Gene interactions and pathways from curated databases and text-mining

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FOS — IL8

Pathways - manually collected, often from reviews:

Text-mined interactions from Literome

Joseph et al., Free Radic Biol Med 2008 (Hyperoxia) : The data indicate that activation of JNK1/AP-1 and subsequent IL-8 induction in hyperoxia are mediated by intracellular ROS, with SOD having significant protective effects
Seo et al., J Physiol Pharmacol 2009 : Nitric oxide induced IL-8 expression is mediated by NF-kappaB and AP-1 in gastric epithelial AGS cells
Shi et al., J Interferon Cytokine Res 1999 (Adenocarcinoma...) : Deletion and point mutation analyses of the IL-8 promoter revealed that both AP-1 and NF-kappaB binding sites were necessary for IL-8 induction by hypoxia
Wang et al., Biochim Biophys Acta 2004 (Sarcoma, Kaposi) : Furthermore, using DNA protein binding experiments, we have shown that IL-8 increased AP-1 and NF Kappa B activity in these cells
Wolf et al., Clin Cancer Res 2001 (Carcinoma, Squamous Cell...) : IL ( interleukin)-1alpha promotes nuclear factor-kappaB and AP-1 induced IL-8 expression, cell survival, and proliferation in head and neck squamous cell carcinomas ... 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 ... IL-1alpha was found to induce coexpression of IL-8 through the activation of NFkappaB and AP-1 , in that mutation of the NFkappaB site within the IL-8 promoter abolished autocrine- and recombinant IL-1alpha induced IL-8 reporter gene activity, whereas mutation in AP-1 partially decreased IL-8 reporter gene activity in UM-SCC-9 cells
Bancroft et al., Clin Cancer Res 2001 (Carcinoma, Squamous Cell...) : Expression of IL-8 and VEGF in the cell lines was associated with coactivation of both NF-kappaB and AP-1, and U0126 inhibited both NF-kappaB and AP-1 reporter activity in UM-SCC-9 and UM-SCC-11B cells
Ren et al., Laryngoscope 2004 (Carcinoma...) : LMP1 induces IL-8 mainly through the activation of NF-kappa B and partly through AP-1 in NPC model cell lines, NPC-KT, and this suggests that LMP1 plays an important role in the angiogenesis of NPC
Bancroft et al., Int J Cancer 2002 (Carcinoma, Squamous Cell...) : Recombinant EGF induced EGFR phosphorylation, activation of NF-kappaB and AP-1 reporter genes and IL-8 and VEGF expression, indicating that EGFR can mediate coactivation of both transcription factors and cytokine genes in HNSCC
Hoffmann et al., J Biol Chem 2005 : c-Fos activates IL-8 transcription and synergizes in this effect with p65 NF-kappaB
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
Sodin-Semrl et al., Int J Immunopathol Pharmacol 2004 (Arthritis, Rheumatoid) : A human IL-8 promoter luciferase construct was transfected into CHO cells stably expressing ALXR in order to determine the role of NF-kappaB and/or AP-1 in the regulation of IL-8 gene expression
Lee et al., Clin Exp Allergy 2007 (Asthma) : IL-8 promoter deletion analysis indicated that position -132 to +41 was essential for GCE induced IL-8 transcription, and mutants with substitutions in activator protein (AP)-1, nuclear factor (NF)-IL6 and NF-kappaB binding sites revealed a requirement for NF-kappaB and NF-IL6, but not AP-1 , in GCE induced activation of the IL-8 promoter
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
Saadane et al., Journal of inflammation (London, England) 2011 : Little is known about regulation of IL-8 by MAPKs or AP-1 in CF
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
Mori et al., Cancer Res 1998 : Furthermore, using several deletion and mutated plasmids of the 5'-flanking regulatory region of the IL-8 gene linked to the luciferase gene as a reporter and mutant tax gene expression vectors, we have established that both AP-1 at -126 to -120 and nuclear factor (NF)-kappaB-like cis-element at -80 to -71 are essential and sufficient for the induction of the IL-8 gene by HTLV-I Tax
