抗Human AGT 抗体:
抗Mouse (Murine) AGT 抗体:
抗Rat (Rattus) AGT 抗体:
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 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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Mouse (Murine) Polyclonal AGT Primary Antibody for WB - ABIN4886440
Lan, Yue, Han, Shi, Yang, Pu, Yao, Kang: Genome-wide identification of TCF7L2/TCF4 target miRNAs reveals a role for miR-21 in Wnt-driven epithelial cancer. in International journal of oncology 2011
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
In the Asian populations, ACE I/D and AGTR1 A1166C may contribute to Diabetic Nephropathy (DN) susceptibility in patients with T2DM by different genetic models. However, the role of AGT M235T needs to be further evaluated. [review & meta-analysis]
In coronary artery disease patients, M235T among several AGT gene polymorphisms is associated with elevated serum-CRP levels with AGT C allele as the significant factor for patients with serum-CRP level of more than 1 mg/L.
High urinary angiotensinogen levels are associated with albuminuria and left ventricular hypertrophy
Renin angiogensin system activation, particularly renal RAS activation indicated by elevated urinary Ang excretion, exerts a fundamental role in the pathogenesis of hypertension in the general population.
AGT C/T and AT2 G/A polymorphisms were not significantly associated with aneurysmal subarachnoid hemorrhage (aSAH) after controlling for potential confounders. However, a strong trend was identified for a dominant effect of the G allele of the AT2 G/A SNP. Downregulation of the local RAS may contribute to the formation of cerebral aneurysms and subsequent presentation with aSAH.
Patients homozygous for the C allele of the AGT C/T polymorphism experienced a higher rate of rupture from aneurysms smaller than 7 mm.
Among East Asians the angiotensinogen variant M235T is associated with cardiovascular disease.
The AGT Thr-Thr genotype frequency was significantly higher among WLs (25.9%) compared with S/J (4.2%) and controls (12.8%).
angiotensinogen-6 A/G and angiotensinogen-20 A/C polymorphisms were not associated with the antihypertensive response to telmisartan treatment in Chinese patients with hypertension.
the T174M polymorphism in the AGT gene was associated with diabetic nephropathy in Asians.
Contractile responses to angiotensin II are preserved in narrow lumen human cirrhotic splanchnic arteries and are comparatively augmented in early disease. Angiotensin-(1-7) had no vasodilatory effect on adrenergic tone, however, attenuated angiotensin II-induced contractility, possibly through an Ang-(1-7)-AT1R interaction, and thus may contribute to pathological vasodilatation in human cirrhosis.
Ang II regulates sympathetic and parasympathetic nerve-mediated excitation and contraction.
AGT gene polymorphism rs5050T>G is associated with the risk of coronary aneurysm in children with Kawasaki disease.
Angiotensinogen (AGT) rs5050 (GG) found to be associated with poor prognosis in astrocytoma patients
Isoliquiritigenin alleviated the Ang II-induced hypertensive renal injury through suppressing inflammation cytokines, excessive deposition of extracellular matrix and oxidative stress-induced apoptosis via Nrf2 and NF-kappaB pathways.
findings indicate that AGT adapts unique serpin features for hormone delivery and binds renin through concerted movements in the N-terminal tail and in its main body to modulate angiotensin release.
The rs7079 C to A substitution reduced the binding of miR-31-5p/miR-584-5p to the 3' UTR of AGT, possibly altering the risk of lead poisoning.
These results suggest that Angiotensin II induces CTGF expression and extracellular matrix accumulation through a special TGF-beta-independent interaction between the NF-kappaB and Smad2/3 signals elicited by the AT1/PKCalpha/p38 MAPK pathway.
The possible contribution of the I/D in the ACE gene, M235T and T174M in the angiotensinogen (AGT) gene polymorphisms with ischemic stroke in young Mexican population.
AGT M235T gene polymorphism may represent a genetic modifier to vascular morbidities in Egyptian patients with sickle cell disease.
a regulatory role of megalin in the intrarenal renin-angiotensin homeostasis and atherogenesis, positing renal Ang II to be an important contributor to atherosclerosis that is mediated through AGT and megalin interactions.
In ULK1 transgenic (TG) mice with ULK1 over-expression, accelerated hypertrophy, reduced cardiac function and promoted fibrosis deposition were observed compared with non-transgenic mice following AngII challenge.
