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EPHB2 — FOS

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

Studies that report less than 10 interactions are marked with *

• IRef Hprd Interaction: FOS — EPHB2 (in vivo) Monje et al., Mol Cell Biol 2003*, Bannister et al., Nucleic Acids Res 1994*
• IRef Hprd Interaction: FOS — EPHB2 (in vitro) Monje et al., Mol Cell Biol 2003*, Bannister et al., Nucleic Acids Res 1994*

Text-mined interactions from Literome

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
Armelin et al., Braz J Med Biol Res 1999 (Adrenal Cortex Neoplasms...) : ACTH, itself a very weak mitogen, blocks the mitogenic response effect of FGF2 in the early and middle G1 phase, keeping both ERK-MAPK activation and c-Fos induction at maximal levels
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
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
Lotfi et al., Braz J Med Biol Res 2000 (Adrenal Cortex Neoplasms) : FGF2 elicits a strong mitogenic response in G0/G1 arrested Y1 adrenocortical cells, that includes a ) rapid and transient activation of extracellular signal regulated kinases-mitogen activated protein kinases ( ERK-MAPK) (2 to 10 min ), b ) transcription activation of c-fos, c-jun and c-myc genes ( 10 to 30 min ), c ) induction of c-Fos and c-Myc proteins by 1 h and cyclin D1 protein by 5 h, and d ) onset of DNA synthesis stimulation within 8 h. ACTH, itself a weak mitogen, interacts with FGF2 in a complex manner, blocking the FGF2 mitogenic response during the early and middle G1 phase, keeping ERK-MAPK activation and c-Fos and cyclin D1 induction at maximal levels, but post-transcriptionally inhibiting c-Myc expression
Lepique et al., Endocr Res 2000 : In G0/G1 cell cycle arrested mouse Y1 adrenocortical tumor cells ACTH39, a weak mitogen and strong anti-mitogenic agent, blocks FGF2 mitogenic activity at G1 phase, keeping untouched ERK-MAPK activation and c-Fos protein induction
Ciapponi et al., Genes Dev 2001 : Drosophila Fos mediates ERK and JNK signals via distinct phosphorylation sites
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
Liu et al., J Biol Chem 2002 : Signaling via the G ( i ) subfamily of G proteins was excluded, as neither ERK activation nor c-Fos and LH beta induction was impaired by treatment with pertussis toxin or a cell-permeable peptide that sequesters G beta gamma-subunits
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
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
Brummer et al., EMBO J 2002 : The Raf-1/B-Raf double deficient DT40 cells show an almost complete block both in ERK activation and in the induction of the immediate early gene products c-Fos and Egr-1
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
Terasawa et al., Genes Cells 2003 : Phosphorylation of c-Fos appears to be mediated by ERK5 and a kinase ( s ) lying downstream of ERK5, and the MEK5-ERK5 pathway dependent phosphorylation sites on c-Fos are different from the ERK1/2 pathway dependent ones
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
Monje et al., Mol Cell Biol 2003 (Cell Transformation, Neoplastic) : Furthermore, we provide evidence that the ERK dependent activation of c-Fos is an integral component of the mitogenic pathway by which PDGF regulates normal and aberrant cell growth
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
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 ... 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 : TPA stimulated ERK dependent increases in c-Fos protein and the c-Fos content of AP-1 complexes ... 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
Burch et al., Mol Cell Biol 2004 : After induction of the immediate-early gene response in the presence of oxidative stress, inhibition of ERK1,2 signaling promoted degradation of c-Fos , recruitment of Fra-1 to chromatin, and expression of cyclin D1
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
Hoffmann et al., J Biol Chem 2005 : Additional experiments reveal that, in conjunction with p65 NF-kappaB, the MEK1-ERK dependent synthesis of c-Fos and Fra-1 serves to adjust the overall expression level of IL-8 in response to two of its physiological inducers, IL-1 and epidermal growth factor
Elia et al., Cell Signal 2005 : Effects of extracellular nucleotides in the thyroid : P2Y2 receptor mediated ERK1/2 activation and c-Fos induction in PC Cl3 cells
