Gene interactions and pathways from curated databases and text-mining

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JUN — JUN

Pathways - manually collected, often from reviews:

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

Studies that report less than 10 interactions are marked with *

Text-mined interactions from Literome

Adunyah et al., J Cell Physiol 1992 (Leukemia) : Like phorbol esters, okadaic acid treatment also activates AP-1 enhancer activity and induces the phosphorylation of c-Jun protein
Ikeo et al., Endocr J 2004 (Multiple Endocrine Neoplasia Type 1) : JunD-menin interaction regulates c-Jun mediated AP-1 transactivation
Haase et al., Radiat Res 2008 (Pulmonary Fibrosis) : Instead, a selective nuclear cleavage of c-Jun by a serine protease caused the loss of AP1 activity
Müller et al., J Cell Biochem 2010 (Insulinoma) : Expression of dominant negative mutants of c-Jun and Elk-1 reduced AP-1 transcriptional activity in INS-1 cells indicating that c-Jun and ternary complex factors are involved in the regulation of AP-1 activity in glucose stimulated insulinoma cells
Chen et al., Mol Carcinog 1999 : Our previous studies have indicated that UVB induced c-fos expression may play a key role in UVB induced activation of the activator protein-1 transcription factor and EGCG inhibited, UVB induced activation of AP-1 in HaCaT cells
Lin et al., Inflamm Bowel Dis 2008 (Crohn Disease) : Probiotic L. reuteri suppressed TNF transcription by inhibiting activation of MAP kinase regulated c-Jun and the transcription factor, AP-1
Dhar et al., Oncogene 2004 (Cell Transformation, Neoplastic...) : Previous studies have established that expression of a dominant negative c-Jun ( TAM67 ) inhibits phorbol 12-tetradecanoyl-13-acetate ( TPA ) -induced AP-1 transactivation as well as transformation in mouse epidermal JB6/P+ cells and tumor promotion in mouse skin carcinogenesis
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
Wu et al., Cell Biochem Funct 2003 : The results from mobility shift assays and Western blotting analysis revealed that this AP-1 binding increase involved c-Jun , but not c-Fos
Yoshioka et al., Proc Natl Acad Sci U S A 1995 : Furthermore, Fra-1 repressed AP-1 activity induced by either TPA or expression of c-Jun and c-Fos
Manna et al., J Immunol 2000 : Leflunomide also inhibited TNF induced activation of AP-1 and the c-Jun N-terminal protein kinase activation
Yi et al., J Immunol 1998 (Lymphoma, B-Cell) : CpG DNA also induces the phosphorylation of activating transcription factor-2, c-Jun , and mitogen activated protein kinase ( MAPK) activated protein kinase 2 as well as the activation of activator protein-1 (AP-1) DNA binding
Andreone et al., J Immunol 2003 : In murine wild-type fibroblasts, oxidative challenge by peroxynitrite and hydrogen peroxide or immunological challenge by IL-1 and 20 % FCS induced phosphorylation of the mitogen activated protein kinase kinase-4, activation of c-Jun N-terminal kinase (JNK) , and DNA binding of AP-1
Hambleton et al., Proc Natl Acad Sci U S A 1996 : As AP-1 activity is regulated in part by activation of the c-Jun N-terminal kinase (JNK) , which phosphorylates and subsequently increases the transcriptional activity of c-Jun, we examined whether LPS treatment of macrophages resulted in activation of this kinase
Kim et al., Circulation 1998 : In vitro studies show that extracellular signal regulated kinases ( ERKs ) and c-Jun NH2-terminal kinases (JNKs) , belonging to the mitogen activated protein kinase ( MAPK ) family, play a critical role in the activation of transcription factor activator protein-1 (AP-1) and cell proliferation or apoptosis
Oguro et al., J Pharmacol Exp Ther 1998 : However, GSH isopropyl ester prevented GSH depletion and abolished both c-Jun phosphorylation and the activation of AP-1 binding evoked by phorone
