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ANGPT2 — JUN

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Deguchi et al., Circ Res 1999 : In newborn rat VSMCs, Ang II activates extracellular signal regulated protein kinase ( ERK ), c-Jun N-terminal protein kinase (JNK) , and p38 mitogen activated protein kinase
Viedt et al., Arterioscler Thromb Vasc Biol 2000 : The study was performed to further characterize the role of ROS in Ang II-mediated MAP kinase activation and the regulation of the transcription factor activator protein-1 (AP-1) ... The results indicate that in VSMCs, Ang II activates MAP kinases and AP-1 through different pathways ; the results further suggest that ROS, generated by p22phox, mediate Ang II-induced JNK and p38 MAPK activation, which may contribute to the pathogenesis of atherosclerosis
Murasawa et al., J Biol Chem 2000 (Calcium Signaling) : In this study, we tested the involvement of Pyk2 and EGF-R in Ang II-induced activation of JNK and c-Jun in cardiac fibroblasts ... Induction of c-Jun gene transcription by Ang II was abolished in PKM, DN-Rac1, and DN-MEKK1, in which Ang II-induced binding of ATF2/c-Jun heterodimer to the activator protein-1 sequence at -190 played a key role ... These results suggest that 1 ) in cardiac fibroblasts activation of JNK and c-Jun by Ang II is initiated by Pyk2 dependent signalings but not by downstream signals of EGF-R or Ras, 2 ) Rac1 but not Cdc42 is required for JNK activation by Ang II upstream of MEKK1, and 3 ) ATF-2/c-Jun binding to the activator protein-1 sequence at -190 plays a key role for induction of c-Jun gene by Ang II
Yoshizumi et al., Mol Pharmacol 2001 : Our findings showed that Ang II stimulated rapid and significant activation of extracellular signal regulated kinase ( ERK ) 1/2, c-Jun N-terminal kinase (JNK) , and p38 in RASMC
Blume et al., Neuropharmacology 2002 : Ang II , injected intracerebroventricularly, induced the expression of c-Fos, c-Jun and Krox-24 in the hypothalamic paraventricular ( PVN ) and supraoptic ( SON ) nuclei
Hautala et al., Pflugers Arch 2002 : These results show that ET-1 and Ang II are required for the stimulation of GATA4 and AP-1 DNA binding activity in response to direct left ventricular wall stretch
Kalra et al., Circulation 2002 : Stimulation with Ang II led to the activation of nuclear factor-kappaB and activator protein-1 (AP-1) , two transcription factors that are important for TNF gene expression
Bataller et al., J Clin Invest 2003 (Liver Cirrhosis, Experimental) : Ang II phosphorylated AKT and MAPKs and increased AP-1 DNA binding in a redox-sensitive manner
Viedt et al., J Mol Med (Berl) 2004 : ANG II and PDGF AA both activated the redox-sensitive transcription factor AP-1 , which was inhibited by p22phox antisense ODNs
Zheng et al., J Cardiovasc Pharmacol 2004 (Cardiomegaly) : EGCG only inhibited Ang II-stimulated activation of c-Jun N-terminal kinase (JNK)
Touyz et al., J Hypertens 2004 : Ang II and ET-1 increased MAPK phosphorylation ( P < 0.01 ). Pre-treatment with Tiron and Tempol, *O2 scavengers, attenuated agonist stimulated phosphorylation of p38MAPK, c-Jun N-terminal kinases (JNK) and ERK5, but not of ERK1/2 ( extracellular signal regulated kinases ). Apocynin and diphenylene iodinium ( DPI ), NAD ( P ) H oxidase inhibitors, decreased Ang II-induced responses 60-70 %. ET-1 mediated MAPK phosphorylation was unaffected by apocynin but was reduced ( > 50 % ) by thenoyltrifluoroacetone ( TIFT ) and carboxyl cyanide-m-chlorophenylhydrazone ( CCCP ), mitochondrial inhibitors
Terebessy et al., Nephrol Dial Transplant 2004 : In these cells Ang II activated both extracellular signal regulated kinase ( ERK ) and the c-Jun-N-terminal kinase (JNK)
Izawa et al., Exp Cell Res 2005 (Hypertension...) : Ang II induced extracellular signal regulated kinase ( ERK ) 1/2 and c-Jun N-terminal kinase (JNK) activation and IRS-1 phosphorylation at Ser307 and Ser616
