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anti-Human Angiotensin II Antikörper:
anti-Rat (Rattus) Angiotensin II Antikörper:
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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.
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
, angiotensinogen (PAT)
, angiotensin ll