Hsu et al., Cancer Res 2001 (Cell Transformation, Neoplastic) : Expression of a transactivation-deficient mutant of Jun or dominant negative extracellular signal regulated kinase suppressed both AP-1 activation and p65-specific transactivation in JB6 cells, suggesting that AP-1 activity is needed for p65 transactivation and consequently for NF-kappaB activation
Srivastava et al., J Clin Invest 1999 : The consequent decrease in the nuclear levels of c-Jun and JunD leads to diminished binding of c-Jun/c-Fos and JunD/c-Fos heterodimers to the AP-1 consensus sequence in the TNF promoter and, thus, to decreased transactivation of the TNF gene
Imafuku et al., J Cell Biol 1999 (Alzheimer Disease) : Here we show that QM/Jun interacting factor (Jif)-1 , a negative regulator of c-Jun , is a candidate to mediate the function of PS1 in the cell
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 )
Gao et al., Biochem Biophys Res Commun 2008 : These data consistently suggest that SIRT1 directly inhibits the transcriptional activity of AP-1 by targeting c-JUN
Suzuki et al., J Virol 1994 (Cell Transformation, Neoplastic) : We further showed that Fra-2-c-Jun heterodimer is mainly responsible for the elevated AP-1 DNA binding activity in these transformed cells, and we propose that this heterodimer play a crucial role in the transformation induced by these oncogenes
Pérez-Sala et al., J Biol Chem 2003 : Here we show that 15d-PGJ2 covalently modifies c-Jun and directly inhibits the DNA binding activity of AP-1
Zhou et al., Mol Endocrinol 1999 : Ligand activated retinoic acid receptor inhibits AP-1 transactivation by disrupting c-Jun/c-Fos dimerization
Behrens et al., Nat Genet 1999 (Seizures) : c-Jun and AP-1 activities are regulated by c-Jun N-terminal phosphorylation (JNP) at serines 63 and 73 through Jun N-terminal kinases(JNKs)
Qi et al., J Biol Chem 2004 (Breast Neoplasms) : Furthermore, inhibition of c-Jun activation by a dominant negative c-Jun blocks AP-1 activity in ER+ cells and attenuates stress induced cell death but not AP-1 activity in ER- cells, suggesting that the c-Jun/AP-1 activity has distinct properties depending on ER status
Xu et al., Carcinogenesis 2006 (Prostatic Neoplasms) : In the present study, we determined the effects of SFN, PEITC and AITC on AP-1 activation, and investigated the roles of extracellular signal regulated protein kinase ( ERK ) and c-Jun N-terminal kinase (JNK) signaling pathways in the regulation of AP-1 activation and cell death elicited by these ITCs in human prostate cancer PC-3 cells
Pober , Pathol Biol (Paris) 1998 : Activation of c-Jun/ATF-2 involves new c-Jun synthesis, and more importantly, phosphorylation of the amino terminus of c-Jun by Jun N-terminal kinase (JNK)
Peng et al., Cell Mol Biol Res 1995 (Myocardial Reperfusion Injury) : The levels of c-Fos and c-Jun proteins increased in nuclei as revealed by immunostaining, and DNA binding activity of nuclear AP-1 increased
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
Abreu-Martin et al., Am J Physiol 1999 : Signaling via Fas receptor, as determined by induction of c-Jun NH2-terminal kinase (JNK) activity and transcriptional activation of AP-1 , is enhanced in IFN-gamma primed cells
De Sarro et al., Neuropharmacology 2000 (Disease Models, Animal...) : In addition, all GABA(B) receptor antagonists were able to induce an increase in Fos and Jun protein expression in pentylenetetrazole ( 25 mg/kg i.p. ) treated mice whilst the GABA(B) receptor agonist R-baclofen ( 2 or 6 mg/kg ) attenuated the expression of Fos and Jun protein, at cortical and limbic structures
Vukic et al., Neurobiol Dis 2009 (Alzheimer Disease) : Western blot analyses showed that c-Jun was activated via JNK mediated phosphorylation, suggesting that as a result of c-Jun phosphorylation, AP-1 was activated and thus up-regulated MCP-1 expression
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
