Gene interactions and pathways from curated databases and text-mining

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JUN — NFKB1

Protein-Protein interactions - manually collected from original source literature:

Studies that report less than 10 interactions are marked with *

Text-mined interactions from Literome

Kim et al., Arch Pharm Res 2009 (Colonic Neoplasms) : NF-kappaB target gene expression of apoptotic cell death proteins ( Bax, caspase-3, caspase-9 ) was significantly enhanced, but the expression of anti-apoptotic genes and cell proliferation marker genes ( Bcl-2, inhibitor of apoptosis protein ( IAP-1 ) and X chromosome IAP (XIAP), Cox-2, c-Fos, c-Jun and cyclin D1 ) was significantly inhibited by the combined treatment compared to Rg3 or docetaxel alone
Yang et al., J Cell Physiol 2010 (Arthritis, Rheumatoid) : IL-1beta induced ICAM-1 expression, extracellular signal regulated kinase ( ERK ) and c-Jun-N-terminal kinase (JNK) phosphorylation, AP-1 activation, and nuclear factor-kappaB (NF-kappaB) p65 translocation were attenuated by the inhibitors of MEK1/2 ( U0126 ), JNK ( SP600125 ), AP-1 ( tanshinone IIA ), and NF-kappaB ( helenalin ) or transfection with respective short hairpin RNA plasmids
Ares et al., BMC immunology 2002 : In contrast, oxidized LDL stimulated AP-1 and PPARgamma but inhibited NF-kappaB , indicating that the effects of lipid loading with ac-LDL were not due to oxidation of lipids
Maggirwar et al., J Neurochem 2000 : Furthermore, the inhibition of endogenous NF-kappaB in NGF maintained neuronal PC12 cells led to the induction of c-Jun synthesis and a marked increase in cell death
Lee et al., Toxicol Lett 2010 (Carcinoma, Hepatocellular...) : Hesperidin suppressed TPA stimulated NF-kappaB translocation into the nucleus through IkappaB inhibitory signaling pathways and also inhibited TPA induced AP-1 activity by the inhibitory phosphorylation of p38 kinase and c-Jun N-terminal kinase (JNK) signaling pathways
Wu et al., FEBS Lett 2002 : In HEK293 cells, proteasome inhibitors could concentration-dependently increase IL-8 promoter and activator protein-1 (AP-1) activities, but inhibited nuclear factor (NF)-kappa B activation induced by cytokines
Bianchi et al., Neurobiol Aging 2010 (Encephalitis...) : We show here that : ( 1 ) S100B also stimulates AP-1 transcriptional activity in microglia via RAGE dependent activation of JNK ; ( 2 ) S100B upregulates IL-1beta and TNF-alpha expression in microglia via RAGE engagement ; and ( 3 ) S100B/RAGE induced upregulation of COX-2, IL-1beta and TNF-alpha expression requires the concurrent activation of NF-kappaB and AP-1
Xiang et al., Zhonghua Gan Zang Bing Za Zhi 2008 (Hepatitis B, Chronic) : Three kinds of immunological adjuvants, TNF alpha, CpG-ODN and CpG-ODN/HBsAg enhanced the expression of nucleic NF-kB and inhibited the expression of AP-1 in DC
Fujioka et al., Mol Cell Biol 2004 : NF-kappaB and AP-1 connection : mechanism of NF-kappaB dependent regulation of AP-1 activity
Mohan et al., J Biol Chem 2000 (Neovascularization, Pathologic) : Using cultured corneal cells, we show that FGF-2 stimulates DNA binding activity of transcription factor AP-1 but not NF-kappaB and that AP-1 stimulation is inhibited by curcuminoids
Wang et al., J Cell Biochem 2009 (Orthostatic Intolerance) : These findings indicate that clinorotation upregulates iNOS in HUVECs by a mechanism dependent on suppression of AP-1 , but not NF-kappaB
