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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 (show ANGPT1 Proteins)-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 (show AGT Proteins) stimulation via MAPK (show MAPK1 Proteins) pathwa
increased Ang-II/Ang-(1 (show ANGPT1 Proteins)-7) ratios may lead to Ang-II (show AGT Proteins) over-activation and aggravate atherosclerosis progression.
urinary angiotensinogen (show AGT Proteins) could be a prognostic marker of the albuminuria reduction effects of olmesartan in patients with metabolic syndrome
AGT (show AGXT Proteins) expression is significantly upregulated in human masticatory mucosa during wound healing
Urinary angiotensinogen reflects intrarenal RAS status, and is of value to assess the severity of acute tubular necrosis .
Data suggest that enhanced survival of normal prostate epithelial cells (PNT1A cell line) in presence of either or both angiotensin II (Ang II) and relaxin 2 (RLN2 (show RLN1 Proteins)) appears to be associated with increased ratio of BCL2 (show BCL2 Proteins)/BAX (show BAX Proteins) messenger RNA expression; thus, Ang II (show AGT Proteins) and/or RLN2 (show RLN1 Proteins) appear to be involved in regulation of apoptosis in prostate epithelium.
increasing the serum levels of AngII increased the risk of acute myocardial infarction (AMI (show CFD Proteins)); the risk of AMI (show CFD Proteins) increased when the serum levels of AngII and KLK1 (show KLK1 Proteins) simultaneously increased; individuals with the combined genotypes of ACE (show ACE Proteins) DD and KLK1 (show KLK1 Proteins) GG showed increased risk of AMI (show CFD Proteins) compared with those with the combined genotypes of ACE (show ACE Proteins) II and KLK1 (show KLK1 Proteins) AA
genetic association study and meta-analysis revealed a significant association between M235T polymorphism of angiotensinogen (show AGT Proteins) and myocardial infarction risk
These results implied that AngII could effectively induce EpiCs to differentiate into vascular smooth muscle-like cells through the AT1 receptor (show AGTRAP Proteins).
Results suggest the involvement of angiotensin II (Ang II), through its angiotensin type-1 receptor (AT1R (show AGTRAP Proteins)) in the inflammation induced by Aah (show ASPH Proteins) venom, in the heart and the aorta.
expression of spinal ACE (show ACE Proteins) increased in streptozotocin-induced diabetic mice, which in turn led to an increase in Ang II (show AGT Proteins) levels and tactile allodynia.
the beneficial actions of insulin (show INS Proteins) in diabetic nephropathy appear to be mediated, in part, by suppressing renal Nrf2 (show NFE2L2 Proteins) and Agt (show AGXT Proteins) gene transcription and preventing Nrf2 (show NFE2L2 Proteins) stimulation of Agt (show AGXT Proteins) expression via hnRNP F (show HNRNPF Proteins)/K.
Angiotensinogen (show AGT Proteins)-mediated downregulation of aquaporin 1 (show AQP1 Proteins) and Nrf2 (show NFE2L2 Proteins) signalling may play an important role in intrarenal renin (show REN Proteins)-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 (show ANGPT1 Proteins)-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 (show AGT Proteins) by Interleukin-10 (show IL10 Proteins), and its implications, has been described.
These results suggest that increased formation of AT1R (show AGTRAP Proteins)-P2Y6R (show P2RY6 Proteins) heterodimers with age may increase the likelihood of hypertension induced by Ang II (show AGT Proteins).
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