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抗Human Angiotensin II 抗体:
抗Rat (Rattus) Angiotensin II 抗体:
抗Mouse (Murine) Angiotensin II 抗体:
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 (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 (显示 AGT 抗体) 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 (显示 AGT 抗体) 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 (显示 AGT 抗体) 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 (显示 CDH5 抗体) and the endothelial skeletal rearrangement
Renin-angiotensin system transgenic mouse model suggests that renal injury in preeclampsia may be mediated through local VEGF.
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 (显示 AGT 抗体) 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 (显示 AGT 抗体)-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 (显示 AGT 抗体) 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.
Angiotensinogen (显示 AGT 抗体)-mediated downregulation of aquaporin 1 (显示 AQP1 抗体) and Nrf2 (显示 NFE2L2 抗体) signalling may play an important role in intrarenal renin (显示 REN 抗体)-angiotensin system-induced hypertension and kidney injury.
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