Zhang et al., Int J Cancer 2009 (Prostatic Neoplasms) : We show that inhibition of NF-kappaB or activation of AP-1 can only partially sensitize resistant prostate cancer cells to proapoptotic effects of TNFalpha or TRAIL ... However, concomitant repression of NF-kappaB and activation of c-Fos/AP-1 significantly enhanced the proapoptotic effects of TNFalpha and TRAIL in resistant prostate cancer cells
Pacurari et al., Environ Health Perspect 2008 (Neoplasms, Mesothelial) : In the present study, we exposed mesothelial cells to SWCNTs and investigated reactive oxygen species ( ROS ) generation, cell viability, DNA damage, histone H2AX phosphorylation, activation of poly(ADP-ribose) polymerase 1 ( PARP-1 ), stimulation of extracellular signal regulated kinase ( ERKs ), Jun N-terminal kinases (JNKs) , protein p38, and activation of activator protein-1 (AP-1), nuclear factor kappaB (NF-kappaB) , and protein serine-threonine kinase ( Akt )
Hsieh et al., Biochim Biophys Acta 2008 : Moreover, thrombin stimulated activation of NF-kappaB, AP-1 , and COX-2 promoter activity was blocked by the inhibitors of c-Src, PKC, EGFR, MEK1/2, AP-1 and NF-kappaB , suggesting that thrombin induces COX-2 promoter activity mediated through PKC ( delta ) /c-Src dependent EGFR transactivation, MEK-ERK1/2, AP-1, and NF-kappaB
Meyer et al., EMBO J 1993 : H2O2 and antioxidants have opposite effects on activation of NF-kappa B and AP-1 in intact cells : AP-1 as secondary antioxidant-responsive factor
Cooper et al., Mol Carcinog 2005 : Expression of the leucine zipper domain of the TAM67 protein inhibited UVB induced NF-kappaB transactivation but not AP-1 transactivation
Onodera et al., Arthritis Rheum 2004 (Arthritis, Rheumatoid...) : The mRNA up-regulation of IL-8 and IL-1beta by MIF was inhibited by 2 tyrosine kinase inhibitors, a protein kinase C ( PKC ) inhibitor, an activator protein 1 (AP-1) inhibitor , and by an NF-kappaB inhibitor
Patel et al., Biochem Biophys Res Commun 2006 : LPS stimulated both AP-1 ( c-Fos, c-Jun ) and NF-kappaB ( p50 and p65 ) activation, but only inhibition of AP-1 attenuated LPS induced CXCR6 expression
Petlickovski et al., Blood 2005 (Leukemia, Lymphocytic, Chronic, B-Cell...) : This response was characterized by transient phosphorylation of extracellular signal related kinase ( ERK ) and Akt ( protein kinase B [ PKB ] ), lack of activation of c-JUN NH2-terminal kinase (JNK) and p38 mitogen activated protein kinase ( MAPK ), and variable activation of phospholipase Cgamma2 ( PLCgamma2 ) and nuclear factor-kappaB (NF-kappaB)
Lee et al., J Biochem Mol Biol 2002 : TAK1 dependent activation of AP-1 and c-Jun N-terminal kinase by receptor activator of NF-kappaB
Gentry et al., J Biol Chem 2004 : Reciprocally, NRIF enhanced TRAF6 mediated activation of the c-Jun NH2-terminal kinase (JNK) by 3-fold, while only modestly increasing the stimulation of NF-kappaB
Jope et al., Brain Res Mol Brain Res 1997 (Neuroblastoma) : Besides being differentially sensitive to inhibition by lithium, activation of AP-1 and NF-kappaB demonstrated different carbachol EC50 concentrations, and carbachol induced activation of AP-1 , but not NF-kappaB, was inhibited by treating cells with Ni2+, which blocks receptor mediated calcium influx
Manna et al., J Immunol 2000 : Vesnarinone also blocked NF-kappa B activation induced by several other inflammatory agents, inhibited the TNF induced activation of transcription factor AP-1 , and suppressed the TNF induced activation of c-Jun N-terminal kinase and mitogen activated protein kinase kinase