Naumann et al., J Exp Med 1998 : Since it is established that phosphorylation of c-Jun , the central component of AP-1, by the stress activated c-Jun NH2-terminal kinase (JNK) increases the transcriptional activity of AP-1 , we studied whether Ngo could induce stress response pathways involving JNK
Kang et al., Free radical research 2007 : Glycitein abrogated the activation of c-Jun N-terminal kinase (JNK) induced by H ( 2 ) O ( 2 ) treatment and inhibited DNA binding activity of activator protein-1 (AP-1) , a downstream transcription factor of JNK
Trejo et al., Mol Cell Biol 1992 : The late induction of c-jun and fra-1 mRNA can be prevented by adding the antagonist hirudin 30 min after thrombin, which results in loss of thrombin stimulated increases in c-Jun protein, AP-1 DNA binding activity, and AP-1 mediated transactivation
Baker et al., Mol Cell Biol 1992 : Phosphorylation of full-length Jun with several kinases did not affect the DNA binding activity of Jun homodimers or Fos-Jun heterodimers
Gupta et al., J Biol Chem 1999 : Our results demonstrated that : ( i ) PGN induced phosphorylation of the transcription factors ATF-1 and CREB; (ii) ATF-1 and CREB bound DNA as a dimer and induced transcriptional activation of a CRE reporter plasmid, which was inhibited by dominant negative CREB and ATF-1 ; ( iii ) PGN induced phosphorylation of c-Jun , protein synthesis of JunB and c-Fos, and transcriptional activation of the AP-1 reporter plasmid, which was inhibited by dominant negative c-Fos ; and ( iv ) PGN induced activation of CREB/ATF and AP-1 was mediated through CD14
Rincón et al., Genes Funct 1997 : Unlike precursor cells, the activation of AP-1 does not appear to be mediated by c-Jun N-terminal kinase (JNK) in effector Th2 cells
Chiu et al., Cell 1988 : The c-Fos protein interacts with c-Jun/AP-1 to stimulate transcription of AP-1 responsive genes
Ding et al., FEMS Immunol Med Microbiol 2008 : extracellular signal related kinase ( ERK ), p38, and c-Jun N-terminal kinase (JNK) each selectively regulated AP-1 subcomponent expression and DNA binding activity
Bennett et al., Curr Opin Pharmacol 2003 (Diabetes Mellitus, Type 2...) : Jun N-terminal kinase (JNK) regulates the transcription factor AP-1 , which is implicated in the controlled expression of many genes involved in the immune response
Ming et al., Cancer Immunol Immunother 2012 (Carcinoma, Non-Small-Cell Lung...) : We found that, in lung cancer cell lines and in nude mice, Interleukin-7/Interleukin-7 receptor increased the expression of cyclin D1 and phosphorylation of c-Fos/c-Jun, induce c-Fos and c-Jun heterodimer formation, and enhanced c-Fos/c-Jun DNA binding activity to regulate cyclin D1
Won et al., Mol Pharmacol 2000 : In AP-1, the basal expression of Fra-2 and c-Jun proteins and AP-1 DNA binding activity in the adrenal medulla was higher than other tissues tested, but CHX reduced these protein levels and AP-1 DNA binding activity
Wang et al., J Virol 2005 : IE1 induced c-Jun phosphorylation, and treatment with SP600125, a selective JNK inhibitor, as well as overexpression of JNK binding domain of JIP1, blocked IE1 mediated induction of AP-1 and relB promoter activity in NIH 3T3 cells and SMCs. Ectopic expression of c-Jun plus Fra-2, but not c-Fos, induced relB promoter activity
Cerezo-Guisado et al., Biochim Biophys Acta 2007 : It also induced c-Jun phosphorylation with a subsequent increase in activator protein-1 (AP-1) binding, AP-1 mediated gene expression and BimEL protein levels
Seong et al., Arch Pharm Res 2006 : The restoring effect of EPO in the RAW264.7 cells was associated with the increased of c-Fos and c-Jun expression as well as AP-1 activation
Li et al., Toxicol Mech Methods 2009 (Silicosis) : Dominant negative mutant c-Jun ( TAM67 ) inhibited silica induced AP-1 DNA binding activity and downregulated the TNF-alpha and TGF-beta1 expression
