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抗Human AGT 抗体:
抗Mouse (Murine) AGT 抗体:
抗Rat (Rattus) AGT 抗体:
Human Polyclonal AGT Primary Antibody for ELISA, IHC - ABIN1583980
Mateos, Ismail, Gil-Bea, Leoni, Winblad, Björkhem, Cedazo-Mínguez: Upregulation of brain renin angiotensin system by 27-hydroxycholesterol in Alzheimer's disease. in Journal of Alzheimer's disease : JAD 2011
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Human Polyclonal AGT Primary Antibody for ICC, IF - ABIN447446
Dimitrijevic, Rissler, Luts, Edvinsson: Reduced expression of angiotensin II and angiotensin receptor type 1 and type 2 in resistance arteries from nasal lesions in granulomatosis with polyangiitis (Wegener's granulomatosis). in Scandinavian journal of rheumatology 2011
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Human Monoclonal AGT Primary Antibody for WB - ABIN1882205
Desong Liu, Fang Lu, Songhui Zhai, Liu Wei, Shi Ma, Xiuying Chen, Liqun Dong, Yannan Guo, Jin Wu, Zheng Wang: Renin-angiotensin system gene polymorphisms in children with Henoch-Schönlein purpura in West China. in Journal of the renin-angiotensin-aldosterone system : JRAAS 2010
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Human Monoclonal AGT Primary Antibody for WB - ABIN1882204
Kieć-Wilk, Olszanecka, Mikołajczyk, Kawecka-Jaszcz et al.: [Role of the M235T (c.704c>T) polymorphism of angiotensynogen gene as well as A724A (c.2171G>A) polymorphism of SERCA2a gene in ethiopathogenesis of left ventricular hypertrophy in essential... in Przegla̧d lekarski 2010
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Human Monoclonal AGT Primary Antibody for ELISA, WB - ABIN968948
Xu, Carretero, Lin, Cavasin, Shesely, Yang, Reudelhuber, Yang: Role of cardiac overexpression of ANG II in the regulation of cardiac function and remodeling postmyocardial infarction. in American journal of physiology. Heart and circulatory physiology 2007
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Human Monoclonal AGT Primary Antibody for ELISA, WB - ABIN559812
Jain, Li, Patil, Kumar: HNF-1alpha plays an important role in IL-6-induced expression of the human angiotensinogen gene. in American journal of physiology. Cell physiology 2007
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Human Polyclonal AGT Primary Antibody for IHC, IHC (p) - ABIN4352882
Bachmann, Burté, Pramana, Conte, Brown, Orimadegun, Ajetunmobi, Afolabi, Akinkunmi, Omokhodion, Akinbami, Shokunbi, Kampf, Pawitan, Uhlén, Sodeinde, Schwenk, Wahlgren, Fernandez-Reyes, Nilsson: Affinity proteomics reveals elevated muscle proteins in plasma of children with cerebral malaria. in PLoS pathogens 2014
Urinary angiotensinogen and renin (显示 REN 抗体) excretion are elevated in CKD patients. Both parameters are negatively associated with eGFR (显示 EGFR 抗体) and these associations are independent of urinary albumin (显示 ALB 抗体) excretion
Reduced IL-18 (显示 IL18 抗体) serum concentration in children after HUS (显示 CFH 抗体) with no difference in its urine concentration may indicate a loss of the protective effects of this cytokine on renal function due to previously occurred HUS (显示 CFH 抗体).
Angiotensin II initiates hepatocyte epithelial-mesenchymal transition by activating the NOX-derived H2O2-mediated NLRP3 (显示 NLRP3 抗体) inflammasome/IL-1ss/Smad (显示 SMAD1 抗体) circuit.
present study has demonstrated, for the first time, that high glucose augments AGT (显示 AGXT 抗体) in human RPTCs through HNF-5, which provides a potential therapeutic target for diabetic nephropathy
AngII-dependent phosphorylation of LCP1 (显示 LCP1 抗体) in cultured podocytes was mediated by the kinases ERK (显示 EPHB2 抗体), p90 (显示 CANX 抗体) ribosomal S6 kinase (显示 RPS6KB1 抗体), PKA, or PKC (显示 PRRT2 抗体). LCP1 (显示 LCP1 抗体) phosphorylation increased filopodia formation.
Autosomal dominant polycystic kidney disease (ADPKD), uniquely increases urinary angiotensinogen and renin (显示 REN 抗体) excretion despite their circulating levels being comparable with those in non-ADPKD chronic kidney disease.
Quaternary interactions and supercoiling modulate the cooperative DNA binding of AGT (显示 AGXT 抗体).
results show that SNPs in the Hap (显示 SAFB 抗体)-I of the hAGT gene promote high-fat diet-induced binding of transcription factors GR, CEBP-beta (显示 CEBPB 抗体) and STAT3 (显示 STAT3 抗体), which lead to elevated expression of the hAGT gene in hepatic and adipose tissues
Angiotensinogen import and subsequent trafficking to the mitochondria occurs in proximal kidney tubules.
Transgenic mice expressing human AGT (显示 AGXT 抗体) in the subfornical organ AGT (显示 AGXT 抗体) and possibly ANG I/ANG II into the cerebral ventricles.
adipocyte-derived Agt (显示 AGXT 抗体) has essentially no contribution to the plasma concentration and no impact on blood pressure compared to liver-derived Agt (显示 AGXT 抗体).
