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EPHB2 — JUN

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Ishida et al., Diabetes 1999 : Stretch induced activation of ERK was inhibited by herbimycin A, a tyrosine kinase inhibitor, but not by GF109203X or calphostin C, the inhibitors of protein kinase C. Mechanical stretch also enhanced DNA binding activity of AP-1 , and this enhancement was inhibited by PD98059, an inhibitor of MAPK or ERK kinase ( MEK )
Huang et al., Oncogene 1999 : Overexpression of wild-type Erk2 in Cl 30.7b cells that contain small amounts of Erks caused a 46.6- or 138.1-fold increase of AP-1 activity by UVB and UVC, respectively ; introduction of a dominant negative Erk2 into Cl 41 cells significantly blocked the UV-induced Erks activation as well as the AP-1 activation
Zeigler et al., J Cell Physiol 1999 : This evidence suggests that while ERK and JNK activity are necessary for AP-1 activation, ERK but not JNK is sufficient in stimulating cell motility
Chen et al., J Biol Chem 1999 : This AP-1 activation was completely blocked by PD 098059, a specific mitogen activated protein kinase/ERK kinase inhibitor , as well as by a dominant negative JNK or a dominant negative Jun , indicating that the AP-1 activation induced by 1,25 ( OH ) ( 2 ) D ( 3 ) was mediated by ERK and JNK ... This AP-1 activation was completely blocked by PD 098059, a specific mitogen activated protein kinase/ERK kinase inhibitor, as well as by a dominant negative JNK or a dominant negative Jun, indicating that the AP-1 activation induced by 1,25 ( OH ) ( 2 ) D ( 3 ) was mediated by ERK and JNK
Wang et al., Hypertension 1999 (MAP Kinase Signaling System) : Tumor necrosis factor-alpha (TNF-alpha) alone can induce extracellular signal regulated kinase ( ERK ), p38 MAPK, and c-Jun N-terminal kinase activity in a rapid and transient manner, whereas interferon-gamma (IFN-gamma) can induce only ERK
Qiao et al., J Biol Chem 2000 (Adenocarcinoma) : Inhibition of ERK by the mitogen activated protein kinase/ERK kinase inhibitor PD 98059 or by expression of a dominant negative mutant ERK suppressed AP-1 activation
Finlay et al., J Biol Chem 2000 : AP-1 binding was dependent on ERK activation, since the MEK-1 ( mitogen activated protein kinase kinase ) inhibitor PD98059 inhibited TGF-beta1 induced binding
Reffas et al., Biochem J 2000 : Compartment-specific regulation of extracellular signal regulated kinase ( ERK ) and c-Jun N-terminal kinase (JNK) mitogen activated protein kinases ( MAPKs ) by ERK dependent and non-ERK dependent inductions of MAPK phosphatase (MKP)-3 and MKP-1 in differentiating P19 cells
Yoshizumi et al., Jpn J Pharmacol 2000 : The ERK1/2 activation was followed by an increase in transcription factor activator protein-1 DNA binding activity
Simeone et al., Am J Physiol Cell Physiol 2001 (MAP Kinase Signaling System) : The biological relevance of ERK activation by TGF-beta was indicated by demonstrating that inhibition of ERK signaling by PD-98059 blocked the ability of TGF-beta to activate the transcription factor activator protein-1
Yu et al., Cancer Res 2001 (Breast Neoplasms...) : Expression of dominant negative mutants of ERK1 , MAPK/ERK activator-1, or JNK1 but not p38 blocked phosphorylation of the substrate glutathione S-transferase-c-Jun and inhibited VES induced apoptosis
Zentrich et al., J Biol Chem 2002 : Truncation analysis and electromobility shift assays established the requirement for a cAMP-response element/activating transcription factor-like site in the NFLC promoter that minimally interacts with constitutively expressed cAMP-response element binding protein and JunD as well as c-Jun which is induced by NGF in an ERK dependent manner
Young et al., Mol Cell Biol 2002 (Cell Transformation, Neoplastic) : These observations suggest that ERK dependent activation of Fra-1 is required for AP-1 transactivation in JB6 cells