Fan et al., Shock 2004 (Inflammation...) : Pretreatment with PTx inhibited TLR4ca induced ERK 1/2 phosphorylation ( 30 +/- 7 %, P < 0.05 ) and AP-1 activation ( 36 +/- 3 %, P < 0.05 ) but did not inhibit NFkappaB activation
Farhana et al., Mol Cancer Ther 2009 : 3-Cl-AHPC induction of c-Fos and c-Jun expression as well as NF-kappaB activation was dependent on SHP protein levels
Thompson et al., J Biol Chem 2008 (Inflammation) : LTC ( 4 ) stimulation induced NF-kappaB and AP-1 DNA binding, which involved the formation of a p50/p65 and a c-JUN.c-FOS complex, respectively
Wang et al., Neurochem Int 2010 (Disease Models, Animal...) : Mechanistically, PSPC strongly inhibited LPS induced phosphorylated extracellular signal regulated kinase ( ERK ) and phosphorylated c-Jun N-terminal kinase (JNK) expression and nuclear factor kappa B (NF-kappaB) activation
Kaneko et al., Biol Pharm Bull 2004 : These results suggest that the MnSOD expression is controlled by ER stress through IRE1 mediated NF-kappaB and AP-1 activation
Kim et al., J Biol Chem 2000 : Taken together with previous observations, these results implicate that, for the assembly of an IFN-beta enhanceosome, MEKK1 can induce IRF3 and ATF2/c-JUN through the JNK pathway, whereas it can induce NF-kappaB through the IKK pathway
O'Suilleabhain et al., Shock 2001 (Burns) : Our findings revealed that changes in mitogen stimulated T-cell AP-1 and NFkappaB factor activation correlated directly with defective mitogen induced IL-2 mRNA expression
You et al., FEMS Immunol Med Microbiol 2008 : The DNA binding activity of NF-kappaB and AP-1 was also assessed by an electrophoretic mobility gel shift assay, and an NF-kappaB specific inhibitor, pyrrolidine dithiocarbamate, profoundly inhibited the synthesis and production of the proinflammatory cytokines
Mattson et al., Int J Hyperthermia 2004 : Heat shock and the activation of AP-1 and inhibition of NF-kappa B DNA binding activity : possible role of intracellular redox status ... Gel electromobility shift assays ( EMSA ) demonstrated that heat shock induced AP-1 DNA binding activity but inhibited IR-induced activation of NF-kappa B
Lu et al., Journal of neuroinflammation 2010 (Inflammation) : Resveratrol inhibited LPS induced NF-kappaB activation in both cell types, but inhibited AP-1 activation only in microglia
Newton et al., FEBS Lett 1997 : Furthermore, equivalent effects were observed on NF-kappaB binding to COX-2 promoter kappaB sites and activation of the Jun N-terminal kinases (JNK) , p54 and p46
Simon et al., Int Immunol 1996 : Second, antigen induced a different pattern of transcription factor binding activities than PMA/lonomycin in DP thymocytes, AP-1 activity being selectively induced by antigen and NF-kappa B by PMA/lonomycin
Yang et al., Oncogene 2001 (Cell Transformation, Neoplastic) : A novel transformation suppressor, Pdcd4, inhibits AP-1 transactivation but not NF-kappaB or ODC transactivation
Kim et al., Biol Chem 2003 : Pyrrolidine dithiocarbamate ( PDTC ) has been shown to have unique reciprocal activities in activating AP-1 and inhibiting NF-kappaB , two oxidative stress-sensitive transcription factors
Knecht et al., Oncology 2001 (Cell Transformation, Neoplastic...) : TRAF2 mediated NF-kappaB activation, AP-1 induction and JAK3/STAT activation may result in sustained proliferation leading to lymphoma
Dudek et al., J Virol 2010 : Rather, PS-341 treatment resulted in an induction of IkappaB degradation and activation of NF-kappaB as well as the JNK/AP-1 pathway
