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JUN — TCF3

Text-mined interactions from Literome

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
Famulski et al., Cell Death Differ 1999 : We propose that ( i ) the up-regulation of an acidic nuclease activity is governed by a regulatory pathway different from that responsible for AP-1 factor induction, caspases activation and intracellular acidification, and ( ii ) activation of an acidic nuclease does not cause any deleterious effects when AP-1 transcription factor induction , caspases activation and intracellular acidification are down-regulated
Troussard et al., Oncogene 2000 (Glioblastoma) : The integrin linked kinase (ILK) induces an invasive phenotype via AP-1 transcription factor dependent upregulation of matrix metalloproteinase 9 (MMP-9)
Sodhi et al., J Interferon Cytokine Res 2002 : Additionally, phosphorylation of JNK and activation of the transcription factor , c-Jun , were also noted in response to MCP-1 treatment
Ventura et al., Mol Cell Biol 2003 (MAP Kinase Signaling System) : The JNK signal transduction pathway is therefore essential for AP-1 transcription factor regulation in cells exposed to TNF
Chen et al., Arterioscler Thromb Vasc Biol 2003 (Arteriosclerosis) : Electrophoretic mobility shift assay demonstrated that both GBE and probucol inhibited transcription factor nuclear factor-kappaB activation in TNF-alpha stimulated HAECs ( 55.2 % and 65.6 % inhibitions, respectively ) but only GBE could inhibit the TNF-alpha stimulated activator protein 1 activation ( 45.1 % inhibition, P < 0.05 )
Kinser et al., J Toxicol Environ Health 2004 (Inflammation) : c-Fos, Fra-, c-Jun , and JunB, components of the activator protein-1 (AP-1) transcription factor complex, were induced by DON as well as another transcription factor , NR4A1
Hwang et al., FEBS Lett 2005 : AP-1 activation suppressed the expression of Sox-9, a major transcription factor regulating type II collagen expression
Sahambi et al., Birth Defects Res A Clin Mol Teratol 2006 (Abnormalities, Drug-Induced) : We hypothesize that oxidative stress and activation of a redox-sensitive transcription factor , activator protein-1 (AP-1) , are early indicators of embryonic stress in response to a teratogenic insult ... We hypothesize that oxidative stress and activation of a redox-sensitive transcription factor , activator protein-1 (AP-1), are early indicators of embryonic stress in response to a teratogenic insult
Tu et al., Am J Physiol Cell Physiol 2007 : Involvement of oxidants and AP-1 in angiotensin II-activated NFAT3 transcription factor
Smart et al., Hepatology 2006 (Carbon Tetrachloride Poisoning...) : JunD is a profibrogenic transcription factor regulated by Jun N-terminal kinase independent phosphorylation
Weinberg et al., Neuroscience 2007 : Differential basal and stress induced expression patterns of the fra-2 and c-fos genes are likely to have important functional consequences for AP-1 transcription factor dependent regulation of neural plasticity
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
Salisbury et al., Mol Endocrinol 2009 : Together, these results indicate that GnRH regulation of Jun transcription requires a functional interaction between TCF/LEF and beta-catenin and that alteration of either impacts expression of JUN downstream targets such as Cga
Jung et al., Biofactors 2008 : Matrine inhibited PMA induced activation of the AP-1 promoter, an important nuclear transcription factor in MMP-1 expression
Hsieh et al., Journal of neuroinflammation 2010 (MAP Kinase Signaling System) : ROS production leads to activation of extracellular signal regulated kinase 1/2 ( ERK1/2 ) and c-Jun-N-terminal kinase (JNK) and then activation of the NF-?B transcription factor
Chae et al., Biosci Biotechnol Biochem 2011 : And, it inhibited DNA binding activity of activator protein-1 (AP-1) , a transcription factor of MMP-1 and downstream of ERK and JNK
Hwang et al., Arthritis Res Ther 2012 (Arthritis, Rheumatoid) : Importantly, the preferential induction of IL-34 rather than M-CSF by TNFa in RAFLS was mediated by the transcription factor nuclear factor kappa B ( NF-?B ) and activation of c-Jun N-terminal kinase (JNK)
Lu et al., J Dermatol 2013 : Importantly, JUN may regulate activating transcription factor 3 expression to involve cell proliferation process ; STAT1 and STAT3 can inhibit tissue inhibitor of metalloproteinases-3 expression to modulate the cell adhesion molecule pathway ; NF-?B and E2F1 can downregulate cyclin D1, but upregulate proliferating cell nuclear antigen expression to promote the cell cycle pathway
Hattori et al., Am J Physiol 1993 (Acute-Phase Reaction...) : These findings demonstrate the complexity of AP-1 hepatic transcription factor responses to humoral regulators with direct hepatocellular effects
Erkel et al., J Antibiot (Tokyo) 1996 : In reporter gene assays nidulal ( 1 ) preferentially activated the transcription factor complex AP-1 mediated expression of secreted alkaline phosphatase in COS-7 cells
Manna et al., J Immunol 1998 : TNF induced activation of another nuclear transcription factor , AP-1 , was suppressed by IL-13
Chen et al., J Biol Chem 1998 : The effects of UVB irradiation on transcription factor activator protein-1 (AP-1) DNA binding and AP-1 transactivation were studied in a human keratinocyte cell line, HaCaT