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Autosomal dominant polycystic kidney disease (ADPKD), uniquely increases urinary angiotensinogen and renin (show REN Proteins) 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 Proteins).
results show that SNPs in the Hap (show SAFB Proteins)-I of the hAGT gene promote high-fat diet-induced binding of transcription factors GR, CEBP-beta (show CEBPB Proteins) and STAT3 (show STAT3 Proteins), which lead to elevated expression of the hAGT gene in hepatic and adipose tissues
Angiotensinogen import and subsequent trafficking to the mitochondria occurs in proximal kidney tubules.
Transgenic mice expressing human AGT (show AGXT Proteins) in the subfornical organ AGT (show AGXT Proteins) and possibly ANG I/ANG II 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 Proteins) 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 (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 stimulation via MAPK (show MAPK1 Proteins) pathwa
Snell, GHKRO, and PAPPA (show PAPPA Proteins)-KO mice express high levels of two proteins involved in DNA repair, O-6-methylguanine-DNA methyltransferase (MGMT (show MGMT Proteins)) and N-myc downstream-regulated gene 1 (NDRG1 (show NDRG1 Proteins)).
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 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-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 by Interleukin-10 (show IL10 Proteins), and its implications, has been described.
NADPH oxidase (show NOX1 Proteins) plays an important role in proMMP-2 expression and activation and MMP-2 (show MMP2 Proteins) mediated SMC (show DYM Proteins) proliferation occurs through the involvement of Spm (show NPC1 Proteins)-Cer (show CBLN1 Proteins)-S1P (show MBTPS1 Proteins) signaling axis under ANG II stimulation of PASMCs
The metabolism of angiotensin II (Ang II) to angiotensin III (Ang III) and its role in the vasorelaxation response in adrenal arteries are reported.
The study identified the serine phosphorylation (p-Ser (show SIGLEC1 Proteins)) sites induced by PKC-Beta (show PRKCB Proteins) activation or AGT, which inhibits insulin (show INS Proteins)-induced p-Tyr (show TYR Proteins) sites on IRS2 (show IRS2 Proteins) and its signals in endothelial cells.
Data suggest up-regulation of AGT in granulosa cells and of Ang II in follicular fluid during preovulatory period; Ang II appears to amplify stimulatory effects of luteinizing hormone on secretion of progesterone/prostaglandins by granulosa cells.
Data suggest that angiotensin II promotes uptake/accumulation of iron (non-transferrin (show Tf Proteins) bound iron) into vascular endothelial cells; such iron accumulation appears to depend on activation of angiotensin type 1 receptor and promotes oxidative stress.
a critical role for H(2)O(2) in angiotensin-II signaling to the endothelial cytoskeleton in a novel pathway that is critically dependent on MARCKS, Rac1, and c-Abl.
The objective of this study was to characterize the profiles of Ang-(1-7), MAS receptor, ACE(2), NEP and PEP during the ovulatory process in cattle.
Fetal adrenal cells in primary culture respond to angiotensin-II by increasing aldosterone production and aldosterone synthase (show CYP11B2 Proteins) [P450c18/CYP11B2 (show CYP11B2 Proteins)] activity.
ANG II inhibits bTREK-1 K(+) channels by a Ca(2+)-dependent mechanism that does not require the depletion of membrane-associated PIP(2).
prostaglandin F2alpha, endothelin-1 (show EDN1 Proteins), and angiotensin II may interact with each other in a local positive feedback manner to activate their secretion in the regressing corpus luteum, thus accelerating and completing luteolysis
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.
zC8A9.1 (angiotensinogen )
, serpin peptidase inhibitor, clade A, member 8
, alanine--glyoxylate aminotransferase
, angiotensin receptor 2
, serine--pyruvate aminotransferase, mitochondrial
, serine--pyruvate aminotransferase, peroxisomal
, serine-pyruvate aminotransferase
, serine:pyruvate aminotransferase SPT
, serine:pyruvate/alanine:glyoxylate aminotransferase
, alpha-1 antiproteinase, antitrypsin
, angiotensin I
, angiotensin II
, serine (or cysteine) proteinase inhibitor
, serpin A8
, angiotensin ll
, angiotensinogen (PAT)
, Serpin A8
, 6-O-methylguanine-DNA methyltransferase
, O-6-alkylguanine-DNA alkyltransferase
, methylated-DNA--protein-cysteine methyltransferase