Matthews et al., Cancer Res 2007 (Skin Neoplasms) : Dominant negative c-Jun ( TAM67 ) blocks AP-1 activation by dimerizing with Jun or Fos family proteins and blocks NFkappaB activation by interacting with NFkappaB p65
Krappmann et al., Mol Cell Biol 2004 : The IkappaB kinase complex and NF-kappaB act as master regulators of lipopolysaccharide induced gene expression and control subordinate activation of AP-1 ... Thus, our data illustrate that NF-kappaB orchestrates immediate-early effects of LPS signaling and controls secondary AP-1 activation to mount an appropriate biological response
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
Zingarelli et al., FASEB J 2002 (Myocardial Infarction...) : These events were preceded by degradation of inhibitor kappaBalpha ( IkappaBalpha ), activation of IkappaB kinase complex (IKK) and c-Jun-NH2-terminal kinase (JNK) , and subsequently activation of nuclear factor-kappaB (NF-kappaB) and activator protein 1 (AP-1) as early as 15 min after reperfusion
Theuer et al., Kidney Int 2005 : EPA treatment reduced activator protein-1 (AP-1) activation and partially inhibited nuclear factor-kappaB (NF-kappaB) activity in kidneys of dTGR
Ding et al., Mol Cell Biochem 2002 (Cell Transformation, Neoplastic) : This article summarizes recent studies from our laboratory on ( a ) the reduction of Cr ( VI ) by ascorbate, diol- and thiol containing molecules, certain flavoenzymes, cell organelles, intact cells, and whole animals ; ( b ) free radical production in both non-cellular and cellular systems ; and ( c) Cr(VI ) -induced DNA damage, activation of nuclear transcription factor KB ( NF-kappaB ), activator protein-1 , p53, hypoxia-inducible factor-1, vascular endothelial growth factor, tyrosine phosphorylation, apoptosis, cell growth arrest, and gene expression profile
Lucio-Cazana et al., J Am Soc Nephrol 2001 : t-RA substantially inhibited the constitutive activity of AP-1 but did not inhibit NF-kappaB activity in mesangial cells
Georganas et al., J Immunol 2000 (Arthritis, Rheumatoid) : Employing gel shift assays, NF-kappaB, C/EBPbeta, and c-Jun were constitutively activated in RA FLS, but only NF-kappaB and c-Jun activity increased after IL-1beta
Kim et al., Rheumatology (Oxford) 2009 (Osteoarthritis) : MAP kinases [ p38, extracellular signal regulated protein kinase ( ERK ) and C-Jun N terminal kinase (JNK) ] and NF-kappaB activation were evaluated by western blotting and by an electrophoretic mobility shift assay, respectively
Ryoo et al., Cardiovasc Res 2004 : These data demonstrated that LDL stimulates SMCs to induce IL-8 production in dose- and time dependent manners at the transcription level and that the LDL signaling in hAoSMCs is conveyed via the generation of H2O2, the phosphorylation of p38 MAPK, the activation of AP-1 , and the participation of NF-kappaB
Jeon et al., Toxicol Lett 1999 : Treatment of AAF to RAW 264.7 cells induced a dose related inhibition of NF-kappa B/Rel in chloramphenicol acetyltransferase activity, while either AP-1 or NF-IL6 activation was not affected by AAF
Kim et al., PLoS Biol 2007 : We conclude that an inhibitory effect of AP-1 and STAT on NF-kappaB is required for properly balanced immune responses and appears to be evolutionarily conserved
Zhou et al., Free Radic Biol Med 2001 : In summary, our results suggest that NF kappa B and AP-1 are important mediators of redox-responsive gene expression in skeletal muscle, and that at least NF kappa B is actively involved in the upregulation of the GPx and CAT in response to oxidative stress