Peakman et al., Brain Res 2003 : However, expression of Deltac-Jun in adult mice blocked the ability of chronic cocaine administration to induce three known targets for AP-1 in the NAc : the AMPA glutamate receptor subunit GluR2, the cyclin dependent protein kinase Cdk5, and the transcription factor nuclear factor-kappaB (NFkappaB), without affecting several other proteins examined for comparison
William et al., J Biol Chem 1990 : We find that, although a single dose of diacylglycerol, like phorbol esters, is sufficient to elevate mRNA levels of both the c-jun and c-fos protooncogenes, in contrast to phorbol esters there is no increase in either Jun protein or activation of AP-1 enhancer activity
Naderi et al., Int J Cancer 2012 (Breast Neoplasms) : In turn, the overexpression of BEX2 led to an increase in both c-Jun mediated induction of ErbB2 and c-Jun binding to the ErbB2 promoter in MCF-7 cells
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
Omori et al., J Biol Chem 2008 (Inflammation) : We found that c-Jun was decreased in TAK1-deficient keratinocytes and that ectopic expression of c-Jun could partially inhibit TNF induced increase of ROS and cell death
Arnould et al., J Biol Chem 1998 (Polycystic Kidney, Autosomal Dominant) : The polycystic kidney disease 1 gene product mediates protein kinase C alpha dependent and c-Jun N-terminal kinase dependent activation of the transcription factor AP-1
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
Harrison et al., Mol Endocrinol 1995 : AP-1 , cAMP response element, and glucocorticoid response element motifs are required for full cooperative activation by either c-Jun or c-Jun/c-Fos and glucocorticoids
Chen et al., Biochem Biophys Res Commun 2001 : In contrast, both troglitazone ( at 10 microM ) and 15-deoxy-Delta ( 12,14 ) -prostaglandin J ( 2 ) ( 15d-PGJ ( 2 ), at 15 microM ), a natural ligand for PPARgamma, induce c-Jun phosphorylation by activation of c-Jun N-terminal kinase (JNK) through a posttranslational regulation of c-Jun activity, therefore increasing AP-1/DNA binding activity and transcriptional responses as results of increasing basal ICAM-1 gene expression
Grimm et al., Cell Death Differ 2001 (Vision, Ocular) : AP-1 mediated retinal photoreceptor apoptosis is independent of N-terminal phosphorylation of c-Jun
Gober et al., J Neurovirol 2005 (Herpes Genitalis) : Up-regulation correlated with activator protein (AP)-1 activation , notably c-Jun and c-Fos that bind cognate elements in the ICP10 promoter
Gao et al., Hepatology 1999 : HGF alone induced moderate levels of c-Jun-N-terminal kinase (JNK) and p44/p42 mitogen activated protein kinase ( MAPK ), resulting in moderate levels of AP-1-DNA binding activity
Collins-Hicok et al., Mol Cell Biol 1994 : Both CRE binding protein ( CREB ) and activator protein 1 (AP-1) can regulate RD, but their effects are in opposite directions ; CREB represses and AP-1 activates RD. CREB induced repression and AP-1 activation require distinct elements within the control region, but their binding and functions overlap at CRE-3
Chae et al., Int Immunopharmacol 2001 : PDTC transiently increased the phosphotransferase activity of c-Jun N-terminal Kinase1 ( JNK1 ) , which might in turn activates transcriptional activity of activating protein-1 (AP-1)
Gough et al., J Biol Chem 2007 (MAP Kinase Signaling System) : Herein we have shown that IFNgamma rapidly activated AP-1 DNA binding that required c-Jun but was independent of JAK1 and STAT1 ... 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
Yi et al., Cancer Res 2005 : Major vault protein, in concert with constitutively photomorphogenic 1, negatively regulates c-Jun mediated activator protein 1 transcription in mammalian cells ... Taken together, we propose that MVP, most likely through its interaction with COP1, suppresses c-Jun mediated AP-1 transcription under unstressed conditions, thereby preventing cells from undergoing stress response
