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anti-Human Angiotensin I Converting Enzyme 1 Antikörper:
anti-Mouse (Murine) Angiotensin I Converting Enzyme 1 Antikörper:
anti-Rat (Rattus) Angiotensin I Converting Enzyme 1 Antikörper:
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Human Monoclonal Angiotensin I Converting Enzyme 1 Primary Antibody für FACS - ABIN2688976
Sinka, Biasch, Khazaal, Péault, Tavian: Angiotensin-converting enzyme (CD143) specifies emerging lympho-hematopoietic progenitors in the human embryo. in Blood 2012
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Human Monoclonal Angiotensin I Converting Enzyme 1 Primary Antibody für ELISA, WB - ABIN560577
Dekanty, Romero, Bertolin, Thomas, Leishman, Perez-Perri, Boccaccio, Wappner: Drosophila genome-wide RNAi screen identifies multiple regulators of HIF-dependent transcription in hypoxia. in PLoS genetics 2010
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Human Polyclonal Angiotensin I Converting Enzyme 1 Primary Antibody für CyTOF, FACS - ABIN4900150
Rockx, Sheahan, Donaldson, Harkema, Sims, Heise, Pickles, Cameron, Kelvin, Baric: Synthetic reconstruction of zoonotic and early human severe acute respiratory syndrome coronavirus isolates that produce fatal disease in aged mice. in Journal of virology 2007
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Mouse (Murine) Polyclonal Angiotensin I Converting Enzyme 1 Primary Antibody für CyTOF, FACS - ABIN4900261
Park, Bivona, Kobori, Seth, Chappell, Lazartigues, Harrison-Bernard: Major role for ACE-independent intrarenal ANG II formation in type II diabetes. in American journal of physiology. Renal physiology 2009
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Cat (Feline) Monoclonal Angiotensin I Converting Enzyme 1 Primary Antibody für IHC (fro), FACS - ABIN2478509
Danilov, Muzykantov, Martynov, Atochina, Sakharov IYu, Trakht, Smirnov: Lung is the target organ for a monoclonal antibody to angiotensin-converting enzyme. in Laboratory investigation; a journal of technical methods and pathology 1991
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Cat (Feline) Monoclonal Angiotensin I Converting Enzyme 1 Primary Antibody für FACS - ABIN2478516
Danilov, Jaspard, Churakova, Towbin, Savoie, Wei, Alhenc-Gelas: Structure-function analysis of angiotensin I-converting enzyme using monoclonal antibodies. Selective inhibition of the amino-terminal active site. in The Journal of biological chemistry 1994
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Human Polyclonal Angiotensin I Converting Enzyme 1 Primary Antibody für IF (p), IHC (p) - ABIN668631
Liu, Jiang, Zhang, Li, Li, Xie, Hu: Pulmonary artery denervation improves pulmonary arterial hypertension induced right ventricular dysfunction by modulating the local renin-angiotensin-aldosterone system. in BMC cardiovascular disorders 2016
Human Polyclonal Angiotensin I Converting Enzyme 1 Primary Antibody für IHC (p), WB - ABIN3042841
Yan, Shen: Aliskiren has chondroprotective efficacy in a rat model of osteoarthritis through suppression of the local renin-angiotensin system. in Molecular medicine reports 2018
Human Monoclonal Angiotensin I Converting Enzyme 1 Primary Antibody für FACS - ABIN4897256
Pelosi, Castelli, Martin-Padura, Bordoni, Santoro, Conigliaro, Cerio, De Santis Puzzonia, Marighetti, Biffoni, Alonzi, Amicone, Alcalay, Bertolini, Testa, Tripodi: Human haemato-endothelial precursors: cord blood CD34+ cells produce haemogenic endothelium. in PLoS ONE 2012
there is a statistically significant association with coronary artery disease disease(CAD) with DD genotypes in Turkish Cypriot population. The results indicated that ACE INDEL polymorphism is an important predictor of coronary artery disease in Turkish Cypriots. Although 47% of the studied Turkish Cypriot population carry the D allele (p=0.07), protocols should be developed for prevention strategies immediately.
Our results showed that the ACE I/D polymorphism was associated with IRPL, and that women that carried DD or ID genotypes had a 72% elevated risk of developing IRPL than women with the II genotype (OR (95% CI): 1.72 (1.181-2.5)). This odds ratio was found to be 1.61 in a case-control study and 1.28 in a meta-analysis study compiling 11 separate studies, which is consistent with our study data.