Okabe et al., Jpn J Cancer Res 1999 : Moreover, SS555 inhibited TNF-alpha gene expression mediated through inhibition of AP-1 activation, but not NF-kappa B activation
Dragomir et al., Vascul Pharmacol 2006 : Together, the findings indicate that in endothelial cells aspirin and PPAR-alpha activators reduce the high glucose increased expression of MCP-1 by a mechanism that includes the inhibition of reactive oxygen species, and decrease of AP-1 and NF-kB activation
Lee et al., Dev Biol 2001 : In contrast, gas1 overexpression in 12.5 day limb cells enhanced AP-1 response while it inhibited NFkappaB and c-myc activities
Pekarsky et al., Proc Natl Acad Sci U S A 2008 (Leukemia, Lymphocytic, Chronic, B-Cell) : The results indicate that Tcl1 overexpression causes B-CLL by directly enhancing NF-kappaB activity and inhibiting AP-1
Blanchette et al., Immunology 2009 (MAP Kinase Signaling System...) : The activation of AP-1 , and not nuclear factor-kappaB (NF-kappaB) or signal transducer and activator of transcription-1 alpha ( STAT-1 alpha ), may explain the enhanced NO generation in SHP-1-deficient cells
Kim et al., Am J Transplant 2005 (Reperfusion Injury) : Induction of MIEP-lacZ expression was preceded by TNFR independent formation of reactive oxygen species ( ROS ), weak and transient activation of NF-kappaB and strong and sustained activation of AP-1
Bierhaus et al., Thromb Haemost 1997 : The dietary pigment curcumin reduces endothelial tissue factor gene expression by inhibiting binding of AP-1 to the DNA and activation of NF-kappa B
Savaskan et al., FASEB J 2003 (Disease Susceptibility...) : Gel shift analysis demonstrates that this effect is connected to the inhibition of glutamate induced NF-kappaB and AP-1 activation
Radoja et al., Mol Cell Biol 2004 (Epidermolysis Bullosa) : We found that C/EBP-beta and AP-1 induced, while retinoic acid, glucocorticoid receptors, and NF-kappaB suppressed , the K15 promoter, along with other keratin gene promoters
Lee et al., Food Chem Toxicol 2008 (Necrosis) : Hydrogen peroxide provoked phosphorylation of extracellular regulated kinase (ERK) and c-Jun NH ( 2 ) -terminal kinase ( JNK ), and activation of nuclear factor-kappaB (NF-kappaB)
Guo et al., Inflammation 2000 : Cotransfection experiments showed that the combination of antisense IRAK-2 ODN and antisense p110 PI 3-kinase ODN resulted in additive inhibition of NF-kappaB as well as AP-1 activation
Jung et al., J Ethnopharmacol 2007 : WHW extract attenuated the phosphorylation of mitogen activated protein kinases ( MAPKs ), extracellular signal regulated kinases 1 and 2 ( ERK1/2 ) and c-Jun N-terminal kinase (JNK) , as well as the activation of nuclear factor-kappa B (NF-kappaB) in LPS stimulated RAW264.7 cells
Janssens et al., FEBS Lett 2003 : Moreover, the regulated expression of a MyD88 splice variant which specifically interferes with NF-kappaB- but not AP-1 dependent gene expression implies an important role for alternative splicing in the fine tuning of TLR/IL-1R responses
Weng et al., J Immunol 1997 : To further explore the ramifications of CD19 signaling, the current study examined whether phosphorylation of Elk-1, activation of activator protein-1 (AP-1) , or activation of nuclear factor-kappaB (NF-kappaB) transcription factors occurred following CD19 cross linking
Matsumoto et al., FEBS J 2007 (MAP Kinase Signaling System) : Selective inhibition of AP-1 did not affect NF-kappaB activation and vice versa, indicating that their activations were not sequential events
