protein-1 (AP-1) and nuclear factor-kappaB (NF-kappaB) activation were inhibited by luteolin
Wall et al., Oxidative medicine and cellular longevity 2013 : Luteolin and kaempferol decreased IL-1ß induced NF- ? B p65 DNA binding activity and nuclear c-Jun expression
Lu et al., Phytother Res 2013 : Importantly, results showed that IL-1ß induced activation of phosphorylated ( p)-c-Jun in chondrocytes was significantly inhibited by cinnamophilin
Zhang et al., PloS one 2012 (MAP Kinase Signaling System) : Gel shift and chromatin immunoprecipitation assays validated that IL-1ß increased the in vitro and ex vivo binding activities of AP1 within rabbit Rgs4 promoter
Sanjo et al., Mol Cell Biol 2003 (Fetal Death...) : Recently, serine/threonine kinase TAK1 and TAK1 binding protein 1 and 2 (TAB1/2) have been identified as molecules involved in IL-1 induced TRAF6 mediated activation of AP-1 and NF-kappa B via mitogen activated protein ( MAP ) kinases and I kappa B kinases, respectively
Sabolek et al., Stem Cells 2009 (MAP Kinase Signaling System) : Surprisingly, IL-1beta did not activate the NF-kappaB pathway or the transcription factor activating protein 1 (AP-1) , but inhibition of nuclear translocation of NF-kappaB by SN50 facilitated IL-1beta induced Nurr1 expression and dopaminergic differentiation of mdNPCs
Böhm et al., Exp Dermatol 2004 : Functional studies have shown that alpha-MSH exerts anti-inflammatory actions in human fibroblastic skin cells by suppressing interleukin-1 (IL-1) induced IL-8 production, activation of the transcription factor activator protein-1 (AP-1) and induction of intercellular adhesion molecule-1 by interferon-alpha
Shen et al., Zhonghua Yan Ke Za Zhi 2007 : The possible mechanism of this effect is the activation of c-Jun by IL-1
Hengartner et al., Mol Med 2013 : IL-1ß induced extracellular signal regulated kinases 1 and 2 ( ERK1/2 ) and c-Jun N-terminal kinases (JNK) activation and inhibition of these signaling pathways suggested an involvement in the IL-1ß effects on osteoblast migration
Eda et al., Rheumatol Int 2011 (MAP Kinase Signaling System) : IL-1ß and TNF-a activated the intracellular mitogen activated protein kinases ( MAPKs ) : p44/42 MAPK, p38, and c-Jun N-terminal kinase (JNK) as well as nuclear factor-?B ( NF-?B ) in osteoblasts
Făgărăsan et al., Proc Natl Acad Sci U S A 1990 : The effect appeared within 30 min, and returned to basal levels after 2 hr. Desensitization of protein kinase C by phorbol ester pretreatment had no effect on the ability of IL-1 to induce Fos and Jun mRNA expression ... Somatostatin, an inhibitor of cAMP and beta-endorphin secretion, did not reduce the IL-1 effect on Fos and Jun mRNA expression
Wang et al., Int J Mol Med 2005 : In this study, we first investigated the effect of IL-1 on MAPK activity, c-Jun and c-Fos mRNA expression, and MMP-1 and MMP-2 production in UVA irradiated human dermal fibroblasts
Guo et al., Inflammation 2000 : As a result, antisense IRAK-2 ODN or antisense p110 PI 3-kinase ODN inhibited IL-1 induced NF-kappaB and AP-1 activation in HepG2 cells
Bertelsen et al., Assay Drug Dev Technol 2005 (Inflammation) : This was supported by RNA interference where co-transfection of small interfering RNA targeting both JNK1 and JNK2, to limit signaling redundancy, significantly inhibited IL-1alpha stimulated translocation of phosphorylated c-Jun without altering phosphorylated p38 and NFkappaB p65/RelA redistribution
Jimi et al., J Immunol 1999 : sODF, as well as IL-1 , activated NF-kappaB and c-Jun N-terminal protein kinase (JNK) in OCLs
Varga et al., Int Immunol 1999 : While the extracellular signal regulated kinase ( ERK ) cascade was activated by both receptors, IL-1 preferentially stimulated Jun-N-terminal kinases (JNK) and p38 mitogen activated kinase or microtubule associated protein kinase ( MAPK )
Ginnan et al., Free Radic Biol Med 2013 : In this study, we tested the hypothesis that NOX4 is a proximal mediator of IL-1ß dependent activation of PKCd and increases IL-1ß stimulated c-Jun kinase (JNK) signaling in primary rat aortic VSM cells
Kanakaraj et al., J Exp Med 1999 (Cytomegalovirus Infections) : Interleukin (IL)-18 is functionally similar to IL-12 in mediating T helper cell type 1 ( Th1 ) response and natural killer ( NK ) cell activity but is related to IL-1 in protein structure and signaling, including recruitment of IL-1 receptor associated kinase (IRAK) to the receptor and activation of c-Jun NH2-terminal kinase (JNK) and nuclear factor (NF)-kappaB
Sawai et al., Oncogene 2006 (Disease Progression...) : In this study, we demonstrated that ILK and beta ( 1 ) -integrin play important roles in interleukin (IL)-1alpha induced enhancement of adhesion and invasion of pancreatic cancer cells through p38 mitogen activated protein kinase ( MAPK ) signaling pathway and activator protein-1 (AP-1) activation ... Alteration of ILK kinase activity controlled IL-1alpha induced p38 MAPK phosphorylation and its downstream AP-1 activation with subsequent regulation of pancreatic cancer cell adhesion and invasion
Reddy et al., J Biol Chem 1997 : Furthermore, two PI 3-kinase-specific inhibitors, wortmannin and a dominant negative mutant of the p85 subunit, inhibited IL-1 induced activation of both NFkappaB and AP-1