Wu et al., Mol Immunol 2008 : IL-8 production and AP-1 transactivation induced by UVA in human keratinocytes : roles of D-alpha-tocopherol
Yamagishi et al., J Cardiovasc Pharmacol 2004 : An inhibitor of AP-1 , curcumin, or an anti-oxidant, N-acetylcysteine, also inhibited the TNF-alpha induced IL-8 expression in HUVEC
Hwang et al., Oncogene 2004 (Stomach Neoplasms) : The above results suggest that MAPK-AP-1 and ROS-NF-kappaB signaling pathways are involved in the IL-1beta induced IL-8 expression and that these paracrine signaling pathways induce endothelial cell proliferation
Chan et al., Cytokine 2006 (Cell Transformation, Viral) : In human bronchial epithelial cells, binding sites for NFkappaB, AP-1 , and NF-IL6 in the 5'-flanking region of the IL-8 promoter are necessary for optimal NaCl induction of IL-8
Ondrey et al., Mol Carcinog 1999 (Carcinoma, Squamous Cell...) : We concluded that the early transcription factors NF-kappaB, AP-1, and NF-IL6 are constitutively activated in human HNSCC cell lines and that NF-kappaB and AP-1 promote expression of the pro-inflammatory and pro-angiogenic cytokine IL-8 in HNSCC
Yoshida et al., Int J Mol Med 2007 : These results indicate that PAR2 activation in HEEC by trypsin induces NFkappaB- and AP-1 dependent IL-8 production in association with activation of p38 MAPK and ERK1/2, suggesting that esophageal inflammation may be induced by PAR2 activation via reflux of trypsin
Kim et al., Am J Physiol Lung Cell Mol Physiol 2006 : Zn2+ induced IL-8 expression involves AP-1 , JNK, and ERK activities in human airway epithelial cells
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
Zhou et al., J Clin Immunol 2004 : IL-8 induction by hyperforin required the activation of AP-1 but not the NF-kappaB transcription factor, thereby distinguishing it from the NF-kappaB dependent IL-8 induction mediated by tumor necrosis factor alpha (TNFalpha)
Kim et al., Mol Immunol 2007 (Ovarian Neoplasms) : Saxatilin inhibits TNF-alpha induced proliferation by suppressing AP-1 dependent IL-8 expression in the ovarian cancer cell line MDAH 2774 ... TNF-alpha induced IL-8 promoter activation that is inhibited by saxatilin treatment was dependent on activating protein-1 (AP-1) instead of nuclear factor-kappa B (NF-kappaB) ... Experimental evidence clearly indicated that saxatilin inhibits TNF-alpha induced proliferation of the ovarian cancer cells by suppressing IL-8 expression in AP-1 dependent manner
Zouki et al., J Leukoc Biol 2001 : The NO synthase inhibitors aminoguanidine and N ( G ) -nitro-L-arginine methyl ester blocked nuclear accumulation of activator protein-1 (AP-1) and nuclear factor (NF)-kappaB in both polymorphonuclear ( PMN ) and mononuclear leukocytes and inhibited IL-8 mRNA expression and IL-8 release by approximately 90 % in response to IL-1beta and TNF-alpha
Fong et al., J Bone Miner Res 2008 (Neoplasms) : Activation of AP-1 and NF-kappaB DNA-protein binding and MAPKs after TGF-beta1 treatment was shown, and TGF-beta1 induced IL-8 promoter activity was inhibited by the specific inhibitors of MAPK cascades
Kadoya et al., Microbiol Immunol 2005 : Deletion mutational analysis of the IL-8 promoter revealed the possible involvement of the transcription factor AP-1 in both NS4A- and NS4B mediated IL-8 gene activation
Le et al., J Interferon Cytokine Res 2000 (Adenocarcinoma...) : Collectively, our data demonstrated that constitutive NF-kappaB and AP-1 activation contributes to the overexpression of IL-8 , which in turn plays an important role in tumor angiogenesis and contributes to the aggressive biology of human pancreatic cancer
