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anti-Human Angiotensin II Anticorps:
anti-Rat (Rattus) Angiotensin II Anticorps:
anti-Mouse (Murine) Angiotensin II Anticorps:
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Human Polyclonal Angiotensin II Primary Antibody pour IHC, ELISA - ABIN1583979
Matsuura-Hachiya, Arai, Ozeki, Kikuta, Nishiyama: Angiotensin-converting enzyme inhibitor (enalapril maleate) accelerates recovery of mouse skin from UVB-induced wrinkles. dans Biochemical and biophysical research communications 2014
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Human Polyclonal Angiotensin II Primary Antibody pour IF (p), IHC (p) - ABIN670521
Anand, Yiangou, Sinisi, Fox, MacQuillan, Quick, Korchev, Bountra, McCarthy, Anand: Mechanisms underlying clinical efficacy of Angiotensin II type 2 receptor (AT2R) antagonist EMA401 in neuropathic pain: clinical tissue and in vitro studies. dans Molecular pain 2015
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Urinary angiotensinogen (Montrer AGT Anticorps) and renin (Montrer REN Anticorps) excretion are elevated in CKD patients. Both parameters are negatively associated with eGFR (Montrer EGFR Anticorps) and these associations are independent of urinary albumin (Montrer ALB Anticorps) excretion
Reduced IL-18 (Montrer IL18 Anticorps) serum concentration in children after HUS (Montrer CFH Anticorps) 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 (Montrer CFH Anticorps).
Angiotensin II initiates hepatocyte epithelial-mesenchymal transition by activating the NOX-derived H2O2-mediated NLRP3 (Montrer NLRP3 Anticorps) inflammasome/IL-1ss/Smad (Montrer SMAD1 Anticorps) circuit.
present study has demonstrated, for the first time, that high glucose augments AGT (Montrer AGXT Anticorps) in human RPTCs through HNF-5, which provides a potential therapeutic target for diabetic nephropathy
AngII-dependent phosphorylation of LCP1 (Montrer LCP1 Anticorps) in cultured podocytes was mediated by the kinases ERK (Montrer EPHB2 Anticorps), p90 (Montrer CANX Anticorps) ribosomal S6 kinase (Montrer RPS6KB1 Anticorps), PKA, or PKC (Montrer PRRT2 Anticorps). LCP1 (Montrer LCP1 Anticorps) phosphorylation increased filopodia formation.
Autosomal dominant polycystic kidney disease (ADPKD), uniquely increases urinary angiotensinogen (Montrer AGT Anticorps) and renin (Montrer REN Anticorps) 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 (Montrer AGXT Anticorps).
results show that SNPs in the Hap (Montrer SAFB Anticorps)-I of the hAGT gene promote high-fat diet-induced binding of transcription factors GR, CEBP-beta (Montrer CEBPB Anticorps) and STAT3 (Montrer STAT3 Anticorps), which lead to elevated expression of the hAGT gene in hepatic and adipose tissues
Angiotensinogen (Montrer AGT Anticorps) import and subsequent trafficking to the mitochondria occurs in proximal kidney tubules.
Transgenic mice expressing human AGT (Montrer AGXT Anticorps) in the subfornical organ AGT (Montrer AGXT Anticorps) and possibly ANG I/ANG II (Montrer AGT Anticorps) into the cerebral ventricles.
adipocyte-derived Agt (Montrer AGXT Anticorps) has essentially no contribution to the plasma concentration and no impact on blood pressure compared to liver-derived Agt (Montrer AGXT Anticorps).
Lung ischemia-reperfusion injury causes a dysregulation of circulating Ang 2 (Montrer ANGPT2 Anticorps) levels and plasma PREP (Montrer PREP Anticorps) activity, although no direct link between both phenomena could be shown.
Inhibition of TLR4 (Montrer TLR4 Anticorps) ameliorates AngII-impaired cavernosal relaxation, decreases TNF-alpha (Montrer TNF Anticorps) levels, and restores Nitric Oxide bioavailability, demonstrating that TLR4 (Montrer TLR4 Anticorps) partly mediates AngII-induced cavernosal dysfunction.
Our study is the first to show the important role of IL-6 (Montrer IL6 Anticorps) in regulating cardiac pathogenesis via inflammation and apoptosis during AngII-induced hypertension. We also provide a novel link between IL-6 (Montrer IL6 Anticorps)/STAT3 (Montrer STAT3 Anticorps) and EndoG (Montrer ENDOG Anticorps)/MEF2A (Montrer MEF2A Anticorps) pathway that affects cardiac hypertrophy during AngII stimulation.
this study demonstrated that Ang II (Montrer AGT Anticorps) could increase TRPC6 (Montrer TRPC6 Anticorps) induced Ca(2 (Montrer CA2 Anticorps)+) influx and enhance autophagy through increasing reactive oxygen species levels in podocytes, and autophagy could protect Ang II (Montrer AGT Anticorps)-treated podocytes.
These results implied that AngII could effectively induce EpiCs to differentiate into vascular smooth muscle-like cells through the AT1 receptor (Montrer AGTRAP Anticorps).
Results suggest the involvement of angiotensin II (Ang II), through its angiotensin type-1 receptor (AT1R (Montrer AGTRAP Anticorps)) in the inflammation induced by Aah (Montrer ASPH Anticorps) 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 (Montrer ACE Anticorps) increased in streptozotocin-induced diabetic mice, which in turn led to an increase in Ang II (Montrer AGT Anticorps) levels and tactile allodynia.
the beneficial actions of insulin (Montrer INS Anticorps) in diabetic nephropathy appear to be mediated, in part, by suppressing renal Nrf2 (Montrer NFE2L2 Anticorps) and Agt (Montrer AGXT Anticorps) gene transcription and preventing Nrf2 (Montrer NFE2L2 Anticorps) stimulation of Agt (Montrer AGXT Anticorps) expression via hnRNP F (Montrer HNRNPF Anticorps)/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