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           Search results for: MOUSE ANTI HUMAN ANGIOTENSIN I_II_III-MONOCLONAL ANTIBODY   

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#28813513   2017/08/16 Save this To Up

Validation of commercial Mas receptor antibodies for utilization in Western Blotting, immunofluorescence and immunohistochemistry studies.

Mas receptor (MasR) is a G protein-coupled receptor proposed as a candidate for mediating the angiotensin (Ang)-converting enzyme 2-Ang (1-7) protective axis of renin-angiotensin system. Because the role of this receptor is not definitively clarified, determination of MasR tissue distribution and expression levels constitutes a critical knowledge to fully understanding its function. Commercially available antibodies have been widely employed for MasR protein localization and quantification, but they have not been adequately validated. In this study, we carried on an exhaustive evaluation of four commercial MasR antibodies, following previously established criteria. Western Blotting (WB) and immunohistochemistry studies starting from hearts and kidneys from wild type (WT) mice revealed that antibodies raised against different MasR domains yielded different patterns of reactivity. Furthermore, staining patterns appeared identical in samples from MasR knockout (MasR-KO) mice. We verified by polymerase chain reaction analysis that the MasR-KO mice used were truly deficient in this receptor as MAS transcripts were undetectable in either heart or kidney from this animal model. In addition, we evaluated the ability of the antibodies to detect the human c-myc-tagged MasR overexpressed in human embryonic kidney cells. Three antibodies were capable of detecting the MasR either by WB or by immunofluorescence, reproducing the patterns obtained with an anti c-myc antibody. In conclusion, although three of the selected antibodies were able to detect MasR protein at high expression levels observed in a transfected cell line, they failed to detect this receptor in mice tissues at physiological expression levels. As a consequence, validated antibodies that can recognize and detect the MasR at physiological levels are still lacking.

1384 related Products with: Validation of commercial Mas receptor antibodies for utilization in Western Blotting, immunofluorescence and immunohistochemistry studies.

IGF-1R Signaling Phospho- Insulin Receptor Phospho- Nuclear Membrane Receptor T-Cell Receptor Signaling Rabbit Anti-Human Androge Goat Anti-Human Androgen Goat Anti-Human Bradykini Goat Anti-Human, Mouse Ca Goat Anti-Rat CCKA Recept Goat Anti- Dopamine recep Goat Anti- EP1 receptor P Goat Anti-Human EP4 prost

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#28610597   2017/06/14 Save this To Up

Anti-connective tissue growth factor (CTGF/CCN2) monoclonal antibody attenuates skin fibrosis in mice models of systemic sclerosis.

Systemic sclerosis (SSc) is characterized by fibrosis of the skin and internal organs. Although the involvement of connective tissue growth factor (CTGF/CCN2) has been well-documented in SSc fibrosis, the therapeutic potential of targeting CTGF in SSc has not been fully investigated. Our aim was to examine the therapeutic potential of CTGF blockade in a preclinical model of SSc using two approaches: smooth muscle cell fibroblast-specific deletion of CTGF (CTGF knockout (KO)) or a human anti-CTGF monoclonal antibody, FG-3019.

2490 related Products with: Anti-connective tissue growth factor (CTGF/CCN2) monoclonal antibody attenuates skin fibrosis in mice models of systemic sclerosis.

Human Connective Tissue G Rat monoclonal anti mouse Rat monoclonal anti mouse Rat monoclonal anti mouse Rat monoclonal anti mouse Rat monoclonal anti mouse Anti C Reactive Protein A Anti AGO2 Human, Monoclon Anti AGO2 Mouse, Monoclon Anti AGO2 Human, Monoclon Anti AGO2 Mouse, Monoclon Anti 3 DG imidazolone Mon

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#28577747   2017/06/04 Save this To Up

[Membranous nephropathy: Pathophysiology and natural history].

