anti-AGT (AGT) Antikörper

Human Angiotensinogen (serpin Peptidase Inhibitor, Clade A, Member 8) (AGT) Interaktionspartner

1. AGT M235T gene polymorphism may represent a genetic modifier to vascular morbidities in Egyptian patients with sickle cell disease.

2. Patients with heart failure and type 2 diabetes mellitus with AGT TT + MT genotype had a higher level of ST2 and a higher probability of unfavorable cardiovascular events during 24 months of observation compared with MM genotype carriers.

3. Unfavorable genotype of polymorphic variants of candidate gene participating in endothelial dysfunction AGT (Thrl74Met and Met23SThr) was associated with changes in levels of their active substances in individuals exposed to mercury.

4. Angiotensin 1-7 can modulate cell adhesion and epithelial-mesenchymal transition of normal prostate epithelial cells.

5. These findings reveal the critical role of hypoxia in producing local angiotensin II by a lactate-chymase-dependent mechanism and highlight the importance of local angiotensin II in regulating radioresistance of hypoxic tumor cells.

6. The reduced urinary AGT/creatinine in Autralian Indigenous pregnant women may reflect subclinical renal dysfunction which limits the ability of the kidney to maintain sodium balance and could indicate an increased risk of pregnancy complications and/or future renal disease.

7. ACE2 and other enzymes can form ANG-(1-7) directly or indirectly from either the decapeptide ANG I or from ANG II. [review]

8. The ACE and AGT gene polymorphisms are not associated with the progress of diabetes developing into retinopathy in Chinese patients with type 2 diabetes.

9. AGT M235T and T174M variants contribute to an increased risk of developing preeclampsia (PE), and for M235T to PE severity.

10. Data, including data using network analysis, suggest that angiotensinogen (AGT), mitogen-activated protein kinase-14 (MAPK14), and prothrombin (F2) in placental villous tissues are core factors in early embryonic development; these studies involved proteomics and bioinformatics analysis of altered protein expression in placental villous tissue from early recurrent miscarriage patients in comparison to control tissues.

11. The AGT (M235T) gene polymorphism do not seem to have a significant effect on the development of clinical properties or cardiovascular comordities of acromegalic patients.

12. Angiotensin II has a role in increasing glomerular permeability by beta-arrestin mediated nephrin endocytosis

13. After donor nephrectomy, increasing uAGT levels can be the result of activation of the intrarenal renin-angiotensin system affecting the compensatory changes in the remaining kidney.

14. M235T polymorphism of the AGT gene seems unrelated to the development or the clinical course of endometriosis.

15. AGT missense polymorphisms are not associated with diabetic nephropathy in our subset of Slovenian type 2 diabetes mellitus patients

16. Association of AGT single nucleotide polymorphism rs3789678 and gestational hypertension in Chinese population.

17. Data suggest that angiotensin-II plays important role in development of albuminuria, particularly in subjects with impaired glucose metabolism; here, serum angiotensin-II levels are up-regulated in subjects with prediabetes and type 2 diabetes as compared to subjects with normal glucose metabolism; elevated serum angiotensin-II level may be early biomarker or risk factor for vasculitis.

18. The T allele of AGT may play a role in the pathogenesis of preeclampsia in South African Black women.

19. These data indicate that Ang II-AT2R regulates human bone marrow MSC migration by signaling through the FAK and RhoA/Cdc42 pathways.

20. Data suggest that up-regulaton of Ang-(1-7) levels in follicular fluid correlates with increases in number of mature oocytes retrieved upon ovarian stimulation in preparation for in vitro fertilization.

Mouse (Murine) Angiotensinogen (serpin Peptidase Inhibitor, Clade A, Member 8) (AGT) Interaktionspartner

1. Our data demonstrate a previously unknown synergy between AngII and BAFF in inducing IL-10 production by B cells, resulting in atheroprotection.

2. Mean blood pressure, plasma Ang II level, and myocardium malondialdehyde (MDA) content of angiotensinogen-renin (AGT-REN) double transgenic hypertension (dTH) mice were higher than those in wild-type (WT) mice.

3. ANG II is up-regulated in serum and heart tissues of mice with EAM and that ANG II significantly drives monocyte/macrophage infiltration through the C-C chemokine receptor 2/5 (CCR2/5) axis.

4. results established that A20 is involved in the renoprotective effect by calcitriol via negatively modulating the NF-kappaB pathway and necroptotic pathway in AngII-induced renal injury.

5. NLRP3 gene deletion attenuates Ang II-induced NLRP3 inflammasome activation, phenotypic transformation from a contractile phenotype to a synthetic phenotype and proliferation in primary mice Vascular Smooth Muscle Cells.

6. adipocyte-derived Agt has essentially no contribution to the plasma concentration and no impact on blood pressure compared to liver-derived Agt.

7. Lung ischemia-reperfusion injury causes a dysregulation of circulating Ang 2 levels and plasma PREP activity, although no direct link between both phenomena could be shown.