Cho et al., Nitric Oxide 2002 (MAP Kinase Signaling System) : These results demonstrated that bovine type I collagen induces iNOS in serum stimulated murine macrophages through JunB/AP-1 and NF-kappa B activation and that activation of ERK1/2 plays an essential role in JunB/AP-1 activation
Granet et al., Cell Signal 2002 : Downregulation of protein kinase C ( PKC ) and COX1/2 or inhibition of ERK1/2 , p38 ( MAPK ) or src kinases had no major effect on AP-1 mRNA expression in the Flexcell
Jijon et al., Am J Physiol Cell Physiol 2002 : Furthermore, AP-1 and NF-kappaB DNA binding was not affected by ERK and p38 inhibition
Iles et al., Free Radic Biol Med 2002 : Together these data suggest that C5a mediated AP-1 activation requires both the activation of the ERK and JNK pathways, whereas activation of the JNK pathway is sufficient to increase AP-1 binding with ADP
Chen et al., J Virol 2002 (Epstein-Barr Virus Infections) : The phosphorylation could be inhibited by the ERK pathway inhibitor PD98059, indicating that ERK may contribute to the phosphorylation of c-Jun in LMP2A expressing cells
Bozinovski et al., J Biol Chem 2002 (MAP Kinase Signaling System) : Granulocyte/macrophage-colony stimulating factor ( GM-CSF ) regulates lung innate immunity to lipopolysaccharide through Akt/Erk activation of NFkappa B and AP-1 in vivo
Budagian et al., J Biol Chem 2003 : ATP failed to stimulate the phosphorylation of ERK and c-Jun N-terminal kinase and activation of AP-1 in the p56 ( lck ) -deficient isogenic T cell line JCaM1, suggesting a critical role for p56 ( lck ) kinase in downstream signaling
Ramachandiran et al., Chem Res Toxicol 2002 : TGHQ increased AP-1 and NFkappaB DNA binding activity, but whereas pharmacological inhibition of ERK1/2 or p38 MAPKs attenuated AP-1 DNA binding activity, it potentiated TGHQ mediated NFkappaB activation
Huang et al., J Cell Physiol 2003 (Melanoma) : Inhibition of ERK1/2 phosphorylation stimulated AP-1 activity, which was not additive to that induced by RA
Jorritsma et al., J Immunol 2003 (MAP Kinase Signaling System) : Interestingly, transient Erk activation resulted in altered AP-1 DNA binding activity and the induction of an AP-1 complex that was devoid of Fos protein and consisted of Jun-Jun dimers
Qiao et al., Mol Cell Biol 2003 : DCA induced ERK1/2 activation was responsible for increased DNA binding of C/EBPbeta, CREB, and c-Jun/AP-1
Qu et al., Blood 2004 : The antigen induced tyrosine phosphorylation of FcepsilonRI, Syk, phospholipase C-gamma (PLC-gamma), activation of c-Jun N-terminal kinase (JNK) , extracellular signal regulated kinase ( ERK ), inhibitor of nuclear factor kappaB kinase ( IKK ), and Ca++ influx were all suppressed in the cells overexpressing Cbl-b in the lipid raft
Vial et al., J Cell Sci 2003 (Colonic Neoplasms) : We show that c-JUN and FRA-1 expression is dependent on ERK activity and that different thresholds of ERK activity control the expression of FRA-1
Chun et al., Carcinogenesis 2004 : In order to clarify the roles of p38 and ERK in TPA induced AP-1 activation, we utilized the pharmacologic inhibitors of these enzymes
Hammaker et al., J Immunol 2004 (Arthritis, Rheumatoid...) : Of interest, MEKK1 immunoprecipitates from IL-1 stimulated FLS appeared to activate c-Jun through the JNK pathway and TAK1 activation of c-Jun was dependent on JNK, ERK , and p38
Karoor et al., J Mol Cell Cardiol 2004 : In contrast, phospho-kinase levels of ERK and Akt were increased at 9-10 months, but phospho-kinase levels of c-Jun N-terminal kinase (JNK) increased only at 15-20 months ( when cardiomyopathy was fully manifest )
Higashi et al., Genes Cells 2004 (MAP Kinase Signaling System) : In contrast, concomitant stimulation of the STAT3 signal and a MEK/Erk-signal markedly increased AP-1 activity with enhanced c-Fos expression