Membranous nephropathy is a major cause of nephrotic syndrome in adults, with various etiologies and outcomes. One third of patients enter spontaneous remission with blockade of the renin-angiotensin system, one third develop a persistent nephrotic syndrome, while another third of patients develop end-stage kidney disease and 40% of them relapse after kidney transplantation. Treatment of membranous nephropathy remains controversial. Immunosuppressive therapy is only recommended in case of renal function deterioration or persistent nephrotic syndrome after 6months of renin-angiotensin system blockade. Therefore, delayed immunosuppressive treatments may lead to significant and potentially irreversible complications. For long, no biological markers could predict clinical outcome and guide therapy. The discovery of autoantibodies to the phospholipase A2 receptor (PLA2R1) in 2009, and to the thrombospondin type 1 domain containing 7A (THSD7A) in 2014 in respectively 70 and 5% of patients with membranous nephropathy were major breakthroughs. The passive infusion of human anti-THSD7A antibodies in mouse induces proteinuria and membranous nephropathy. The identification of these antigens has allowed developing diagnostic and prognostic tests. High anti-PLA2R1 titers at time of diagnosis predict a poor renal outcome. Anti-PLA2R1 antibodies can bind at least three different domains of PLA2R1. Epitope spreading with binding of two or three of these antigenic domains is associated with active membranous nephropathy and poor renal survival. These new tools could help us to monitor disease severity and to predict renal prognosis for a better selection of patients that should benefit of early immunosuppressive therapy.

1542 related Products with: [Membranous nephropathy: Pathophysiology and natural history].

CELLKINES Natural Human I TCGF (Natural T Cell Grow Androgen Receptor (Phosph Androgen Receptor (Phosph Rabbit Anti-Human Androge Rabbit Anti-Human Androge Androgen Receptor (Ab 650 96-well FastPlate Low Pro AZD-3514 Mechanisms: Andr 17β-Acetoxy-2α-bromo-5 (5α,16β)-N-Acetyl-16-[2 (5α,16β)-N-Acetyl-16-ac

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#28433633   2017/04/23 Save this To Up

Angiotensin-converting enzyme 2 is a potential therapeutic target for EGFR-mutant lung adenocarcinoma.

EGFR-mutant lung adenocarcinomas contain a subpopulation of cells that have undergone epithelial-to-mesenchymal transition and can grow independently of EGFR. To kill these cancer cells, we need a novel therapeutic approach other than EGFR inhibitors. If a molecule is specifically expressed on the cell surface of such EGFR-independent EGFR-mutant cancer cells, it can be a therapeutic target. We found that a mesenchymal EGFR-independent subline derived from HCC827 cells, an EGFR-mutant lung adenocarcinoma cell line, expressed angiotensin-converting enzyme 2 (ACE2) to a greater extent than its parental cells. ACE2 was also expressed at least partially in most of the primary EGFR-mutant lung adenocarcinomas examined, and the ACE2 expression level in the cancer cells was much higher than that in normal lung epithelial cells. In addition, we developed an anti-ACE2 mouse monoclonal antibody (mAb), termed H8R64, that was internalized by ACE2-expressing cells. If an antibody-drug conjugate consisting of a humanized mAb based on H8R64 and a potent anticancer drug were produced, it could be effective for the treatment of EGFR-mutant lung adenocarcinomas.

2700 related Products with: Angiotensin-converting enzyme 2 is a potential therapeutic target for EGFR-mutant lung adenocarcinoma.

PERMANENT AQUEOUS MOUNTIN MOUSE ANTI CANINE DISTEMP MOUSE ANTI HUMAN CD15, Pr MOUSE ANTI HUMAN CD15, Pr MOUSE ANTI BOVINE ROTAVIR MOUSE ANTI BORRELIA BURGD NATIVE HUMAN PROLACTIN, P RABBIT ANTI GSK3 BETA (pS Lung adenocarcinoma (grad 10x ELISA WASH BUFFER, Pr 10X PHOSPHATE BUFFERED SA Human Angiotensin convert

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#28330983   2017/03/23 Save this To Up

γδ T Cells Mediate Angiotensin II-Induced Hypertension and Vascular Injury.

Innate antigen-presenting cells and adaptive immune T cells have been implicated in the development of hypertension. However, the T-lymphocyte subsets involved in the pathophysiology of hypertension remain unclear. A small subset of innate-like T cells expressing the γδ T cell receptor (TCR) rather than the αβ TCR could play a role in the initiation of the immune response in hypertension. We aimed to determine whether angiotensin (Ang) II caused kinetic changes in γδ T cells; deficiency in γδ T cells blunted Ang II-induced hypertension, vascular injury, and T-cell activation; and γδ T cells are associated with human hypertension.

2359 related Products with: γδ T Cells Mediate Angiotensin II-Induced Hypertension and Vascular Injury.

ELISA Agtr2,Angiotensin I Anti-Angiotensin II Recep Anti Angiotensin II Recep Anti-Angiotensin II Recep Angiotensin II Type 1 (AT Angiotensin II Type 1 (AT Angiotensin II Type 1 (AT Angiotensin II Type 1 (AT Topoisomerase II; Clone Topoisomerase II; Clone Topoisomerase II; Clone Angiotensin II [Lys0](Hum

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#28069388   2017/01/10 Save this To Up

Vitamin D receptor deficit induces activation of renin angiotensin system via SIRT1 modulation in podocytes.