Lung ischemia-reperfusion injury causes a dysregulation of circulating Ang 2 (显示 ANGPT2 抗体) levels and plasma PREP (显示 PREP 抗体) activity, although no direct link between both phenomena could be shown.
Inhibition of TLR4 (显示 TLR4 抗体) ameliorates AngII-impaired cavernosal relaxation, decreases TNF-alpha (显示 TNF 抗体) levels, and restores Nitric Oxide bioavailability, demonstrating that TLR4 (显示 TLR4 抗体) partly mediates AngII-induced cavernosal dysfunction.
Our study is the first to show the important role of IL-6 (显示 IL6 抗体) in regulating cardiac pathogenesis via inflammation and apoptosis during AngII-induced hypertension. We also provide a novel link between IL-6 (显示 IL6 抗体)/STAT3 (显示 STAT3 抗体) and EndoG (显示 ENDOG 抗体)/MEF2A (显示 MEF2A 抗体) pathway that affects cardiac hypertrophy during AngII stimulation.
this study demonstrated that Ang II could increase TRPC6 (显示 TRPC6 抗体) induced Ca(2 (显示 CA2 抗体)+) influx and enhance autophagy through increasing reactive oxygen species levels in podocytes, and autophagy could protect Ang II-treated podocytes.
These results implied that AngII could effectively induce EpiCs to differentiate into vascular smooth muscle-like cells through the AT1 receptor (显示 AGTRAP 抗体).
Results suggest the involvement of angiotensin II (Ang II), through its angiotensin type-1 receptor (AT1R (显示 AGTRAP 抗体)) in the inflammation induced by Aah (显示 ASPH 抗体) venom, in the heart and the aorta.
Angiotensin II stimulates PYY secretion, in turn inhibiting epithelial anion fluxes, thereby reducing net fluid secretion into the colonic lumen.
expression of spinal ACE (显示 ACE 抗体) increased in streptozotocin-induced diabetic mice, which in turn led to an increase in Ang II levels and tactile allodynia.
the beneficial actions of insulin (显示 INS 抗体) in diabetic nephropathy appear to be mediated, in part, by suppressing renal Nrf2 (显示 NFE2L2 抗体) and Agt (显示 AGXT 抗体) gene transcription and preventing Nrf2 (显示 NFE2L2 抗体) stimulation of Agt (显示 AGXT 抗体) expression via hnRNP F (显示 HNRNPF 抗体)/K.
Data suggest that intra-adrenal metabolism of Ang II to Ang III is required for zona glomerulosa cell-mediated relaxation of adrenal arterioles but not for aldosterone secretion.
NADPH oxidase (显示 NOX1 抗体) plays an important role in proMMP-2 expression and activation and MMP-2 (显示 MMP2 抗体) mediated SMC (显示 DYM 抗体) proliferation occurs through the involvement of Spm (显示 NPC1 抗体)-Cer (显示 CBLN1 抗体)-S1P (显示 MBTPS1 抗体) signaling axis under ANG II stimulation of PASMCs
The metabolism of angiotensin II (Ang II) to angiotensin III (Ang III) and its role in the vasorelaxation response in adrenal arteries are reported.
The study identified the serine phosphorylation (p-Ser (显示 SIGLEC1 抗体)) sites induced by PKC-Beta (显示 PRKCB 抗体) activation or AGT, which inhibits insulin (显示 INS 抗体)-induced p-Tyr (显示 TYR 抗体) sites on IRS2 (显示 IRS2 抗体) and its signals in endothelial cells.
Data suggest up-regulation of AGT in granulosa cells and of Ang II in follicular fluid during preovulatory period; Ang II appears to amplify stimulatory effects of luteinizing hormone on secretion of progesterone/prostaglandins by granulosa cells.
Data suggest that angiotensin II promotes uptake/accumulation of iron (non-transferrin (显示 Tf 抗体) bound iron) into vascular endothelial cells; such iron accumulation appears to depend on activation of angiotensin type 1 receptor and promotes oxidative stress.
a critical role for H(2)O(2) in angiotensin-II signaling to the endothelial cytoskeleton in a novel pathway that is critically dependent on MARCKS, Rac1, and c-Abl.
The objective of this study was to characterize the profiles of Ang-(1-7), MAS receptor, ACE(2), NEP and PEP during the ovulatory process in cattle.
Fetal adrenal cells in primary culture respond to angiotensin-II by increasing aldosterone production and aldosterone synthase (显示 CYP11B2 抗体) [P450c18/CYP11B2 (显示 CYP11B2 抗体)] activity.
ANG II inhibits bTREK-1 K(+) channels by a Ca(2+)-dependent mechanism that does not require the depletion of membrane-associated PIP(2).
The protein encoded by this gene, pre-angiotensinogen or angiotensinogen precursor, is expressed in the liver and is cleaved by the enzyme renin in response to lowered blood pressure. The resulting product, angiotensin I, is then cleaved by angiotensin converting enzyme (ACE) to generate the physiologically active enzyme angiotensin II. The protein is involved in maintaining blood pressure and in the pathogenesis of essential hypertension and preeclampsia. Mutations in this gene are associated with susceptibility to essential hypertension, and can cause renal tubular dysgenesis, a severe disorder of renal tubular development. Defects in this gene have also been associated with non-familial structural atrial fibrillation, and inflammatory bowel disease.
alpha-1 antiproteinase, antitrypsin
, angiotensin I
, angiotensin II
, serine (or cysteine) proteinase inhibitor
, serpin A8
, angiotensin ll
, angiotensinogen (PAT)
, zC8A9.1 (angiotensinogen )
, Serpin A8