In primary hypertension,ACE ID/DD genotype may be associated with carotid atherosclerotic plaque.
ACE mutations were identified in three cases of renal tubular dysgenesis with microcolon abnormalities.
observed a positive correlation between Ndel1 activity and the total YMRS score in BD group (p = 0.030) and a positive correlation between ACE activity and Ham-D score
SNP-by-ACE-I /ARB interaction analyses uncovered loci that, if replicated, could have future implications for the prevention of arrhythmias.
For the ENOS (rs1799983) SNP, the genotype GT was positively associated with protection for development of the clinical form in DHF compared to dengue fever (OR=0.39, 95% CI = (0.13-1.14), p=0.0058) in codominant GG/GT/TT and overdominant model GT vs GG+TT (OR=0.35, 95% CI =(0.12-1.02), p=0.04).
in the sample studied there is no association of the I/D polymorphism of the ACE gene and Polycystic ovarian syndrome.
Angiotensin Converting Enzyme Insertion/Deletion Polymorphism is Associated with Breast Cancer Risk.
Polymorphism of angiotensin I converting enzyme gene are associated with multiple sclerosis risk.
The possible contribution of the I/D in the ACE gene, M235T and T174M in the angiotensinogen (AGT) gene polymorphisms with ischemic stroke in young Mexican population.
The results showed that rs4343 and rs4351 in ACE gene were risk factors of high level of pulse pressure.
The current study suggests that ACE polymorphism, particularly the homozygote variant (DD), might contribute to the risk of chronic obstructive pulmonary disease and chronic obstructive pulmonary disease with pulmonary hypertension among Asians.
ACE and ACTN3 genes do not have a role in determining power/strength performance of elite athletes.
The authors identified CD143 as a marker exclusively expressed on Mesenchymal stromal cells derived from adult tissue sources.
The study suggests that the ACE I/D polymorphism may contribute to mechanisms and intensity of DNA damage in hypertensive and normotensive individuals.
study found a significant association between the ACE insertion/deletion polymorphism and Kawasaki disease risk - meta-analysis
ACE gene I/D polymorphism was not associated with the risk of chronic obstructive pulmonary disease.
aerobic exercise training differentially affects the ACE C- and N-domain activities, and the N-domain activity is dependent on ACE polymorphism.
A significant difference was found between the patients with familial Mediterranean fever (FMF)-related amyloidosis and the control group as for genotype distribution of angiotensin converting enzyme (ACE) I/D variant. Based on these observations, the ACE I/D variant D/D genotypes implicate a possible risk in the FMF-related amyloidosis among Turkish population.
Endothelial ACE is a central regulator of the glomerular filtration rate while tubular ACE is a key player in the development of tubular injury and albuminuria in diabetic mice.
ACE expression/phosphorylation in the bone-marrow niche interface negatively regulates G-CSF-induced signaling and hematopoietic progenitor cell mobilization.
first evidence indicating the causation between ACE DD or B2R+9bp genotype and the increased risk for diabetic nephropathy, broadening our horizon about the role of genetic modulators in this disease.
a small increase in angiotensin-converting enzyme activity in diabetic animals leads to greater impairment of autonomic function, as demonstrated by increased sympathetic modulation and reduced cardiac vagal modulation along with increased renal expression of Ang II.
Resveratrol upregulated ACE2 and inhibited abdominal aortic aneurysm growth in a mouse model.
In mice with renal injury induced by L-NAME pretreatment, renal tubular epithelial ACE is essential for renal angiotensin II accumulation and salt-sensitive hypertension
Studied ACE role in peptide processing and for MHC class II antigen presentation; found ACE level effects efficiency of antigen presentation, and overexpression or inhibition of ACE alters the CD4(+) T-cell and antibody response.
ACE enhances the oxidative response and bactericidal activity of neutrophils.
this study shows that angiotensin-converting enzyme inhibitor captopril rescues mice from endotoxin-induced lethal hepatitis
Smooth muscle cell-derived ACE contributes to atherosclerosis, independent of circulating ACE activity and blood pressure.
Intestinal ACE shedding is increased by DSS-induced intestinal inflammation and parallels local corticosterone production. ACE product angiotensin II stimulates corticosterone formation in healthy intestine.
Renin angiostensin system contributes to 20-HETE-mediated microvascular remodeling in hypertension and that 20-HETE-driven microvascular remodeling independent of blood pressure elevation does not fully rely on ACE activity in the vascular endothelium.
angiotensin-converting enzyme has an essential role in hypertension induced by nitric oxide synthesis inhibition
Suggest that the ACE2-ACE imbalance plays an important role in the pathogenesis of severe acute pancreatitis and that pancreatic ACE2 is an important factor in determining the severity of SAP.