Vitamin D receptor (VDR) deficient status has been shown to be associated with the activation of renin angiotensin system (RAS). We hypothesized that lack of VDR would enhance p53 expression in podocytes through down regulation of SIRT1; the former would enhance the transcription of angiotensinogen (Agt) and angiotensinogen II type 1 receptor (AT1R) leading to the activation of RAS. Renal tissues of VDR mutant (M) mice displayed increased expression of p53, Agt, renin, and AT1R. In vitro studies, VDR knockout podocytes not only displayed up regulation p53 but also displayed enhanced expression of Agt, renin and AT1R. VDR deficient podocytes also displayed an increase in mRNA expression for p53, Agt, renin, and AT1R. Interestingly, renal tissues of VDR-M as well as VDR heterozygous (h) mice displayed attenuated expression of deacetylase SIRT1. Renal tissues of VDR-M mice showed acetylation of p53 at lysine (K) 382 residues inferring that enhanced p53 expression in renal tissues could be the result of ongoing acetylation, a consequence of SIRT1 deficient state. Notably, podocytes lacking SIRT1 not only showed acetylation of p53 at lysine (K) 382 residues but also displayed enhanced p53 expression. Either silencing of SIRT1/VDR or treatment with high glucose enhanced podocyte PPAR-y expression, whereas, immunoprecipitation (IP) of their lysates with anti-retinoid X receptor (RXR) antibody revealed presence of PPAR-y. It appears that either the deficit of SIRT1 has de-repressed expression of PPAR-y or enhanced podocyte expression of PPAR-y (in the absence of VDR) has contributed to the down regulation of SIRT1.

1072 related Products with: Vitamin D receptor deficit induces activation of renin angiotensin system via SIRT1 modulation in podocytes.

EIA for Quantitative Dete EtBr Destaining Bag Kit A Human integrin aVb3, affi Digestive system tissue a Goat Anti- Dopamine recep Digestive system carcinom DiscoveryPak™ Receptor Male genitourinary system Anti-AICDA(Activation-ind Anti AICDA(Activation ind SensiTek HRP Anti-Mouse SensiTek HRP Anti-Rabbit

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#27975141   2016/12/15 Save this To Up

Glucose and angiotensin II-derived endothelial extracellular vesicles regulate endothelial dysfunction via ERK1/2 activation.

In various diseases, including diabetes, extracellular vesicles (EVs) have been detected in circulation and tissues. EVs are small membrane vesicles released from various cell types under varying conditions. Recently, endothelial cell-derived EVs (EEVs) were identified as a marker of endothelial dysfunction in diabetes, but the ensuing mechanisms remain poorly understood. In this study, we dissected the ensuing pathways with respect to nitric oxide (NO) production under the condition of type 2 diabetes. Human umbilical vein endothelial cells (HUVECs) were stimulated with glucose alone and with glucose in combination with angiotensin II (Ang II) for 48 h. In supernatants from glucose + Ang II-stimulated HUVECs, release of EEVs was assessed using Western blotting with an anti-CD144 antibody. EEV release was significantly increased after stimulation of HUVECs, and high glucose + Ang II-derived EEVs impaired ACh-induced vascular relaxation responses and NO production in mice aortic rings. Furthermore, high glucose + Ang II-derived EEVs induced ERK1/2 signalling and decreased endothelial NO synthase (eNOS) protein expression in mice aortas. Furthermore, in the presence of the MEK/ERK1/2 inhibitor PD98059, high glucose plus Ang II treatment stimulated EEVs in HUVECs and those EEVs prevented the impairments of ACh-induced relaxation and NO production in mice aortas. These data strongly indicate that high glucose and Ang II directly affect endothelial cells and the production of EEVs; the resultant EEVs aggravate endothelial dysfunction by regulating eNOS protein levels and ERK1/2 signalling in mice aortas.

2503 related Products with: Glucose and angiotensin II-derived endothelial extracellular vesicles regulate endothelial dysfunction via ERK1/2 activation.

CD31, Endothelial Cell; CD34, Endothelial Cell; Human Vascular Endothelia Human Vascular Endothelia Mouse Vascular Endothelia Mouse Vascular Endothelia Rat Vascular Endothelial Human Cord Blood CD34+ Ce Recombinant Human Vascula Rabbit Anti-Human Angiote Anti-Angiotensin II Recep Anti Angiotensin II Recep

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#27001297   2016/04/14 Save this To Up

Angiotensin II Stimulation of Cardiac Hypertrophy and Functional Decompensation in Osteoprotegerin-Deficient Mice.