Qian et al., Mol Cell Endocrinol 2007 : Lastly, the pharmacological AP-1 activator phorbol myristate acetate increased AP-1 binding, trans activated the wild-type but not the AP-1 mutant NOS3 promoter and dose-dependently stimulated UAEC NOS3 and c-Jun protein expression
Eilers et al., J Neurosci 1998 : Thus, activation of Jun kinase and increases in c-Jun phosphorylation and c-Jun protein levels occur at the same time after NGF withdrawal, but c-Jun levels and phosphorylation are regulated by an SEK1 independent pathway
Billiet et al., J Mol Biol 2008 : The interference of PPARalpha/retinoid X receptor alpha with the AP-1 transcription factor elements c-Jun/c-Fos resulted in the inhibition of AP-1 binding and down-regulation of the VDUP-1 gene expression
Son et al., Mol Cells 2009 (Lymphoma...) : The c-Jun-NH ( 2 ) -terminal kinase ( JNK ) -mediated activation of c-Jun was shown to be related to the H ( 2 ) O ( 2 ) -induced cell death
Boyd et al., Brain Res 2007 (Disease Models, Animal...) : Recent studies have described the activation of a stress induced signal cascade, c-Jun N-terminal kinase (JNK) mediated activation of c-Jun , and an increase in the expression of a downstream effector, cyclooxygenase 2 (COX-2), in postmortem PD brains
Ellsworth et al., Endocrinology 2003 : c-Jun N-terminal kinase activation of activator protein-1 underlies homologous regulation of the gonadotropin releasing hormone receptor gene in alpha T3-1 cells
Kim et al., Carcinogenesis 2005 (Colorectal Neoplasms...) : In addition, the polyphenol triggered the phosphorylation of c-JUN ( Ser63 and Ser73 ) and induced c-JUN/c-FOS , thereby increasing the DNA binding activity of activator protein-1 (AP-1), as shown by an AP-1 luciferase reporter assay
Gallo et al., Oncogene 2002 : Furthermore, Menin expression inhibits Jun N-terminal kinase (JNK) mediated phosphorylation of both JunD and c-Jun
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
Zhu et al., Arterioscler Thromb Vasc Biol 1998 : This AP-1 binding increase involves c-Jun , but not c-Fos, as shown by gel supershift, Northern hybridization, and Western blotting analyses
Song et al., Toxicology 2012 : Phosphorylated c-Jun , in turn, increases AP-1 activity, which results in activation of ARE mediated transcription
Brach et al., Blood 1992 (Leukemia, Myeloid) : Taken together, these findings indicate that : ( 1 ) enhancement of JUN/AP-1 activity in ara-C treated cells involves a posttranslational modification of JUN/AP-1 ; and ( 2 ) binding of activated JUN/AP-1 to the AP-1 site in the c-jun promoter confers ara-C inducibility of this gene
Santibañez , FEBS Lett 2006 (Cell Transformation, Neoplastic) : TGF-beta1 induces JNK phosphorylation, c-Jun transactivation and AP1 activation
Erdös et al., J Cell Physiol 1995 : Furthermore, the increased AP-1 binding activity does not require new protein synthesis but activation of the preexisting c-Jun proteins
Yang et al., Pigment Cell Res 2004 (Melanoma) : There are progressive variations in AP-1 composition in different melanoma cell lines compared with normal melanocytes, in which c-Jun , JunD and FosB were involved in AP-1 complexes ... In w3211, c-Jun , JunD and Fra-1 were involved in AP-1 binding, while in w1205, overall AP-1 binding activity was decreased significantly and supershift binding was detected only with JunD antibodies
Andrew et al., Am J Physiol Lung Cell Mol Physiol 2001 : Addition of nickel to BEAS-2B human airway epithelial cells stimulated intracellular oxidation, induced c-Jun and c-Fos mRNA levels, increased phospho- and total c-Jun protein levels, and elevated PAI-1 mRNA levels over a 24-h time course
Chiu et al., J Immunol 2009 (Arthritis, Rheumatoid) : PGN mediated an increase in the accumulation of phosphorylated c-Jun in the nucleus, AP-1-luciferase activity, and c-Jun binding to AP-1 element was inhibited by Ly294002, Akt inhibitor, and FAK mutant
Cripe et al., New Biol 1990 : Each AP-1 site as well as a third AP-1 site near the promoter bound c-Jun and Jun/Fos in vitro, and was activated by c-Jun and c-Fos in transfections