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
Kim et al., J Lipid Res 2005 : Moreover, inhibition of ERK and JNK by EPA resulted in the decrease of c-Fos expression and c-Jun phosphorylation/expression induced by UV, respectively, which led to the inhibition of UV-induced activator protein-1 DNA binding activity
Iles et al., Free Radic Biol Med 2005 : Whereas inhibiting the ERK pathway with the MEK inhibitor PD98059 significantly decreased HNE mediated ERK phosphorylation, c-Fos protein induction , AP-1 binding, and HO-1 protein induction, inhibition of the ERK pathway had no effect on HNE induced HO-1 mRNA
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
Radwanska et al., Eur J Neurosci 2005 : Additionally, chronic blocking of ERK activation affected cocaine induced c-Fos and JunB but not Zif268 expression
Cao et al., Pain 2005 (MAP Kinase Signaling System...) : The spinal ERK inhibition or knockdown also reduced morphine withdrawal induced phosphorylation of cAMP response element binding protein ( CREB ), which is one of the important downstream substrates of ERK pathway, and Fos expression
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
Moon et al., FEBS Lett 2006 : Moreover, inhibitions of ERK and JNK by 2',4',7-THF resulted in the decrease of c-Fos expression and c-Jun phosphorylation/expression induced by UV, respectively, which led to the inhibition of UV-induced AP-1 DNA binding activity
Fanzo et al., J Clin Invest 2006 (Disease Models, Animal...) : In the absence of IBP, T cells respond suboptimally to TCR engagement, as demonstrated by diminished ERK1/2 activation, decreased c-Fos induction , impaired immunological synapse formation, and defective actin polymerization
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
Vlotides et al., Mol Endocrinol 2006 (Pituitary Neoplasms) : EGF induced EGFR and ERK1/2 phosphorylation was followed by rapid MAPK kinase/ERK kinase dependent activation of Elk-1 and c-Fos
Sasaki et al., Mol Cell 2006 : Spatiotemporal regulation of c-Fos by ERK5 and the E3 ubiquitin ligase UBR1, and its biological role ... We show that sustained ERK5 activity and the E3 ligase UBR1 regulate the stability and subcellular localization of c-Fos ... Thus, this spatiotemporal regulation of c-Fos by ERK5 and UBR1 is critical for the regulation of c-Fos/AP-1 ... 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
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 : Whereas initial induction of c-FOS protein required ERK1/2 dependent activation of c-fos transcription and de novo protein synthesis, persistent accumulation of c-FOS under sustained stimulation did not ... 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
Zhou et al., Cell Prolif 2007 (MAP Kinase Signaling System) : The suppression of MEK1/ERK1/2 activation inhibited UV-induced expression of c-Fos and JunD and increased caspase 3 activity and cell death
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
Sun et al., Brain Res 2007 : A single cocaine administration ( 30 mg/kg ) increased ERK mediated signaling proteins, phosphoryation of cAMP response element binding protein ( CREB ) kinase, pp90 ribosomal S6 kinase ( RSK ), and c-Fos protein levels in the caudate/putamen of Fischer rats
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
Gu et al., Invest Ophthalmol Vis Sci 2007 (Dog Diseases...) : The parallel phosphorylation of c-Fos and activation of ERK1/2 was detected only in exposed mutant retinas
Yin et al., J Biol Chem 2008 (MAP Kinase Signaling System) : BCR activation results in the induction of c-Fos , FosB, and JunB, and expression of these are suppressed by ERK and JNK inhibitors
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
Ailing et al., J Psychiatr Res 2008 (Disease Models, Animal) : Inhibition of ERK phosphorylation blocked the anxiety induced c-Fos expression
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
Park et al., Biochem Pharmacol 2008 (Bone Resorption) : In conclusion, bavachalcone inhibits osteoclastogenesis by interfering with the ERK and Akt signaling pathways and the induction of c-Fos and NFATc1 during differentiation
Guan et al., Neurosci Lett 2008 (Cocaine-Related Disorders...) : Furthermore, using an immunofluorescent staining approach, we found that inhibition of ERK activation completely abolished cocaine induced increase in number of c-Fos positive cells in the core region of NAc, whereas, in shell region of NAc, inhibition of ERK activation partially attenuated cocaine induced c-Fos expression