Bmal1 in PVAT regulates angiotensinogen expression and the ensuing increase in angiotensin II, which acts on smooth muscle cells in the vessel walls to regulate vasoactivity and blood pressure in a circadian fashion during the resting phase.
In conclusion, hematopoietic deficiency of Psgl-1 attenuates Ang II-induced hypertension, an effect that may be mediated by reduced IL-17.
Data suggest that urinary angiotensinogen (UAGT) enables the dynamical monitoring of renal structural recovery after an AKI episode and may serve as an early predictor for acute kidney injury (AKI)- chronic kidney disease (CKD) progression.
Our data demonstrate a previously unknown synergy between AngII and BAFF in inducing IL-10 production by B cells, resulting in atheroprotection.
Mean blood pressure, plasma Ang II level, and myocardium malondialdehyde (MDA) content of angiotensinogen-renin (AGT-REN) double transgenic hypertension (dTH) mice were higher than those in wild-type (WT) mice.
ANG II is up-regulated in serum and heart tissues of mice with EAM and that ANG II significantly drives monocyte/macrophage infiltration through the C-C chemokine receptor 2/5 (CCR2/5) axis.
results established that A20 is involved in the renoprotective effect by calcitriol via negatively modulating the NF-kappaB pathway and necroptotic pathway in AngII-induced renal injury.
NLRP3 gene deletion attenuates Ang II-induced NLRP3 inflammasome activation, phenotypic transformation from a contractile phenotype to a synthetic phenotype and proliferation in primary mice Vascular Smooth Muscle Cells.
adipocyte-derived Agt has essentially no contribution to the plasma concentration and no impact on blood pressure compared to liver-derived Agt.
Lung ischemia-reperfusion injury causes a dysregulation of circulating Ang 2 levels and plasma PREP activity, although no direct link between both phenomena could be shown.
Inhibition of TLR4 ameliorates AngII-impaired cavernosal relaxation, decreases TNF-alpha levels, and restores Nitric Oxide bioavailability, demonstrating that TLR4 partly mediates AngII-induced cavernosal dysfunction.
Our study is the first to show the important role of IL-6 in regulating cardiac pathogenesis via inflammation and apoptosis during AngII-induced hypertension. We also provide a novel link between IL-6/STAT3 and EndoG/MEF2A pathway that affects cardiac hypertrophy during AngII stimulation.
this study demonstrated that Ang II could increase TRPC6 induced Ca(2+) 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.
Results suggest the involvement of angiotensin II (Ang II), through its angiotensin type-1 receptor (AT1R) in the inflammation induced by Aah 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 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 in diabetic nephropathy appear to be mediated, in part, by suppressing renal Nrf2 and Agt gene transcription and preventing Nrf2 stimulation of Agt expression via hnRNP F/K.
Angiotensin-II promotes Na+ uptake in larval in acidic and ion-poor water.
In conclusion, endothelial vWF knockdown prevented angiotensin II-induced ET-1 upregulation through attenuation of NOX-mediated O2- production.
In remodeled myocardium angiotensin II (ANGII) and endothelin contribute to coronary resistance vessel tone in nolinear redundant fashion.
Cyclosporine-A stimulates angiotensin I/II secretion by kidney glomeruli.
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 plays an important role in proMMP-2 expression and activation and MMP-2 mediated SMC proliferation occurs through the involvement of Spm-Cer-S1P 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) sites induced by PKC-Beta activation or AGT, which inhibits insulin-induced p-Tyr sites on IRS2 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 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.
The AngII concentration increased in the follicular fluid of the dominant follicle.
Fetal adrenal cells in primary culture respond to angiotensin-II by increasing aldosterone production and aldosterone synthase [P450c18/CYP11B2] 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).
prostaglandin F2alpha, endothelin-1, and angiotensin II may interact with each other in a local positive feedback manner to activate their secretion in the regressing corpus luteum, thus accelerating and completing luteolysis
Suggest that the activation of a local positive feedback mechanism in the corpus luteum among ET-1, Ang II and PGF2alpha might play a functional role in the paracrine modulation of luteolytic cascade.
MKP-1 is the specific phosphatase induced by AngII and involved in the negative feedback mechanism ensuring adequate ERK1/2-mediated aldosterone production in response to the hormone.
In normotensive donors with a normal compensatory response to nephrectomy, baseline renal reactivity to angiotensin II can influence renal and glomerular hemodynamics 1 year after nephrectomy.
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