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ANGPT2 — FOS

Text-mined interactions from Literome

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
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
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
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
Lu et al., Neuroscience 2009 : Results showed that the Fos immunoreactivity (Fos-ir) expression in forebrain areas such as subfornical organ ( SFO ), paraventricular hypothalamic nuclei ( PVN ), supraoptic nucleus (SON) and organum vasculosum laminae terminalis ( OVLT ) all increased significantly and that the levels of ANG I, ANG II and ALD also increased in plasma and forebrain in rats fed with low sodium diet
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 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
Badoer et al., Am J Physiol 1997 : In the medulla, ANG II did not significantly increase Fos production in the nucleus of the solitary tract (NTS) or ventrolateral medulla ( VLM )
Natarajan et al., Hypertension 1999 : Furthermore, Ang II and HG combined had additive effects on AP-1 activity