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These data indicate that Ang II (zeige AGT Proteine)-AT2R (zeige AGTR2 Proteine) regulates human bone marrow MSC (zeige MSC Proteine) migration by signaling through the FAK (zeige PTK2 Proteine) and RhoA (zeige RHOA Proteine)/Cdc42 (zeige CDC42 Proteine) pathways.
Data suggest that up-regulaton of Ang-(1 (zeige ANGPT1 Proteine)-7) levels in follicular fluid correlates with increases in number of mature oocytes retrieved upon ovarian stimulation in preparation for in vitro fertilization.
Urinary angiotensinogen (zeige AGT Proteine) and renin (zeige REN Proteine) excretion are elevated in CKD patients. Both parameters are negatively associated with eGFR (zeige EGFR Proteine) and these associations are independent of urinary albumin (zeige ALB Proteine) excretion
Reduced IL-18 (zeige IL18 Proteine) serum concentration in children after HUS (zeige CFH Proteine) with no difference in its urine concentration may indicate a loss of the protective effects of this cytokine on renal function due to previously occurred HUS (zeige CFH Proteine).
Angiotensin II initiates hepatocyte epithelial-mesenchymal transition by activating the NOX-derived H2O2-mediated NLRP3 (zeige NLRP3 Proteine) inflammasome/IL-1ss/Smad (zeige SMAD1 Proteine) circuit.
present study has demonstrated, for the first time, that high glucose augments AGT (zeige AGXT Proteine) in human RPTCs through HNF-5, which provides a potential therapeutic target for diabetic nephropathy
AngII-dependent phosphorylation of LCP1 (zeige LCP1 Proteine) in cultured podocytes was mediated by the kinases ERK (zeige EPHB2 Proteine), p90 (zeige CANX Proteine) ribosomal S6 kinase (zeige RPS6KB1 Proteine), PKA, or PKC (zeige PRRT2 Proteine). LCP1 (zeige LCP1 Proteine) phosphorylation increased filopodia formation.
Autosomal dominant polycystic kidney disease (ADPKD), uniquely increases urinary angiotensinogen (zeige AGT Proteine) and renin (zeige REN Proteine) 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 (zeige AGXT Proteine).
results show that SNPs in the Hap (zeige SAFB Proteine)-I of the hAGT gene promote high-fat diet-induced binding of transcription factors GR, CEBP-beta (zeige CEBPB Proteine) and STAT3 (zeige STAT3 Proteine), which lead to elevated expression of the hAGT gene in hepatic and adipose tissues
NLRP3 (zeige NLRP3 Proteine) gene deletion attenuates Ang II (zeige AGT Proteine)-induced NLRP3 (zeige NLRP3 Proteine) inflammasome activation, phenotypic transformation from a contractile phenotype to a synthetic phenotype and proliferation in primary mice Vascular Smooth Muscle Cells.
adipocyte-derived Agt (zeige AGXT Proteine) has essentially no contribution to the plasma concentration and no impact on blood pressure compared to liver-derived Agt (zeige AGXT Proteine).
Lung ischemia-reperfusion injury causes a dysregulation of circulating Ang 2 (zeige ANGPT2 Proteine) levels and plasma PREP (zeige PREP Proteine) activity, although no direct link between both phenomena could be shown.
Inhibition of TLR4 (zeige TLR4 Proteine) ameliorates AngII-impaired cavernosal relaxation, decreases TNF-alpha (zeige TNF Proteine) levels, and restores Nitric Oxide bioavailability, demonstrating that TLR4 (zeige TLR4 Proteine) partly mediates AngII-induced cavernosal dysfunction.
Our study is the first to show the important role of IL-6 (zeige IL6 Proteine) in regulating cardiac pathogenesis via inflammation and apoptosis during AngII-induced hypertension. We also provide a novel link between IL-6 (zeige IL6 Proteine)/STAT3 (zeige STAT3 Proteine) and EndoG (zeige ENDOG Proteine)/MEF2A (zeige MEF2A Proteine) pathway that affects cardiac hypertrophy during AngII stimulation.
this study demonstrated that Ang II (zeige AGT Proteine) could increase TRPC6 (zeige TRPC6 Proteine) induced Ca(2 (zeige CA2 Proteine)+) influx and enhance autophagy through increasing reactive oxygen species levels in podocytes, and autophagy could protect Ang II (zeige AGT Proteine)-treated podocytes.
These results implied that AngII could effectively induce EpiCs to differentiate into vascular smooth muscle-like cells through the AT1 receptor (zeige AGTRAP Proteine).
Results suggest the involvement of angiotensin II (Ang II), through its angiotensin type-1 receptor (AT1R (zeige AGTRAP Proteine)) in the inflammation induced by Aah (zeige ASPH Proteine) 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 (zeige ACE Proteine) increased in streptozotocin-induced diabetic mice, which in turn led to an increase in Ang II (zeige AGT Proteine) levels and tactile allodynia.
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