Zeliadt et al., Biochem Biophys Res Commun 2004 : These studies show that in mouse keratinocytes MMP-13 gene expression can be induced through a Runx independent pathway that involves the ERK dependent modulation of AP-1
Zheng et al., Leukemia 2004 (Leukemia, Erythroblastic, Acute...) : HQ also induces ERK dependent AP-1 activation with concomitant increased transcriptional activity of AP-1 reporter gene
Wang et al., J Biol Chem 2004 (MAP Kinase Signaling System) : PKC and ERK1/2 independently down-regulated JNK/c-Jun , since inhibition of either kinase failed to affect activation of the other kinase, and simultaneous inhibition of both pathways caused additive JNK/c-Jun activation and cell death
Ingram et al., Kidney Int 2004 (MAP Kinase Signaling System) : Erk induces increases in activator protein-1 (AP-1) transcription factor activity which may augment mesangial cell proliferation and ECM protein production
Lee et al., Blood 2005 (MAP Kinase Signaling System) : Application of N-acetylcysteine (NAC) or blocking the activity of Nox, a protein leading to the formation of ROS, with diphenylene iodonium ( DPI ) inhibits the responses of BMM cells to RANKL, including ROS production, activation of c-Jun N-terminal kinase (JNK) , p38 mitogen activated protein ( MAP ) kinase, and extracellular signal regulated kinase ( ERK ), and osteoclast differentiation
Tian et al., Blood 2005 (Lymphoma, B-Cell) : Induction of Bcl10 activity caused rapid activation of nuclear factor-kappaB (NF-kappaB) and c-Jun N-terminal kinase (JNK) , but not activation of extracellular signal regulated kinase ( ERK ) or p38 mitogen activated protein ( MAP ) kinases
Zhao et al., J Biol Chem 2005 (Cell Transformation, Neoplastic) : The AP-1 stimulation appeared to be mediated by ERK but not JNK or p38 kinase
Sharma-Walia et al., J Virol 2005 (Herpesviridae Infections...) : Several MAPK regulated host transcription factors such as c-Jun, STAT1alpha, MEF2, c-Myc, ATF-2 and c-Fos were induced early during infection, and ERK inhibition significantly blocked the c-Fos, c-Jun , c-Myc, and STAT1alpha activation in the infected cells
Kobayashi et al., Exp Dermatol 2005 : We show ( i ) UV induced up-regulation of TNF-alpha mRNA and protein expression in keratinocytes ; ( ii ) cells treated with KTI before UV irradiation showed a significantly lower accumulation of TNF-alpha protein in a dose dependent manner and a reduced UV-induced up-regulation of TNF-alpha mRNA expression ; ( iii ) KTI inhibited the induction of TNF-alpha target molecules interleukin-1beta (IL-1beta) and IL-6 proteins ; ( iv ) UV irradiation transiently activated c-Jun N-terminal kinase (JNK) and Akt signaling but only weakly activated extracellular signal regulated kinase ( ERK ) and p38 ; ( v ) KTI specifically inhibited UV-induced activation of ERK , JNK, and p38, but not Akt ; ( vi ) treatment of cells with SP600125, a pharmacological inhibitor of JNK, predominantly suppressed UV-induced up-regulation of TNF-alpha expression ; and ( vii ) KTI did not enhance suppression of UV-induced JNK phosphorylation by SP600125
Li et al., Zhonghua Gan Zang Bing Za Zhi 2005 : Stimulation of HSC by Aldo results in activation of AP-1 via ERK1/2 pathway, leading to up-regulation of AP-1 target gene alpha1 ( 1 ) procollagen mRNA expression
Lee et al., J Biomed Sci 2006 : The c-Jun mRNA, which is also driven by AP-1, was also induced by HBO, and the induction of c-Jun was blocked by ERK and JNK inhibitors
Pearson et al., Mol Cell Biol 2006 : Transcription of c-Jun is induced by ERK5 , and like ERK5, c-Jun induction is also blocked by cAMP
Gao et al., Zhonghua lao dong wei sheng zhi ye bing za zhi = Zhonghua laodong weisheng zhiyebing zazhi = Chinese journal of industrial hygiene and occupational diseases 2006 : ERK and JNK, but not p38, mediated benzo ( a ) pyrene induced cell cycle changes by AP-1 transactivation in HELF