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
Vaysberg et al., J Biol Chem 2008 (Neoplasms) : Point mutation of either amino acids 212 ( glycine to serine ) or 366 ( serine to threonine ) from the B95.8 isoform to the tumor variant version of LMP1 was sufficient for gain of function characterized by sustained activation of Erk and subsequent c-Fos induction and binding to the AP1 site
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
Gu et al., Invest Ophthalmol Vis Sci 2009 (Disease Models, Animal...) : AP-1 DNA binding activity was determined by electrophoresis mobility shift assay ( EMSA ) and phosphorylation of c-Fos and activation of ERK1/2 were determined by immunoblot analyses
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
Jack et al., Blood 2009 (MAP Kinase Signaling System) : Inhibition of ERK prevented induction of c-Fos by M-CSF and reduced C/EBPalpha phosphorylation and formation of colony forming unit-monocytes ... In summary, M-CSF activates ERK more potently than G-CSF, and thereby induces higher levels of c-Fos and phospho-C/EBPalpha ( S21 ), which may directly interact to favor monopoiesis, whereas G-CSF activates signal transducer and activator of transcription 3 and SHP2, potentially shifting the balance to granulopoiesis via gene induction by C/EBPalpha homodimers and via effects of SHP2 on regulators besides 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
Liu et al., Toxicol Lett 2009 (Calcium Signaling) : AA treatment repressed ERK mediated c-Fos phosphorylation but evoked p38 MAPK mediated ATF-2 phosphorylation
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
He et al., Am J Physiol Heart Circ Physiol 2010 : PGE ( 2 ) stimulation of c-Fos was dependent on EP4, PKA, ERK1/2 , and p90RSK, whereas only the latter two kinases were involved in PGE ( 2 ) regulation of early growth response-1
Campillo et al., Mol Pharmacol 2010 (Pain, Postoperative) : These findings suggest that activated ERK1/2 could induce c-Fos expression and trigger the transcription of prodynorphin in the spinal cord
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
Moldrup et al., J Neurochem 2010 : Our data strongly indicate that Galpha ( q/11 ) -mediated ERK1/2 activation is essential for expression of Fos upon illumination of melanopsin expressing PC12 cells
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
Liu et al., J Cell Physiol 2010 : Caffeine treatment repressed ERK mediated c-Fos phosphorylation but evoked p38 MAPK mediated c-Jun phosphorylation
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
Liu et al., Int J Biochem Cell Biol 2010 : Piceatannol treatment repressed ERK mediated c-Fos phosphorylation but evoked p38alpha MAPK mediated c-Jun and ATF-2 phosphorylation
Annunziata et al., Blood 2011 (Multiple Myeloma) : ERK activates transcription of FOS , part of the AP-1 transcription factor
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
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
Yen et al., J Biol Chem 2011 (MAP Kinase Signaling System) : PKA, PI3K, and ERK inhibitors abolished PGE2- and cAMP induced c-Fos and MMP-9 up-regulation, and ERK activation was required for the binding of activator protein 1 (AP-1) transcription factor to the MMP-9 promoter
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
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
Hasegawa et al., J Dent Res 2012 (Disease Models, Animal...) : ERK is involved in tooth-pressure induced Fos expression in Vc neurons
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
Zhang et al., J Biol Chem 2013 (Breast Neoplasms) : Moreover, we revealed that the nuclear import of HBXIP was required for phosphorylation of c-Fos at Thr ( 232 ), Thr ( 325 ), Thr ( 331 ), and Ser ( 374 ) by ERK1/2
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
Ito et al., Hepatology 1998 (Carcinoma, Hepatocellular...) : Furthermore, in 25 of 26 cases of HCC which genomic DNA was available, 22 cases without genomic DNA amplification exhibited positive correlation, not only between protein expression of c-Fos and cyclin D1, but also between MAPK/ERK activation and cyclin D1 expression
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