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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 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
Show all 2 Pubmed References
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.
AngII could induce pulmonary injury by triggering endothelial barrier injury, and such process may be related to the dephosphorylation of Y685-VE-cadherin (Montrer CDH5 Anticorps) and the endothelial skeletal rearrangement
Renin-angiotensin system transgenic mouse model suggests that renal injury in preeclampsia may be mediated through local VEGF.
endoplasmic reticulum stress induces apoptosis in human alveolar epithelial cells through mediation of unfolded protein response pathways, which in turn regulate the autocrine ANGII/ANG1 (Montrer ANGPT1 Anticorps)-7 system.
Angiotensin II stimulates PYY secretion, in turn inhibiting epithelial anion fluxes, thereby reducing net fluid secretion into the colonic lumen.
NOXs had two time-dependent reactions in response to Ang II (Montrer AGT Anticorps) stimulation via MAPK (Montrer MAPK1 Anticorps) pathwa
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.
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.
Angiotensinogen (Montrer AGT Anticorps)-mediated downregulation of aquaporin 1 (Montrer AQP1 Anticorps) and Nrf2 (Montrer NFE2L2 Anticorps) signalling may play an important role in intrarenal renin (Montrer REN Anticorps)-angiotensin system-induced hypertension and kidney injury.
This study suggests that deletion of AT2R decreases the expression of the beneficial ACE2/Ang-(1-7)/MasR.
an inverse correlation was found between Ang-(1 (Montrer ANGPT1 Anticorps)-7) level and tau hyperphosphorylation, a pathological hallmark of Alzheimer's disease, in cerebral cortex and hippocampus of SAMP8 mice.
The inhibition of pathological autophagy in the heart in response to chronic Ang II (Montrer AGT Anticorps) by Interleukin-10 (Montrer IL10 Anticorps), and its implications, has been described.
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