Yu et al., Toxicol Appl Pharmacol 2006 (MAP Kinase Signaling System) : In addition, atRA treatment caused a strong and sustained activation of c-Jun N-terminal kinase (JNK) and p38 kinase ( p38 ), as well as an early but transient activation of extracellular signal regulated kinase ( ERK )
Jiang et al., J Ocul Pharmacol Ther 2006 : EGF induced cell migration in a dose dependent manner ; EGF induced EGFR phosphorylation and downstream activation of c-Jun N-terminal protein kinase (JNK) , p38 MAP kinase ( p38 ), extracellular signal regulated kinase ( ERK1/2 ) and AKT, were inhibited by PD153035 ( EGFR inhibitor ), JNKi ( JNK inhibitor ), SB203580 ( p38 inhibitor ), U0126 ( MEK/ERK inhibitor ), and LY294002 ( PI3K/AKT inhibitor ), respectively
Sasaki et al., Mol Cell 2006 : Thus, this spatiotemporal regulation of c-Fos by ERK5 and UBR1 is critical for the regulation of c-Fos/AP-1
Gough et al., J Biol Chem 2007 (MAP Kinase Signaling System) : Thus, IFNgamma induced JAK1- and STAT1 independent activation of the ERK mitogen activated protein kinase pathway, phosphorylation of c-Jun, and activation of AP-1 DNA binding, which are important for the induction of a subset of ISGs
Kim et al., Biol Pharm Bull 2007 (Atherosclerosis) : Pre-treatment of VSMCs with NQ304 ( 1-10 microM ) was found to significantly inhibit the 5 % FBS induced phosphorylations of ERK1/2 and Akt, the activation of AP-1 and the expression of c-fos
Gazi et al., Clin Chim Acta 2007 (Prostatic Neoplasms) : Interestingly, although sodium selenite did not show effect on activation of both STAT3 and ERK1/2 in the presence of IL-6, an increased expression of c-Jun was detected in cells after treatment with sodium selenite
Wu et al., Cancer Lett 2007 (MAP Kinase Signaling System) : Specific blockade of MEK1/MEK2 cascade upstream from ERK1/2 abrogated 1,25D activation of AP-1 and p21, and subsequent antiproliferative effects, even in the presence of a nuclear VDR
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
Kang et al., Biol Pharm Bull 2007 : KIOM-79 inhibited activation of extracellular regulated kinase (ERK) induced by STZ and inhibited DNA binding activity of an activator protein-1 (AP-1) , a downstream transcription factor of ERK
Glauser et al., FASEB J 2007 : Altogether these findings reveal a sequential regulation of AP-1 by ERK1/2 , which initially increases transcription of c-fos and, if stimulation persists, stabilizes freshly synthesized c-FOS protein to efficiently activate the transcription of AP-1 regulated genes
Song et al., Gut 2007 (Adenocarcinoma...) : Unconjugated bile acids induce CREB and AP-1 dependent COX-2 expression in Barrett 's oesophagus and OA through ROS mediated activation of PI3K/AKT and ERK1/2
Peng et al., Toxicology 2007 (Glioma) : Inhibition of ERK , p38 and JNK block the activation of AP-1 and NF-kappaB, suggesting these MAPKs are involved in ( Ac ) ( 5 ) GP-induced transcription regulation
Jiao et al., Zhonghua lao dong wei sheng zhi ye bing za zhi = Zhonghua laodong weisheng zhiyebing zazhi = Chinese journal of industrial hygiene and occupational diseases 2007 : Moreover, B ( a ) P-induced activation of c-Jun was inhibited by stable expression of dominant negative mutants of JNK or ERK , but not by dominant negative mutant of p38
Cortez et al., Am J Physiol Heart Circ Physiol 2007 : Our data indicate that IL-17 induces MMP-1 in human cardiac fibroblasts directly via p38 MAPK- and ERK dependent AP-1 , NF-kappaB, and C/EBP-beta activation and suggest that IL-17 may play a critical role in myocardial remodeling
Mukherjee et al., Chem Biol Interact 2008 : We observed that ERK and JNK, but not p38 MAP kinase, are involved in BPDE induced AP-1 activation