Dahan et al., Infect Immun 2002 (Escherichia coli Infections) : These findings demonstrate that ( i ) EHEC can induce in vitro a potent proinflammatory response by secretion of IL-8 and ( ii ) the secretion of IL-8 is due to the involvement of MAPK, AP-1 , and NF-kappaB signaling pathways
Ju et al., Ann N Y Acad Sci 2006 : Role of mitogen activated protein kinases, NF-kappaB, and AP-1 on cerulein induced IL-8 expression in pancreatic acinar cells
Oda et al., J Immunol 2002 : While AP-1 is involved in regulating the IL-1alpha induced expression of IL-8 , but not MCP-1, alprazolam potentiated the binding of c-Jun/c-Fos to the AP-1 oligonucleotide probe
Jang et al., Inflamm Res 2013 (Helicobacter Infections) : The RK-I-123 suppressed the H. pylori induced IL-8 expression and activation of MAPKs, NF-?B, and AP-1 by reducing ROS levels in AGS cells
Buchholz et al., Cell Microbiol 2006 : The AP-1 , NFIL6 ( C/EBPbeta ) and NFkappaB transcriptional regulatory sites of the IL-8 promoter and the host NFkappaB signalling pathway were necessary for IL-8 induction by C. trachomatis
Shen et al., J Asian Nat Prod Res 2003 : The suppression of IL-8 gene transcription by resveratrol was, at least partly, due to inhibition of AP-1 activation
Zhao et al., J Biol Chem 2001 (Colonic Neoplasms...) : By using reporter gene constructs containing targeted substitutions in the IL-8 promoter, we show that the NF-kappaB, AP-1 , and to a lesser degree the C/EBP sites in the IL-8 promoter region are required for IL-8 gene expression induced by NT
Yoshida et al., J Pharmacol Sci 2008 (Gastroenteritis...) : PAR(2) activation in human esophageal epithelial cells by trypsin induces NFkappaB- and AP-1 dependent IL-8 production in association with activation of p38 MAPK and ERK1/2, suggesting that esophageal inflammation may be induced by PAR(2) activation via reflux of trypsin
Schmeck et al., Respir Res 2006 : AP-1 repressor A-Fos reduced IL-8 release by TLR2 overexpressing HEK293 cells induced by pneumococci but not by TNFalpha
Dahan et al., Infect Immun 2003 : In a previous study, it was demonstrated that EHEC induced IL-8 secretion is due to the involvement of the mitogen activated protein kinase ( MAPK ), AP-1 , and NF-kappaB pathways
Lemaire-Ewing et al., Cell Biol Toxicol 2009 (MAP Kinase Signaling System) : These results demonstrate that oxysterol induced IL-8 secretion is a calcium dependent phenomenon involving the MEK/ERK1/2 pathway leading to the activation of IL-8 gene via AP-1 ( c-fos )
Choi et al., Mol Cell Biol 2002 (Astrocytoma...) : These findings collectively indicate that DR5 ligation on human glioma cells leads to apoptosis and that the activation of AP-1 and NF-kappaB leads to the induction of IL-8 expression ; these responses are dependent on caspase activation
Takemura et al., Mol Hum Reprod 2004 : The stretch induced augmentation of both IL-8 and MCP-3 expression was significantly suppressed by an activator protein-1 (AP-1) inhibitor, curcumin
Vitiello et al., Cytokine 2004 (MAP Kinase Signaling System) : Our results elucidate some of the molecular mechanisms by which AP-1 and NF-kappaB regulate IL-8 release and open new strategies for the design of specific molecules that will modulate IL-8 effects in various infectious diseases
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
He et al., Zhonghua Yi Xue Za Zhi 2001 (Pulmonary Disease, Chronic Obstructive) : Enhancement of activity of NF kappa B and AP-1 may positively regulate the production of IL-8 and IL-1 beta in the airflow obstruction
Bian et al., Invest Ophthalmol Vis Sci 2004 : To investigate the role of the phosphatidylinositol 3-kinase (PI3K) pathway and the signal mediator AP-1 in monocyte chemotactic protein (MCP)-1 and interleukin (IL)-8 gene expression in human retinal pigment epithelial ( hRPE ) cells