Chen et al., Cardiovasc Res 2006 : Ang II induced activation of NF-kappaB and AP-1 in untransfected VSMCs, however, Ang II induced significantly higher activities of these pro-inflammatory transcription factors in HSF-1 siRNA transfected cells
Chen et al., Inflamm Res 2005 (Hypertension...) : The Ang II-induced activation of SP-1 and AP-1 were significantly suppressed by HS treatment
Li et al., Zhonghua Yi Xue Za Zhi 2005 : Stimulation of HSC by Ang II and Aldo results in activation of AP-1 via ERK1/2 pathway leading to up-regulation of AP-1 target gene alpha1 ( I ) procollagen mRNA expression
Neves et al., Can J Physiol Pharmacol 2005 (Fibrosis...) : Ang II significantly increased cardiac AP-1 activity and ED-1 expression, which was prevented by spironolactone only
Su et al., Kidney Int 2006 : Ang II ( 5 min, 10 ( -7 ) M ) stimulated phosphorylation of the three MAPK ( p38, extracellular signal related kinase ( ERK 1/2 ), and c-Jun N-terminal kinase (JNK) )
Li et al., Regul Pept 2007 (Liver Cirrhosis, Experimental) : The present study aims to investigate the signal transduction mechanism underlying effects of Ang II and Aldo on NF-kappaB and AP-1 pathway during hepatic fibrogenesis
Ding et al., American journal of physiology. Renal physiology 2007 : ANG II induces c-Jun NH2-terminal kinase activation and proliferation of human mesangial cells via redox-sensitive transactivation of the EGFR
Clark et al., Brain Res Bull 2008 : In the current study, we investigated whether Ang II activates c-Jun N-terminal kinase (JNK) and determined if JNK mediates Ang II-induced astrocyte growth in cultured brainstem astrocytes
Nie et al., Mol Immunol 2009 : Both Ang- ( 1-7 ) and Ang II had no effect on p38 and c-Jun N-terminal kinase (JNK) phosphorylation
Jiménez et al., Biochem Biophys Res Commun 2009 : Furthermore, Ang II-induced MMP 2 activation was markedly blocked by SP600125, a selective c-Jun N-terminal kinase (JNK) inhibitor, or pre-treatment of cells with antisense oligonucleotide to focal adhesion kinase ( FAK ), indicating that both molecules were important for the activation of MMP 2 by Ang II receptor stimulation
Krug et al., Biochim Biophys Acta 2012 : Most likely, the stimulation of Ang-2 is in part mediated by increased activation of AP-1 but different signal transduction pathways may also be involved since we found opposite activation of PI3K/Akt/mTOR and MAPK7ERK pathways ( both known to regulate in Ang-2 expression )
Valente et al., J Mol Cell Cardiol 2012 (Cardiomegaly...) : Since Ang-II is a potent activator of NF-?B and AP-1 , we investigated whether CIKS is critical in Ang-II mediated cardiac hypertrophy ... Further, Ang-II induced IKK/p65 and JNK/c-Jun phosphorylation, NF-?B and AP-1 activation, and IL-18 and MMP-9 expression were also markedly attenuated in CIKS-null mice
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
Lebrun et al., Regul Pept 1996 : Ang II ( 1, 10, 100 ng ) induced after 90 min a dose dependent expression of c-Fos, FosB, c-Jun , JunB and Krox-24, which was confined to four specific brain areas, namely the subfornical organ ( SFO ), median preoptic area ( MnPO ), paraventricular nucleus ( PVN ) and supraoptic nucleus (SON)
Kudoh et al., Circ Res 1997 : In the present study, to elucidate the mechanism by which Ang II regulates gene expression in cardiac myocytes, we examined whether Ang II activates c-Jun NH2-terminal kinase (JNK) , which is a member of the mitogen activated protein kinase family and activates the transcription factor, activator protein-1 (AP-1) ... In conclusion, Ang II may activate JNK in cultured cardiac myocytes through an increase in intracellular Ca2+ and activation of protein kinase C, and the activated JNK may regulate gene expression by activating AP-1 during Ang II-induced cardiac hypertrophy
Natarajan et al., Hypertension 1999 : Furthermore, Ang II and HG combined had additive effects on AP-1 activity