Tang et al., Mol Cell Biol 2002 (MAP Kinase Signaling System) : The absence of NF-kappaB mediated inhibition of c-Jun N-terminal kinase activation contributes to tumor necrosis factor alpha induced apoptosis
Medvedev et al., J Biol Chem 1999 : The lipopolysaccharide antagonist, Rhodobacter sphae-roides diphosphoryl lipid A, inhibited lipopolysaccharide activation of NF-kappaB and AP-1 but did not block C2-ceramide induced AP-1
Pindolia et al., Hematopathol Mol Hematol 1996 : Whereas AP-1 and SP-1 are constitutively expressed in stromal cells, NF-kB is detected only after stimulation with IL-1
Tang et al., J Exp Med 2008 (Bone Marrow Diseases...) : Activation of TAK1 by proinflammatory cytokines and T and B cell receptors induces the nuclear localization of nuclear factor kappaB (NF-kappaB) and the activation of c-Jun N-terminal kinase (JNK)/AP1 and P38, which play important roles in mediating inflammation, immune responses, T and B cell activation, and epithelial cell survival
Jang et al., J Cell Physiol 2004 (Leukemia, Erythroblastic, Acute) : We show that : ( 1 ) downregulation of Notch-1 sensitizes MEL cells to apoptosis induced by a Ca ( 2+ ) influx or anti-neoplastic drugs ; ( 2 ) Notch-1 downregulation induces phosphorylation of c-Jun N-terminal kinase (JNK) while constitutive activation of Notch-1 or prolonged exposure to a soluble Notch ligand abolishes it ; ( 3 ) Notch-1 has dose- and time dependent effects on the levels of apoptotic inhibitor Bcl-x ( L ) and cell cycle regulators p21 ( cip1/waf1 ), p27 ( kip1 ), and Rb ; and ( 4 ) Notch-1 activation by a cell associated ligand is accompanied by rapid and transient induction of NF-kappaB DNA binding activity
Martin et al., Osteoarthritis Cartilage 2005 : IL-1beta enhanced both AP-1 and NF-kappaB binding, whereas H ( 2 ) O ( 2 ) only activated AP-1
Jeon et al., Immunopharmacology 2000 : These results suggest that DEX may inhibit IL-1beta gene expression by a mechanism involving the blocking of LPS induced NF-kappaB/Rel and AP-1 activation
Shibata et al., J Am Soc Nephrol 2006 (Disease Models, Animal...) : Fluvastatin also mitigated tubulointerstitial damage in PAN nephrosis, with the repression of PAN induced NF-kappaB and activator protein-1 activation in the kidneys
Nold-Petry et al., Proc Natl Acad Sci U S A 2009 : Increasing evidence demonstrates that interleukin (IL)-32 is a pro-inflammatory cytokine, inducing IL-1alpha, IL-1beta, IL-6, tumor necrosis factor (TNF)-alpha, and chemokines via nuclear factor (NF)-kappaB , p38 mitogen activated protein kinase ( MAPK ), and activating protein (AP)-1 activation
Tran-Thi et al., Hepatology 1995 : The results indicate a direct participation of NF-kappa B in the regulation of TNF-alpha synthesis and a differential effect of LPS on NF-kappa B and AP-1 , respectively
Jung et al., Food Chem Toxicol 2009 (Inflammation) : The molecular mechanisms that underlie GHE mediated attenuation are related to the inhibition of the phosphorylation of three mitogen activated protein kinases ( MAPKs ), extracellular signal regulated kinases 1 and 2 ( ERK1/2 ), p38 MAPK, and c-Jun N-terminal kinase (JNK) , and the activation of nuclear factor-kappaB (NF-kappaB)
Li et al., Free Radic Biol Med 2005 (Cardiomegaly) : Our results revealed that pretreatment with ISO significantly inhibited Ang II-mediated NF-kappaB through affecting the degradation and phosphorylation of IkappaBalpha and the activity of IKKbeta and AP-1 activation by influencing the expression of c-Fos and c-Jun proteins