Jia et al., Zhonghua lao dong wei sheng zhi ye bing za zhi = Zhonghua laodong weisheng zhiyebing zazhi = Chinese journal of industrial hygiene and occupational diseases 2008 : Furthermore we found expression of dominant negative mutant of ERK and JNK impaired silica induced AP-1 activation, whereas, dominant negative mutant of p38 did not show the effect
Ouyang et al., Cancer Res 2008 (Disease Models, Animal...) : Forced expression of c-Fos and c-Jun in prostate cancer cells promotes tumorigenicity and results in activation of extracellular signal regulated kinase ( Erk ) MAPK signaling
Adiseshaiah et al., Biochem Biophys Res Commun 2008 (Neoplasms) : ERK signaling regulates tumor promoter induced c-Jun recruitment at the Fra-1 promoter
Yu et al., Invest Ophthalmol Vis Sci 2008 : Pretreatment of cells with SB203580, an inhibitor for p38MAP kinase, reduced the H ( 2 ) O ( 2 ) - and TGF-beta2 stimulated Hsp27 expression, whereas pretreatment with PD98059 and U0126, specific inhibitors of ERK1/2 , and SP600125, a specific c-Jun N-terminal kinase inhibitor , had no effects
Xu et al., Toxicol Lett 2008 : Collectively, these data favor the notion that alpha-ZAL antagonizes oxLDL induced upregulation of ET-1 gene expression and secretion via suppression of oxLDL induced ROS accumulation, ERK phosphorylation, and activation of the endothelial transcriptional factor AP-1
Kogut et al., Innate Immun 2008 : Flagellin and lipopolysaccharide up-regulation of IL-6 and CXCLi2 gene expression in chicken heterophils is mediated by ERK1/2 dependent activation of AP-1 and NF-kappaB signaling pathways ... Taken together these data demonstrate that FLG and LPS stimulate the up-regulation of expression of IL-6 and CXCLi2 through an ERK1/2 dependent activation of both NF-kappaB and AP-1
Shim et al., Planta Med 2008 (MAP Kinase Signaling System) : Moreover, inhibition of ERK , JNK and p38 by panduratin A resulted in decreased c-Fos expression and c-Jun phosphorylation induced by UV, which led to inhibition of activator protein-1 (AP-1) DNA binding activity
Choi et al., Stem Cells Dev 2008 (MAP Kinase Signaling System) : As a consequence of PI3K-Akt and ERK1/2 , the upregulation of c-Jun in the Sca-1 ( + ) BMMSCs, after stimulation with FGF-2 or FGF-4, was observed after 12 and 24 h
Kirchmeyer et al., Arthritis Res Ther 2008 (MAP Kinase Signaling System) : Among RAR and RXR agonists, only ATRA inhibited IL-1 induced IL-6 expression in rat synovial fibroblasts by inhibiting ERK1/2 pathway and subsequent activation of AP-1 and NF-IL-6 independently of RAR
Schnidar et al., Cancer Res 2009 (Cell Transformation, Neoplastic...) : EGFR/MEK/ERK signaling induces JUN/activator protein 1 activation, which is essential for oncogenic transformation, in combination with the GLI activator forms GLI1 and GLI2
Park et al., Carcinogenesis 2009 (Breast Neoplasms...) : KPS-A decreased PMA induced transcriptional activation of NF-kappaB and AP-1 and inhibited PMA induced phosphorylation of ERK1/2 and Akt
Hasegawa et al., J Immunol 2009 : ASC mediated AP-1 activation was inhibited by chemical or protein inhibitors for caspase-8, caspase-8 targeting small interfering RNA, and p38 and JNK inhibitors, but not by a caspase-1 inhibitor, caspase-9 or Fas associated death domain protein ( FADD ) dominant negative mutants, FADD- or RICK targeting small interfering RNAs, or a MEK inhibitor, indicating that the ASC induced AP-1 activation is mediated by caspase-8, p38, and JNK, but does not require caspase-1, caspase-9, FADD, RICK, or ERK
Shim et al., J Med Food 2009 : Moreover, inhibition of phosphorylated ERK , JNK, and p38 by K. pandurata extract resulted in decreased c-Fos expression and c-Jun phosphorylation induced by UV light
Hong et al., Mol Cell Biochem 2010 : Further, ERK inhibitor inhibited significantly OPN expression, Elk1 phosphorylation, and activator protein-1 (AP-1)-DNA binding activation, but not FAK phosphorylation, in the force applied cells