Tanaka et al., Biochem Biophys Res Commun 1997 (Astrocytoma) : Redox regulation of lipopolysaccharide (LPS) induced interleukin-8 (IL-8) gene expression mediated by NF kappa B and AP-1 in human astrocytoma U373 cells
Choi et al., J Cell Biochem 2007 : In summary, our results indicate that iron chelator induced IL-8 generation in IECs involves activation of ERK1/2 and p38 kinase and downstream activation of AP-1
Chu et al., Dig Dis Sci 2003 (Helicobacter Infections...) : Role of NF-kappaB and AP-1 on Helicobater pylori induced IL-8 expression in AGS cells ... The present study aims to investigate whether H. pylori induced IL-8 expression is regulated by NF-kappaB and AP-1 in gastric epithelial AGS cells and whether this transcriptional regulation of IL-8 is inhibited by N-acetylcysteine (NAC)
Lindenmeyer et al., Bioorg Med Chem 2006 : p38 MAPK, which plays a role in AP-1 activation as well as in IL-8 regulation , was not influenced by SLs
Lee et al., J Biol Chem 1998 (Ovarian Neoplasms) : We reported previously that paclitaxel can induce interleukin (IL)-8 promoter activation in subgroups of ovarian cancer through the activation of both AP-1 and nuclear factor kappaB
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
Venza et al., Invest Ophthalmol Vis Sci 2007 : Transcriptional regulation of IL-8 by Staphylococcus aureus in human conjunctival cells involves activation of AP-1
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
Tsuchiya et al., Laryngoscope 2007 : However, the PGPS induced IL-8 promoter activation in rodent middle ear epithelial cells required NF-kappaB and NF-IL6 but not AP-1
Henriquet et al., Lung Cancer 2007 (Adenocarcinoma...) : An AP-1 and a NF-kappaB recognition sites were necessary for full induction of IL-8 promoter activity by TNF-alpha and TPA
O'Hara et al., J Immunol 2006 (Helicobacter Infections) : In contrast, overexpression of APE-1/Ref-1 enhanced basal and H. pylori induced IL-8 gene transcription, and the relative involvement of AP-1 in inducible IL-8 promoter activity was greater in APE-1/Ref-1 overexpressing cells than in cells with basal levels of APE-1/Ref-1
Bobrovnikova-Marjon et al., Cancer Res 2004 (Breast Neoplasms) : Blocking NFkappaB and AP-1 activation with curcumin as well as expression of dominant inhibitors, inhibitor of nuclear factor-kappaB ( IkappaB ) super repressor ( IkappaBM ), and a mutant form of c-Fos ( A-Fos ) demonstrated that the activation of NFkappaB and AP-1 transcription factors was necessary for the induction of IL-8 expression but dispensable for the induction of VEGF expression
Zhu et al., J Biol Chem 2003 : Transcriptional regulation of interleukin (IL)-8 by bradykinin in human airway smooth muscle cells involves prostanoid dependent activation of AP-1 and nuclear factor (NF)-IL-6 and prostanoid independent activation of NF-kappaB
Boggaram et al., J Biol Chem 2013 (MAP Kinase Signaling System...) : ESAT-6 induction of IL-8 promoter activity was dependent on nuclear factor-?B ( NF-?B ) and activator protein-1 (AP-1) binding and sensitive to pharmacological inhibition of PKC and ERK and p38 MAPK pathways
Swiergiel et al., Brain Res Bull 1996 : The role of cerebral noradrenergic systems in the Fos response to interleukin-1
Abdel-Malak et al., Blood 2008 : Angiopoietin-1 promotes endothelial cell proliferation and migration through AP-1 dependent autocrine production of interleukin-8
Zhang et al., Cell Biol Int 2012 : AP-1 and NF-?B transcriptionally regulate interleukin-8 in EA.Hy926 cells under shear stress
Matsumoto et al., FEBS J 2007 (MAP Kinase Signaling System) : Caspase-8- and JNK dependent AP-1 activation is required for Fas ligand induced IL-8 production ... These results demonstrate that FasL induced AP-1 activation is required for optimal IL-8 production, and this process is mediated by FADD, caspase-8, and JNK