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JUN — NOX1

Text-mined interactions from Literome

Chou et al., Toxicol Appl Pharmacol 2002 : Western data showed that NOx increased the expressions of c-Fos, c-Jun , and signaling kinases including MEKK1, JNK1, and p38 ( with induction fold of 3.3, 2.8, and 3.2, respectively ) in the cells 12 h after treatment
Yamagishi et al., J Cardiovasc Pharmacol 2004 : These results demonstrated that azelnidipine inhibited TNF-alpha induced IL-8 expression in HUVEC by blocking NADPH oxidase mediated ROS generation and subsequent AP-1 activation
Shiner et al., Free Radic Biol Med 2004 : The present study demonstrates, for the first time, that PON2 expression increases in monocytes during their maturation into macrophage as a result of NADPH-oxidase activation, and this process is partly regulated by the transcription factor AP-1
Nakamura et al., Med Hypotheses 2005 (Arteriosclerosis...) : In the process of the search for such a unique anti-hypertensive drug, we have recently found that azelnidipine, a newly developed and commercially used long acting dihydropyridine based calcium antagonist ( DHP ), inhibited TNF-alpha induced activator protein-1 activation and interleukin-8 expression in human umbilical vein endothelial cells by suppressing NADPH oxidase mediated reactive oxygen species generation
Liu et al., Free radical research 2006 (Inflammation) : We show here that the NADPH oxidase dependent production of O2* ( - ) and H2O2 or respiratory burst in alveolar macrophages ( AM ) ( NR8383 cells ) is required for ADP stimulated c-Jun phosphorylation and the activation of JNK1/2, MKK4 ( but not MKK7 ) and apoptosis signal regulating kinase-1 ( ASK1 )
Wu et al., Br J Pharmacol 2009 : Effects of tripterine were investigated on endothelial barrier function, inducible nitric oxide synthase (iNOS) expression, nicotinamide adenine dinucleotide phasphate ( NADPH ) oxidase activity, 3-nitrotyrosine formation, protein phosphatase type 2A (PP2A) activity, activation of extracellular regulated kinase (ERK), c-Jun terminal kinase (JNK) and Janus kinase ( Jak2 ), and degradation of IkappaB in microvascular endothelial cells exposed to pro-inflammatory stimulus [ lipopolysaccharide (LPS) + interferon gamma (IFNgamma) ] and on vascular permeability in air pouches of mice injected with LPS + IFNgamma
Vendrov et al., J Biol Chem 2010 (Atherosclerosis) : Thrombin induced CD44 expression is mediated by transcription factor AP-1 in a NADPH oxidase dependent manner
Valente et al., Am J Physiol Heart Circ Physiol 2012 (Hyperplasia) : Similar to ANG II, addition of IL-18 also induced superoxide generation, activated NF-?B and AP-1, and stimulated SMC migration and proliferation, in part via Nox1, and both ANG II and IL-18 induced NOX1 transcription in an AP-1 dependent manner
Hsieh et al., Journal of neuroinflammation 2012 : These results demonstrated that in RBA-1 cells, activation of ATF2/AP-1 by the PKC ( a ) -mediated Nox ( 2 ) /ROS signals is essential for upregulation of MMP-9 and cell migration enhanced by LTA
Lin et al., Cell communication and signaling : CCS 2012 : These results demonstrated that in RBA-1 cells, activation of AP-1 ( c-Fos/c-Jun ) by the PKC-a mediated Nox2/ROS signals is essential for up-regulation of MMP-9 and cell migration enhanced by BK
Valente et al., Cell Signal 2013 : IL-18 induced Nox1 dependent ROS generation, TRAF3IP2 expression, and IKK/NF-?B and JNK/AP-1 activation