Madeo et al., Oncogene 2010 (Breast Neoplasms) : In addition, OHT induced ERK dependent expression of c-Fos and transactivation of an AP-1-responsive promoter
Lim et al., American journal of translational research 2009 : Ras-Raf1-ERK1/2 dependent AP-1 activation positively regulates MUC5AC mucin induction by S. pneumoniae, whereas MEKK3-JNK1/2 dependent AP-1 activation negatively regulates it
Koh et al., J Pharmacol Exp Ther 2010 (Acute Disease...) : Furthermore, we found that specific ERK1/2 and JNK inhibitors reduce NF-kappaB and AP-1 activity
Lau et al., Planta Med 2010 (Breast Neoplasms) : ERK can activate the transcriptional factor binding of AP-1 or CRE, which can be located at the COX-2 promoter region ( - 72/- 53 )
Boucher et al., Viral Immunol 2010 (HIV Infections...) : In primary monocytes, ERK and p38 inhibition increased binding of AP-1 and Sp1, respectively, to the IL-12p40 promoter, while JNK inhibition increased NF-kappaB, AP-1, and Sp1 binding
Vlahos et al., Am J Respir Crit Care Med 2010 (Pneumonia) : We have previously shown that granulocyte/macrophage colony stimulating factor ( GM-CSF ) regulates lung innate immunity to LPS through Akt/Erk activation of nuclear factor-kappaB and activator protein (AP)-1
Yang et al., Cancer Sci 2010 (Lung Neoplasms...) : Moreover, c-Fos and c-Jun , the major downstream components of MAPKs, were up-regulated by ERK and JNK, respectively
Wiesner et al., Circ Res 2010 (Atherosclerosis...) : In a nuclear factor-DNA binding assay, the cooperative effect of mmLDL and LPS costimulation on c-Jun and c-Fos DNA binding, but not on p65 or p50, was dependent on mmLDL induced activation of extracellular signal regulated kinase ( ERK ) 1/2
Lee et al., Antivir Ther 2011 (Herpesviridae Infections) : To clarify the signal transduction pathways related to the regulation of the viral genes by alloferon, we confirmed that the calcium influx into BCBL-1 was apparently inhibited by alloferon, which preceded the suppression of the phosphorylation of ERK and the activation of AP-1 by TPA
Ibrahim et al., Diabetes 2011 (Diabetes Mellitus, Experimental...) : The results showed that formation of reactive oxygen species and subsequent activation of ERK and P38, but not Jun NH2-terminal kinase, are molecular events underpinning retinal microglial TNF-a release during AGA treatment
Cai et al., PloS one 2011 : EMSA showed that JNK and ERK1/2 were involved in MCP-1 induced AP1 activation ... These results suggest that MCP-1 induces murine amylin expression through AP1 activation mediated by ERK1/2 or JNK
Ho et al., International journal of biological sciences 2011 (Adenocarcinoma...) : Dimerumic acid inhibits SW620 cell invasion by attenuating H2O2 mediated MMP-7 expression via JNK/C-Jun and ERK/C-Fos activation in an AP-1 dependent manner
Fu et al., J Biol Chem 2011 (Carcinoma, Hepatocellular...) : The increased expression of c-JUN was dependent on ATF2 and on activation of the MEK-ERK and JNK arms of the MAPK signaling pathways
Thaikoottathil et al., Mol Immunol 2011 : Inhibition of ERK1/2 significantly reduced Pam ( 3 ) CSK ( 4 ) -mediated c-Jun activation and SPLUNC1 expression
Yen et al., J Biol Chem 2011 (MAP Kinase Signaling System) : We show that PGE2 induced MMP-9 expression is mediated primarily through the EP2/EP4  cAMP  protein kinase A (PKA)/PI3K  ERK signaling pathway, leading to c-Fos expression, and through JNK mediated activation of c-Jun in a PKA/PI3K/ERK independent manner
Saadane et al., Journal of inflammation (London, England) 2011 : This was associated with enhanced phosphorylation of p38, ERK1/2 and JNK and increased activation of AP-1
Oh et al., J Immunol 2012 (Otitis Media) : ERK2 dependent activation of c-Jun is required for nontypeable Haemophilus influenzae induced CXCL2 upregulation in inner ear fibrocytes
