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anti-Human Angiotensin II Antibodies:
anti-Rat (Rattus) Angiotensin II Antibodies:
anti-Mouse (Murine) Angiotensin II Antibodies:
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Human Polyclonal Angiotensin II Primary Antibody for IHC, ELISA - ABIN1583979
Matsuura-Hachiya, Arai, Ozeki, Kikuta, Nishiyama: Angiotensin-converting enzyme inhibitor (enalapril maleate) accelerates recovery of mouse skin from UVB-induced wrinkles. in Biochemical and biophysical research communications 2014
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Human Polyclonal Angiotensin II Primary Antibody for 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. in Molecular pain 2015
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Angiotensin II initiates hepatocyte epithelial-mesenchymal transition by activating the NOX-derived H2O2-mediated NLRP3 (show NLRP3 Antibodies) inflammasome/IL-1ss/Smad (show SMAD1 Antibodies) circuit.
present study has demonstrated, for the first time, that high glucose augments AGT (show AGXT Antibodies) in human RPTCs through HNF-5, which provides a potential therapeutic target for diabetic nephropathy
AngII-dependent phosphorylation of LCP1 (show LCP1 Antibodies) in cultured podocytes was mediated by the kinases ERK (show EPHB2 Antibodies), p90 (show CANX Antibodies) ribosomal S6 kinase (show RPS6KB1 Antibodies), PKA, or PKC (show PRRT2 Antibodies). LCP1 (show LCP1 Antibodies) phosphorylation increased filopodia formation.
Autosomal dominant polycystic kidney disease (ADPKD), uniquely increases urinary angiotensinogen (show AGT Antibodies) and renin (show REN Antibodies) 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 (show AGXT Antibodies).
results show that SNPs in the Hap (show SAFB Antibodies)-I of the hAGT gene promote high-fat diet-induced binding of transcription factors GR, CEBP-beta (show CEBPB Antibodies) and STAT3 (show STAT3 Antibodies), which lead to elevated expression of the hAGT gene in hepatic and adipose tissues
Angiotensinogen (show AGT Antibodies) import and subsequent trafficking to the mitochondria occurs in proximal kidney tubules.
Transgenic mice expressing human AGT (show AGXT Antibodies) in the subfornical organ AGT (show AGXT Antibodies) and possibly ANG I/ANG II (show AGT Antibodies) into the cerebral ventricles.
AngII could induce pulmonary injury by triggering endothelial barrier injury, and such process may be related to the dephosphorylation of Y685-VE-cadherin (show CDH5 Antibodies) and the endothelial skeletal rearrangement
Renin-angiotensin system transgenic mouse model suggests that renal injury in preeclampsia may be mediated through local VEGF.
adipocyte-derived Agt (show AGXT Antibodies) has essentially no contribution to the plasma concentration and no impact on blood pressure compared to liver-derived Agt (show AGXT Antibodies).
Lung ischemia-reperfusion injury causes a dysregulation of circulating Ang 2 (show ANGPT2 Antibodies) levels and plasma PREP (show PREP Antibodies) activity, although no direct link between both phenomena could be shown.
Inhibition of TLR4 (show TLR4 Antibodies) ameliorates AngII-impaired cavernosal relaxation, decreases TNF-alpha (show TNF Antibodies) levels, and restores Nitric Oxide bioavailability, demonstrating that TLR4 (show TLR4 Antibodies) partly mediates AngII-induced cavernosal dysfunction.
Our study is the first to show the important role of IL-6 (show IL6 Antibodies) in regulating cardiac pathogenesis via inflammation and apoptosis during AngII-induced hypertension. We also provide a novel link between IL-6 (show IL6 Antibodies)/STAT3 (show STAT3 Antibodies) and EndoG (show ENDOG Antibodies)/MEF2A (show MEF2A Antibodies) pathway that affects cardiac hypertrophy during AngII stimulation.
this study demonstrated that Ang II (show AGT Antibodies) could increase TRPC6 (show TRPC6 Antibodies) induced Ca(2 (show CA2 Antibodies)+) influx and enhance autophagy through increasing reactive oxygen species levels in podocytes, and autophagy could protect Ang II (show AGT Antibodies)-treated podocytes.
These results implied that AngII could effectively induce EpiCs to differentiate into vascular smooth muscle-like cells through the AT1 receptor (show AGTRAP Antibodies).
Results suggest the involvement of angiotensin II (Ang II), through its angiotensin type-1 receptor (AT1R (show AGTRAP Antibodies)) in the inflammation induced by Aah (show ASPH Antibodies) 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 (show ACE Antibodies) increased in streptozotocin-induced diabetic mice, which in turn led to an increase in Ang II (show AGT Antibodies) levels and tactile allodynia.
the beneficial actions of insulin (show INS Antibodies) in diabetic nephropathy appear to be mediated, in part, by suppressing renal Nrf2 (show NFE2L2 Antibodies) and Agt (show AGXT Antibodies) gene transcription and preventing Nrf2 (show NFE2L2 Antibodies) stimulation of Agt (show AGXT Antibodies) expression via hnRNP F (show HNRNPF Antibodies)/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