8. Inhibition of TLR4 ameliorates AngII-impaired cavernosal relaxation, decreases TNF-alpha levels, and restores Nitric Oxide bioavailability, demonstrating that TLR4 partly mediates AngII-induced cavernosal dysfunction.

9. Our study is the first to show the important role of IL-6 in regulating cardiac pathogenesis via inflammation and apoptosis during AngII-induced hypertension. We also provide a novel link between IL-6/STAT3 and EndoG/MEF2A pathway that affects cardiac hypertrophy during AngII stimulation.

10. this study demonstrated that Ang II could increase TRPC6 induced Ca(2+) influx and enhance autophagy through increasing reactive oxygen species levels in podocytes, and autophagy could protect Ang II-treated podocytes.

11. These results implied that AngII could effectively induce EpiCs to differentiate into vascular smooth muscle-like cells through the AT1 receptor.

12. Results suggest the involvement of angiotensin II (Ang II), through its angiotensin type-1 receptor (AT1R) in the inflammation induced by Aah venom, in the heart and the aorta.

13. Angiotensin II stimulates PYY secretion, in turn inhibiting epithelial anion fluxes, thereby reducing net fluid secretion into the colonic lumen.

14. expression of spinal ACE increased in streptozotocin-induced diabetic mice, which in turn led to an increase in Ang II levels and tactile allodynia.

15. the beneficial actions of insulin in diabetic nephropathy appear to be mediated, in part, by suppressing renal Nrf2 and Agt gene transcription and preventing Nrf2 stimulation of Agt expression via hnRNP F/K.

16. Angiotensinogen-mediated downregulation of aquaporin 1 and Nrf2 signalling may play an important role in intrarenal renin-angiotensin system-induced hypertension and kidney injury.

17. This study suggests that deletion of AT2R decreases the expression of the beneficial ACE2/Ang-(1-7)/MasR.

18. an inverse correlation was found between Ang-(1-7) level and tau hyperphosphorylation, a pathological hallmark of Alzheimer's disease, in cerebral cortex and hippocampus of SAMP8 mice.

19. The inhibition of pathological autophagy in the heart in response to chronic Ang II by Interleukin-10, and its implications, has been described.

20. These results suggest that increased formation of AT1R-P2Y6R heterodimers with age may increase the likelihood of hypertension induced by Ang II.

Zebrafish Angiotensinogen (serpin Peptidase Inhibitor, Clade A, Member 8) (AGT) Interaktionspartner

1. Angiotensin-II promotes Na+ uptake in larval in acidic and ion-poor water.

Pig (Porcine) Angiotensinogen (serpin Peptidase Inhibitor, Clade A, Member 8) (AGT) Interaktionspartner

1. In conclusion, endothelial vWF knockdown prevented angiotensin II-induced ET-1 upregulation through attenuation of NOX-mediated O2- production.

2. In remodeled myocardium angiotensin II (ANGII) and endothelin contribute to coronary resistance vessel tone in nolinear redundant fashion.

3. Cyclosporine-A stimulates angiotensin I/II secretion by kidney glomeruli.

Cow (Bovine) Angiotensinogen (serpin Peptidase Inhibitor, Clade A, Member 8) (AGT) Interaktionspartner

1. Data suggest that intra-adrenal metabolism of Ang II to Ang III is required for zona glomerulosa cell-mediated relaxation of adrenal arterioles but not for aldosterone secretion.

2. NADPH oxidase plays an important role in proMMP-2 expression and activation and MMP-2 mediated SMC proliferation occurs through the involvement of Spm-Cer-S1P signaling axis under ANG II stimulation of PASMCs

3. The metabolism of angiotensin II (Ang II) to angiotensin III (Ang III) and its role in the vasorelaxation response in adrenal arteries are reported.

4. The study identified the serine phosphorylation (p-Ser) sites induced by PKC-Beta activation or AGT, which inhibits insulin-induced p-Tyr sites on IRS2 and its signals in endothelial cells.

5. 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.

6. Data suggest that angiotensin II promotes uptake/accumulation of iron (non-transferrin bound iron) into vascular endothelial cells; such iron accumulation appears to depend on activation of angiotensin type 1 receptor and promotes oxidative stress.

7. 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.

8. 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.

9. The AngII concentration increased in the follicular fluid of the dominant follicle.

10. Fetal adrenal cells in primary culture respond to angiotensin-II by increasing aldosterone production and aldosterone synthase [P450c18/CYP11B2] activity.

11. ANG II inhibits bTREK-1 K(+) channels by a Ca(2+)-dependent mechanism that does not require the depletion of membrane-associated PIP(2).

12. prostaglandin F2alpha, endothelin-1, 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

13. Suggest that the activation of a local positive feedback mechanism in the corpus luteum among ET-1, Ang II and PGF2alpha might play a functional role in the paracrine modulation of luteolytic cascade.

14. MKP-1 is the specific phosphatase induced by AngII and involved in the negative feedback mechanism ensuring adequate ERK1/2-mediated aldosterone production in response to the hormone.

15. In normotensive donors with a normal compensatory response to nephrectomy, baseline renal reactivity to angiotensin II can influence renal and glomerular hemodynamics 1 year after nephrectomy.