Show that tissue-specific targets are critical for the effects of miR-143/145 on smooth muscle differentiation and that angiotensin converting enzyme is one such target.
Tissue-specific expression of transgenic secreted ACE in vasculature can restore normal kidney functions, but not blood pressure, of Ace-/- mice.
ACE-null mice produce large numbers of myeloid-derived suppressor cells during chronic inflammation.
Myelomonocytic expression of catalytically active ACE, prevents cognitive decline in a murine model of Alzheimer disease.
ACE mediates angiotensin I-induced atherosclerosis, and ACE expression in leukocytes modestly contributes to atherosclerotic development in hypercholesterolemic mice.
TEX101 is a unique specific substrate for ACE that is essential for the production of fertile mouse spermatozoa
Maintaining the balance of the ACE2/ACE axis is important for inhibiting pulmonary apoptosis during acute pulmonary embolism.
The molecular model shows for the first time the relative orientation of the sACE catalytically active domains and their spatial distance.
Tissue Ang I-II conversion depends exclusively on the ACE C-domain, whereas both domains contribute to conversion by soluble ACE and to bradykinin degradation at tissue sites.
The contributions of the C-domain and N-domain differ between DDs and IIs genotype
Corneal cells express ACE, AT(1) and AT(2)receptors. ACE inhibitor enalapril decreased corneal angiogenesis in VEGF-induced corneal neovascularization. ACE inhibitors may be novel therapy to treat corneal angiogenesis.
Angiotensin-converting enzyme (ACE) residues encompassing 343 to 655 of the germinal form are required for its cleavage-secretion.
a portion of the extracellular region of tACE (containing its catalytic site) is released from bovine sperm during capacitation, and tACE activity may be required for sperm capacitation.
The results indicate that the two active sites within bovine somatic ACE exhibit strong negative cooperativity.
Phorbol 12-myristate 13-acetate (PMA) induced Egr-1 and ATF-2 binding to the ACE promoter, whereas Ets-1 binding was suppressed by PMA.
Precompetition angiotensin converting enzyme (ACE) activity in endurance horses competing in an 80 km event was not associated with either finishing position or heart rates, indicating that the enzyme is not a good predictor of performance.
This research investigated angiotensin-converting enzyme activity in the plasma of racehorses and demonstrated that its activity is increased in horses with higher degrees of hemorrhage and is a promising biomarker for pulmonary hemorrhage.
These results show an increase in ACE activity up to fatigue and a return to baseline values at 30 min post exercise.
The aim of this study was to investigate the correlation between angiotensin-converting enzyme (ACE) activity in the equine endometrium and the degree of endometrial periglandular fibrosis.
This gene encodes an enzyme involved in catalyzing the conversion of angiotensin I into a physiologically active peptide angiotensin II. Angiotensin II is a potent vasopressor and aldosterone-stimulating peptide that controls blood pressure and fluid-electrolyte balance. This enzyme plays a key role in the renin-angiotensin system. Many studies have associated the presence or absence of a 287 bp Alu repeat element in this gene with the levels of circulating enzyme or cardiovascular pathophysiologies. Multiple alternatively spliced transcript variants encoding different isoforms have been identified, and two most abundant spliced variants encode the somatic form and the testicular form, respectively, that are equally active.
, angiotensin I converting enzyme (peptidyl-dipeptidase A) 1
, angiotensin I converting enzyme peptidyl-dipeptidase A 1 transcript
, angiotensin converting enzyme, somatic isoform
, angiotensin-converting enzyme
, dipeptidyl carboxypeptidase 1
, dipeptidyl carboxypeptidase I
, kininase II
, peptidase P
, testicular ECA
, dipeptidyl peptidase
, Dipeptidyl carboxypeptidase 1 (Angiotensin I-converting enzyme)
, angiotensin 1 converting enzyme 1
, angiotensin I converting enzyme 1
, angiotensin I-converting enzyme (Dipeptidyl carboxypeptidase 1)
, Angiotensin-converting enzyme, testis-specific isoform
, dipeptidyl carboxy peptidase 1
, angiotensin converting enzyme
, angiotensin-I converting enzyme
, peptidyl dipeptidase i
, angiotensin I-converting enzyme
, Dipeptidyl carboxypeptidase I
, Kininase II
, LOW QUALITY PROTEIN: angiotensin-converting enzyme