Nakamizo et al., Dig Dis Sci 2012 : Gastric mucosal cell proliferation induced by exposure to high transmural pressure may be related to early activation of ERK , the induction of c-fos and c-myc, and the activation of AP-1
Ma et al., Molecular cancer 2012 (Carcinoma, Ductal, Breast) : Individually, epidermal growth factor (EGF), and interleukin (IL)-1ß activated ERK1/2 , increased cell migration and invasion, MMP-9 expression and activity, AP-1 activation in vitro and the expression of p-ERK1/2 was positively correlated with EGF expression levels, as well as IL-1ß, MMP-9 and c-fos in IBDC tissue samples
Mou et al., J Biol Chem 2013 (Brain Neoplasms...) : Reporter gene assays indicated hHK-1 enhanced both AP-1 and NF-?B activity ; inhibition of ERK, JNK, and Akt dose-dependently suppressed the NF-?B activity ; only the inhibition of ERK significantly suppressed the AP-1 activity
Franklin et al., Pharmacol Res 2013 : The CB(2) receptor mediated upregulation of ß-Arrestin 2 would be mediated, at least in part, by an ERK1/2 dependent activation of AP-1
Liu et al., Biochim Biophys Acta 2013 (Inflammation...) : CTGF mediated increase of NF-?B and AP-1 luciferase activity was inhibited by FAK, MEK, and ERK inhibitors or mutants
Qing et al., Arch Toxicol 2013 (MAP Kinase Signaling System...) : SP600125 and U0126, by blocking the phosphorylation of c-Jun and MEK1/2, inhibited JNK and ERK phosphorylation, respectively, and attenuated apoptosis significantly
Chien et al., Prostaglandins Leukot Essent Fatty Acids 2013 : Furthermore, activation of extracellular regulated kinase (ERK) and c-Jun N-terminal kinase (JNK) by TPA+AA was identified in HL-60 cells, and the ERK inhibitor, PD98059, but not the JNK inhibitor, SP600125, inhibited TPA+AA induced NBT positive cells
Frost et al., Mol Cell Biol 1994 : We found that coexpression of small t and either ERK1 , MEK1, or BXB resulted in an increase in AP-1 activity, whereas expression of either small t or any of the kinases alone did not have any effect ... In contrast to REF52 cells, we observed that overexpression of either small or ERK1 alone in CV-1 cells was sufficient to stimulate AP-1 activity and that this stimulation was not enhanced by expression of small t and ERK1 together
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
Isono et al., Kidney Int 1998 : These results indicate that ANP is able to inhibit ET-1 induced activation of AP-1 by inhibiting both ERK and JNK, suggesting that ANP might be able to counteract the expression of AP-1 dependent genes induced by ET-1
Kim et al., Circulation 1998 : JNK and ERK activations were followed by a 3.9-fold increase in arterial AP-1 DNA binding activity, which contained c-Jun and c-Fos proteins
Leppä et al., EMBO J 1998 : Differential regulation of c-Jun by ERK and JNK during PC12 cell differentiation ... Consistently, MEK induced ERK activation in PC12 cells induces c-Jun expression, while JNK signalling does not
Yoshizumi et al., Br J Pharmacol 1998 : 4. Gel-mobility shift analysis revealed that the ERK1/2 activation was followed by an increase in transcription factor activator protein-1 DNA binding activity in HCASMCs
Shenoy et al., Endocrinology 1999 : Concurrent activation of c-Jun N-terminal kinase (JNK) and inhibition of Erk mitogen activated protein kinase activities is important for apoptosis in many cells, and we previously demonstrated that stimulation of AT2 receptors causes decreased mitogen activated protein kinase activity in neurons cultured from newborn rat hypothalamus and brain stem
Abe et al., Mol Cell Biol 1999 : Although it has the signature TEY activation motif of ERK1 and ERK2, ERK7 is not activated by extracellular stimuli that typically activate ERK1 and ERK2 or by common activators of c-Jun N-terminal kinase (JNK) and p38 kinase