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AGTR1 — NFKB1

Text-mined interactions from Literome

Ruiz-Ortega et al., Circ Res 2000 : AT(1) ( DUP753 ) and AT(2) ( PD123319 and CGP42112 ) receptor antagonists inhibited Ang II-induced NF-kappaB DNA binding in a dose dependent manner ( approximately 85 % for each one ; 10 ( - ) ( 5 ) mol/L at 1 hour )
Cowling et al., J Biol Chem 2002 : The use of pharmacologic inhibitors and a degradation-resistant mutant I kappa B-alpha demonstrated that the transcription factor nuclear factor-kappa B (NF-kappa B) is necessary for cytokine induced AT(1) up-regulation
Lorenzo et al., J Am Soc Nephrol 2002 : In cultured rat mesangial cells, both AT(1) and AT(2) receptor antagonists inhibited AngII induced NF-kappaB DNA binding activity, whereas NF-kappaB activation elicited by AngIII was mainly blocked by the AT(2) receptor antagonist ... These data demonstrate that, in mesangial cells, NF-kappaB activation is mediated by AT(1) and AT(2) receptors, suggesting a novel intracellular signaling mechanism for AT(2) receptors in the kidney
Ramesh et al., Toxicol Lett 2002 : Activation of NF-kappaB DNA binding activity by Mn ( 2+ ) at 1.0 microM correlated with proteolytic degradation of the inhibitory subunit IkappaB(alpha) as evidenced in cytosol
Dechend et al., Circulation 2003 (Pre-Eclampsia) : To elucidate their role further, we studied the effects of AT1-AA on reactive oxygen species ( ROS ), NADPH oxidase expression, and nuclear factor-kappaB (NF-kappaB) activation ... We next tested if AT1-AA lead to NF-kappaB activation in VSMC and trophoblasts ... VSMC from p47phox-/- mice showed markedly reduced ROS generation and NF-kappaB activation in response to Ang II and AT1-AA
Wu et al., Mol Endocrinol 2004 : Transfection of a dominant negative Src homology protein tyrosine phosphatase-1 mutant into vascular smooth muscle cells inhibited the AT(2) receptor mediated increase in IkappaB, leading to a significant increase in AT(1) receptor induced NF-kappaB activation and MCP-1 expression
Zhuo et al., Ann N Y Acad Sci 2006 : Our results therefore suggest that AT(1) receptor mediated endocytosis of extracellular Ang II may be required for Ang II-induced NF-kappaB activation and subsequent cell proliferation in renal proximal tubule cells
Chan et al., J Pharmacol Exp Ther 2007 (Acute Disease...) : This study sought to elucidate the mechanism mediating angiotensin II involvement in angiotensin II type 1 (AT1) receptor mediated NF-kappaB activation, and ultimately in proinflammatory actions of AP pathogenesis
Vaziri et al., J Pharmacol Exp Ther 2007 (Disease Models, Animal...) : The untreated group exhibited hypertension, deterioration of renal function and structure, reduced or unchanged plasma renin activity, aldosterone concentration, marked up-regulations of AT1r ( 250 % ), Ang II-expressing cell count ( > 20-fold ), NAD ( P ) H oxidase subunits ( gp91(phox,) p22(phox), and P47 ( phox ) ; 20-40 % ), COX-2 ( 250 % ), 12-lipooxygenase ( 100 % ), MCP-1 ( 400 % ), and PAI-1 ( > 20-fold ), activation of NFkappaB , and interstitial infiltrations of T cells and macrophages in the remnant kidneys
Skultetyova et al., Recent Pat Cardiovasc Drug Discov 2007 (Inflammation) : AT(1) receptor enhances the activation of nuclear factor NF-kappaB , which stimulates the production of proinflammatory cytokines
Zhang et al., Zhonghua Xue Ye Xue Za Zhi 2008 (Multiple Myeloma) : The activity of NF-kappaB was enhanced by BDNF in a dose dependent manner, and pretreatment with K252 alpha could significantly inhibit this activation at 1 , 6, 12 and 24 h ( P < 0.05 ) in a time dependent manner
Miguel-Carrasco et al., Journal of inflammation (London, England) 2010 : To understand the mechanisms involved in the effect of captopril, mRNA expression of ACE, angiotensin II type I receptor (AT1R) and p22phox ( a subunit of NADPH oxidase ), as well as NF-kappaB activation and expression, were measured in the left ventricle of these animals
Wang et al., Zhonghua Shao Shang Za Zhi 2010 (Acute Lung Injury) : To explore the role of angiotensin II type 1 (AT1) receptor in activation of nuclear factor-kappaB (NF-kappaB) and activator protein-1 (AP-1) in lung of mice with LPS induced acute lung injury ( ALI )