Da Costa et al., Mol Cell Biol 2010 (MAP Kinase Signaling System...) : The AP-1 transcription factor c-Jun is phosphorylated at multiple sites within its transactivation domain by the JNKs, and c-Jun phosphorylation is required for JNK induced neurotoxicity
Lauricella et al., Apoptosis 2006 (Liver Neoplasms) : Interestingly, siRNA silencing of c-Jun or JNK1 reduced HepG2 cell susceptibility to apoptosis and prevented the increase in AP-1 activity
Hipp et al., Eur J Immunol 2002 : These results show that proteasome inhibitors can not only lead to functional AP-1 induction by enhanced c-Jun phosphorylation, but also transactivate the IL-8 gene in human endothelial cells despite complete suppression of NF-kappaB activity
Fan et al., Cancer Res 2001 : KB3-TAM67 cell lines displayed normal growth kinetics and essentially unaltered basal AP-1 activity, but vinblastine induced phosphorylation of c-Jun and activating transcription factor-2, and AP-1 activation, were strongly inhibited
Grabiec et al., Ann Rheum Dis 2012 (Arthritis, Rheumatoid...) : Phosphorylation of mitogen activated protein kinases and inhibitor of ?Ba ( I?Ba ) following IL-1ß stimulation were unaffected by HDACi, as were AP-1 composition and binding activity, and c-Jun induction
Kesavan et al., J Cell Physiol 2004 : Thus, MEKK2 regulates AP-1 activity at two levels, by regulating both expression of AP-1 components and c-Jun N-terminal phosphorylation
Zingarelli et al., Immunology 2004 (Colitis) : These inflammatory events were associated with activation of c-Jun-NH ( 2 ) terminal kinase ( JNK ), phosphorylation of c-Jun and activation of the nuclear transcription factor activator protein-1 (AP-1) in the colon
Conrad et al., Mol Cell Biol 1994 : In contrast, we show that intact c-Jun expression inhibited the Ras induced activation of the prolactin promoter, defining it as a negative regulator of this pathway, whereas c-Jun was able to enhance the Ras activation of an AP-1-driven promoter in GH4 cells
Zhang et al., BMC cancer 2007 (Breast Neoplasms...) : Recently, it has been reported that overexpression of c-Jun in breast cancer cell line MCF-7 resulted in increased AP-1 activity, motility and invasiveness of the cells in vitro and tumor formation in nude mice
Francastel et al., Oncogene 1997 (Leukemia, Erythroblastic, Acute) : In non-erythroid cells, c-Jun activates and NF-E2p18 inhibits both AP-1 and NF-E2 activities, suggesting that NF-E2/AP-1 sites function as AP-1 binding sites in these cells
Li et al., Food Chem Toxicol 2005 (Urinary Bladder Neoplasms) : The role of c-Jun in the AP-1 activation induced by naturally occurring isothiocyanates ... However, whereas c-Jun was identified as the predominant component in the AP-1 DNA binding complex, Fra-2 was not detected, suggesting that c-Jun may be mainly responsible for ITC induced AP-1 activation
Hsu et al., Mol Cell Biol 1992 : LRF-1/c-Jun , c-Fos/c-Jun, and c-Fos/JunB activate specific AP-1 and ATF site containing promoters, and in contrast, LRF-1/JunB potently represses c-Fos- and c-Jun mediated activation of these promoters
Watabe et al., Oncogene 1998 (Leukemia) : Both curcumin ( 1,7-bis [ 4-hydroxy-3-methoxy-phenyl ] -1,6-heptadiene-3,5-dione ), an inhibitor of the biosynthesis of AP-1, and the expression of dominant negative c-Jun inhibited the activation of AP-1 and the induction of apoptosis by bufalin
Deng et al., Proc Natl Acad Sci U S A 1992 : Construction and expression of a monomeric c-Jun protein that binds and activates transcription of AP-1-responsive genes
Kaufmann et al., J Cell Biochem 2013 (MAP Kinase Signaling System...) : AP-1 activity was controlled by TCFs and c-Jun in cells expressing an activated Ga ( q ) -coupled designer receptor