Circulating and myocardial expressions of receptor activator of nuclear factor-κb ligand and osteoprotegerin are activated in heart failure; however, it remains to be determined their pathophysiological roles on left ventricular structure and function in interaction with renin-angiotensin system. We conducted experiments using 8-week-old osteoprotegerin(-/-) mice and receptor activator of nuclear factor-κb ligand-transgenic mice to assess whether they affect the angiotensin II-induced left ventricular remodeling. Subcutaneous infusion of angiotensin II to osteoprotegerin(-/-) mice progressed the eccentric hypertrophy, resulting in left ventricular systolic dysfunction for 28 days, and this was comparable with wild-type mice, showing concentric hypertrophy, irrespective of equivalent elevation of systolic blood pressure. The structural alteration was associated with reduced interstitial fibrosis, decreased procollagen α1 and syndecan-1 expressions, and the increased number of apoptotic cells in the left ventricle, compared with wild-type mice. In contrast, angiotensin II infusion to the receptor activator of nuclear factor-κb ligand-transgenic mice revealed the concentric hypertrophy with preserved systolic contractile function. Intraperitoneal administration of human recombinant osteoprotegerin, but not subcutaneous injection of anti-receptor activator of nuclear factor-κb ligand antibody, to the angiotensin II-infused osteoprotegerin(-/-) mice for 28 days ameliorated the progression of heart failure without affecting systolic blood pressure. These results underscore the biological activity of osteoprotegerin in preserving myocardial structure and function during the angiotensin II-induced cardiac hypertrophy, independent of receptor activator of nuclear factor-κb ligand activity. In addition, the antiapoptotic and profibrotic actions of osteoprotegerin that emerged from our data might be involved in the mechanisms.

2923 related Products with: Angiotensin II Stimulation of Cardiac Hypertrophy and Functional Decompensation in Osteoprotegerin-Deficient Mice.

Angiotensin II [Lys0](Hum anti HSV (II) gB IgG1 (mo Human Insulin-like Growth EMAP-II Inhibitor Z-ASTD- EMAP-II Inhibitor Z-ASTD- EMAP II Inhibitor Z ASTD EMAP II Inhibitor Z ASTD EIA for Quantitative Dete IKK-ε Kinase Inhibitor I IKK-ε Kinase Inhibitor I HIV I&II test strip, Infe Beta Amyloid (1 40) ELISA

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#26771341   2016/01/28 Save this To Up

ATRQβ-001 vaccine prevents atherosclerosis in apolipoprotein E-null mice.

Angiotensin II (AngII) type 1 receptor (AT1R) blockers have been proved to reduce atherosclerosis. Previously, we have invented ATRQβ-001 vaccine which showed a desirable blocking effect for AT1R. The purpose of this study was to investigate whether ATRQβ-001 vaccine would prevent atherosclerosis in apolipoprotein E-null (ApoE-/-) mice.

1464 related Products with: ATRQβ-001 vaccine prevents atherosclerosis in apolipoprotein E-null mice.

Goat Anti-Human Apolipopr Goat Anti- apolipoprotein Atherosclerosis (Human) A Atherosclerosis (Mouse) A Goat Anti- apolipoprotein Interleukin-34 IL34 (N-t Interleukin-34 IL34 anti Apolipoprotein B (Apo B) Sterile filtered goat se Sterile filtered goat se Sterile filtered mouse s Sterile filtered rat ser

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#26509357   2016/01/15 Save this To Up

Genetic variants in the renin-angiotensin system predict response to bevacizumab in cancer patients.

Currently, there are no predictive biomarkers for anti-angiogenic strategies in cancer, but response to anti-angiogenic drugs is associated with development of hypertension secondary to treatment. Therefore, this study explored the clinical relevance of genetic polymorphisms in some components of the renin-angiotensin system (RAS).

1695 related Products with: Genetic variants in the renin-angiotensin system predict response to bevacizumab in cancer patients.

Top five cancer tissue ar FDA Standard Frozen Tissu FDA Standard Frozen Tissu FDA Standard Frozen Tissu FDA Standard Frozen Tissu Male genitourinary system Oral squamous cell cancer Head & Neck cancer test t Top 4 types of cancer (co Top 4 types of cancer (co Rat TGF-beta-inducible ea Rat TGF-beta-inducible ea

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