Hirai et al., Osaka City Med J 2006 : AP-1 DNA binding activities in the FW and SW of group R significantly increased at POD 5, and NF-kappaB DNA binding activities of group R significantly increased at PODs 3 and 5
Roccaro et al., Blood 2010 (Lymphoma...) : Primary WM cells express higher level of i20S compared with c20S, and that ONX0912 inhibited the CT-L activity of both i20S and c20S, leading to induction of toxicity in primary WM cells, as well as of apoptosis through c-Jun N-terminal kinase activation, nuclear factor kappaB (NF-kappaB) inhibition , caspase cleavage, and initiation of the unfolded protein response
Arsura et al., Oncogene 2003 (Carcinoma, Hepatocellular...) : Transient activation of NF-kappaB through a TAK1/IKK kinase pathway by TGF-beta1 inhibits AP-1/SMAD signaling and apoptosis : implications in liver tumor formation ... Inhibition of NF-kappaB following TGF-beta1 treatment increased AP-1 complex transcriptional activity through sustained c-Jun phosphorylation, thereby potentiating AP-1/SMADs mediated cell killing
Zuscik et al., Environ Health Perspect 2007 : Although Pb had no effect on basal CREB or Wnt/beta-catenin pathway activity, it induced NFkappaB signaling and inhibited AP-1 signaling
Meng et al., Toxicol Lett 2009 : Mechanistic studies indicate that B [ a ] P-induced transcriptional activation of MMP-3 is not mediated by AP-1 , NF-kappaB
Kriehuber et al., Blood 2005 : Ligation of tumor necrosis factor receptor superfamily ( TNFR-SF ) members on DCs and cognate contact with T cells resulted in quantitatively balanced nuclear factor-kappaB (NF-kappaB) and c-Jun N-terminal kinase (JNK) mediated activator protein-1 (AP-1) induction and strongly enhanced DC longevity
Shah et al., Int J Cancer 2006 (Colonic Neoplasms) : UDCA did not increase DNA binding of NF-kappaB and AP-1 and UDCA pretreatment inhibited DCA induced NF-kappaB and AP-1 DNA binding
Arch et al., Biochem Biophys Res Commun 2000 : After recruitment to a receptor, TRAFs initiate formation of multiprotein complexes that induce downstream events, such as translocation of transcription factor nuclear factor kappaB (NF-kappaB) and activation of c-Jun N-terminal kinase (JNK)
Heo et al., J Immunol 2007 : This leads to NFkappaB activation as a result of IkappaBalpha degradation and/or JNK/AP-1 activation, and ultimately results in the expression of genes required for cell survival, cytokine production, or cell proliferation
Granado-Serrano et al., Nutr Cancer 2010 (Carcinoma, Hepatocellular...) : These data suggest that NF-kappa B and AP-1 play a main role in the tight regulation of survival/proliferation pathways exerted by quercetin and that the sustained JNK/AP-1 activation and inhibition of NF-kappa B provoked by the flavonoid induced HepG2 death
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
Ahmed et al., Molecular cancer 2010 (Breast Neoplasms) : Osteopontin selectively regulates p70S6K/mTOR phosphorylation leading to NF-kappaB dependent AP-1 mediated ICAM-1 expression in breast cancer cells ... We also observed that OPN induced NF-kappaB further controls AP-1 transactivation, suggesting that there is cross talk between NF-kappaB and AP-1 which is unidirectional towards AP-1 that in turn regulates ICAM-1 expression in these cells
Jung et al., Ann N Y Acad Sci 1995 : Integration of the signals generated by TCR and CD28 engagement occurs along this pathway, which then bifurcates to induce I kappa B phosphorylation and NF-kappa B activation on the one hand, and JNK activation and c-Jun phosphorylation on the other