Cho et al., Dig Dis Sci 2010 (Adenocarcinoma...) : We investigated whether H. pylori in a Korean isolate ( HP99 ), a cagA ( + ), vacA ( + ) strain, induces the expression of c-Fos and c-Jun for AP-1 activation to induce COX-2 and iNOS and whether HP99 induced expressions of COX-2 and iNOS are mediated by Ras and AP-1 , determined by the expressions of c-Fos and c-Jun, in gastric epithelial AGS cells, using transfection with mutant genes for Ras ( ras N-17 ) and c-Jun ( TAM-67 )
Faour et al., J Biol Chem 2005 (Arthritis, Rheumatoid) : PGE2 suppression of IL-17 induced ATF-2/c-Jun transactivation and DNA binding was dependent on Egr-1 mediated inhibition of induced c-Jun expression
Chambers et al., Exp Cell Res 2013 (Periodontitis) : Here we show that IL-1 induced binding of transcription factor AP-1 to the MMP-3 promoter consists primarily of c-Jun, JunB, and c-Fos and that binding of c-Jun and c-Fos is inhibited by the combination of cytokines while binding of Jun B is not
Tong et al., Neurochem Res 2003 (Hyperoxia) : These results suggest that AP-1 activation via c-Jun binding to DNA is an important component of brain responses to oxidative stress
Hahm et al., Biochem Biophys Res Commun 2004 (Neoplasm Invasiveness...) : These curcumin analogs have been observed to repress the AP-1 transcription in AP-1 transfected cells and they also inhibited the increased expression of Jun/AP-1 protein by 12-O-tetradecanoylphorbol-13-acetate ( TPA ) in the same cells
Young et al., J Biol Chem 2004 : We show that this Raf dependent protection occurred through activation of c-Jun and thus AP-1 activation
Frank et al., Oncogene 1999 (Cell Transformation, Neoplastic...) : Mutational analysis revealed that the runt homology domain (RHD) and a C-terminal transcriptional repression domain in AML1/ETO are required for transformation, activation of c-Jun and increased AP-1 activity
Valesio et al., J Appl Toxicol 2013 (Abnormalities, Drug-Induced...) : SP600125 ( anthrapyrazolone ) is a synthetic polyaromatic chemical that inhibits c-Jun N-terminal kinase (JNK) signaling by interfering with phosphorylation of c-Jun
Lindwall et al., Mol Cell Neurosci 2004 : Here we report that c-Jun N-terminal kinase (JNK) mediated c-Jun activation is important for axonal outgrowth of sensory neurons in rat nodose and dorsal root ganglia ( DRG )
Clerc et al., Virology 2009 : In conclusion, we demonstrate that the repression of c-Jun activity in vivo is mainly due to the HBZ-SP1 mediated sequestration of c-Jun to the HBZ-NBs
Nakahira et al., J Immunol 2002 : An increase in c-Jun , a component of AP-1, in the nuclear compartment was elicited by stimulation with either IL-12 or IL-18, but accumulation of serine phosphorylated c-Jun was induced only by IL-18 capable of activating c-Jun N-terminal kinase
Bianchi et al., J Biol Chem 2003 : As a functional consequence of this interaction, expression of huCOP1 in mammalian cells down-regulates c-Jun dependent transcription and the expression of the AP-1 target genes, urokinase and matrix metalloproteinase 1
Chen et al., Kidney Int 2003 : In contrast, curcumin, an activating protein (AP)-1 inhibitor, attenuated TNF-alpha stimulated phospho-c-Jun levels and fractalkine expression without discernible effects on TNF-alpha induced degradation of I-kappaBalpha or NF-kappaB nuclear translocation
Kim et al., Oncogene 1996 : In the absence of hormone, TAM-67ER produced complete inhibition of c-Jun induced AP-I transactivation
Guo et al., Am J Physiol Gastrointest Liver Physiol 2012 : Chemical inhibitors of JNK and ERK pathways, dominant negative JNK and c-Jun , and c-Jun shRNA significantly inhibited CCK induced DNA synthesis, CCK induced AP-1 activation, and cyclin D1 expression
Kaminuma et al., Mol Cell Biol 2001 : On the other hand, Vav induced the activation of Rac1 or Cdc42 and c-Jun N-terminal kinase (JNK), enhanced the transcriptional and DNA binding activities of AP-1 , and induced increased phosphorylation of c-Jun
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