Gene interactions and pathways from curated databases and text-mining

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FOS — IL1A

Text-mined interactions from Literome

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
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
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
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
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
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
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
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
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
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
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
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
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 ... 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
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
Granet et al., Cytokine 2004 : IL-1 and TNF-alpha induced egr-1 and all AP-1 member expression, except fosB and junD
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
Hoffmann et al., J Biol Chem 2005 : We report here that c-Fos and Fos related antigen-1 (Fra-1), two inducible components of AP-1, are recruited to the endogenous interleukin (IL)-8 promoter in an IL-1 dependent manner
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
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
Sawai et al., Med Sci Monit 2005 (Pancreatic Neoplasms) : EMSA confirmed that IL-1alpha increased DNA binding activity of AP-1 and NF-kappaB
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
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
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
Sakoda et al., J Dent Res 2006 : Dominant negative Rac1 severely inhibited interleukin-1alpha induced NF-kappaB and AP-1 promoter activity
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
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
Mohan et al., Endocrinology 2007 : In contrast, IL-1beta increased both AP-1 and NF-kappaB DNA binding at 1 h only
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
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
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
Kim et al., J Immunol 2009 : However, we demonstrate that overexpression of the IL-1RI receptor in BMMs or induction of IL-1RI by c-Fos overexpression enables IL-1 alone to induce the formation of authentic osteoclasts by a RANKL/RANK independent mechanism ... Interestingly, IL-1/IL-1RI does not induce expression of c-Fos or NFATc1 during osteoclast differentiation, although basal levels of c-Fos and NFATc1 seem to be required
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
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
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
Zhang et al., J Ethnopharmacol 2012 : 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
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
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
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
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
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
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
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
Ericsson et al., J Neurosci 1994 : Discrete and unilateral interruption of ascending catecholaminergic projections from the medulla attenuated IL-1 stimulated increases in Fos immunoreactivity and CRF mRNA in the PVH on the ipsilateral side ... Disruption of descending projections from circumventricular structures associated with the lamina terminalis did not affect IL-1 mediated Fos induction in the PVH
Chang et al., Brain Res 1993 : Within the magnocellular neurons of the SON and PVN, activation of FOS by IL-1 appeared to be greater in areas known to have a high proportion of oxytocin containing cells than in those of vasopressin containing cells
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
Swiergiel et al., Brain Res Bull 1996 : Because cerebral noradrenergic systems have been implicated in Fos induction, we studied the IL-1 induced appearance of Fos in mice pretreated with 6-hydroxydopamine ( 6-OHDA ) which depleted cerebral norepinephrine ( NE ) by more than 90 %, but did not significantly alter dopamine ... Pretreatment with 6-OHDA substantially reduced the IL-1 induced Fos increase in the PVN which was no longer statistically significant ... These results suggest that the noradrenergic innervation of the PVN is involved in the IL-1 induced induction of Fos in the PVN
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
Hui et al., Arthritis Rheum 1998 : Further, IL-1 induced AP-1 activation and AP-1 binding were inhibited by paclitaxel
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