anti at1r antibody  (Alomone Labs)


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    Name:
    Anti Angiotensin II Receptor Type 1 extracellular Antibody
    Description:
    Anti Angiotensin II Receptor Type 1 extracellular Antibody AAR 011 is a highly specific antibody directed against an epitope of the human protein The antibody can be used in western blot immunohistochemistry immunocytochemistry and indirect flow cytometry applications It has been designed to recognize AT1 receptor from rat mouse and human samples
    Catalog Number:
    AAR-011
    Price:
    397.0
    Category:
    Primary Antibody
    Applications:
    Immunocytochemistry, Immunofluorescence, Indirect Flow Cytometry, Immunohistochemistry, Live Cell Imaging, Western Blot
    Purity:
    Affinity purified on immobilized antigen.
    Immunogen:
    Synthetic peptide
    Size:
    25 mcl
    Antibody Type:
    Polyclonal Primary Antibodies
    Format:
    Lyophilized Powder
    Host:
    Rabbit
    Isotype:
    Rabbit IgG
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    Structured Review

    Alomone Labs anti at1r antibody
    Anti Angiotensin II Receptor Type 1 extracellular Antibody
    Anti Angiotensin II Receptor Type 1 extracellular Antibody AAR 011 is a highly specific antibody directed against an epitope of the human protein The antibody can be used in western blot immunohistochemistry immunocytochemistry and indirect flow cytometry applications It has been designed to recognize AT1 receptor from rat mouse and human samples
    https://www.bioz.com/result/anti at1r antibody/product/Alomone Labs
    Average 93 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    anti at1r antibody - by Bioz Stars, 2021-10
    93/100 stars

    Images

    1) Product Images from "Soluble RAGE attenuates AngII-induced endothelial hyperpermeability by disrupting HMGB1-mediated crosstalk between AT1R and RAGE"

    Article Title: Soluble RAGE attenuates AngII-induced endothelial hyperpermeability by disrupting HMGB1-mediated crosstalk between AT1R and RAGE

    Journal: Experimental & Molecular Medicine

    doi: 10.1038/s12276-019-0312-5

    Schematic diagram of signal transduction pathways involved in Ang II-induced endothelial hyperpermeability via AT1R/RAGE/mDia1/Src/β-catenin/VE-cadherin. a As Ang II binds to and stimulates AT1R, the expression and secretion of HMGB1 can be increased by NF-κB activation. NF-κB-mediated expression of proinflammatory molecules, including RAGE itself, can occur. HMGB1 binds to RAGE, which can induce RAGE-mediated activation of Src/β-catenin/VE-cadherin via mDia1. b Blockade of RAGE activation by sRAGE attenuates the Ang II-induced increase in endothelial hyperpermeability by inhibiting RAGE-mediated signaling pathways
    Figure Legend Snippet: Schematic diagram of signal transduction pathways involved in Ang II-induced endothelial hyperpermeability via AT1R/RAGE/mDia1/Src/β-catenin/VE-cadherin. a As Ang II binds to and stimulates AT1R, the expression and secretion of HMGB1 can be increased by NF-κB activation. NF-κB-mediated expression of proinflammatory molecules, including RAGE itself, can occur. HMGB1 binds to RAGE, which can induce RAGE-mediated activation of Src/β-catenin/VE-cadherin via mDia1. b Blockade of RAGE activation by sRAGE attenuates the Ang II-induced increase in endothelial hyperpermeability by inhibiting RAGE-mediated signaling pathways

    Techniques Used: Transduction, Expressing, Activation Assay

    Importance of the AT1R-RAGE axis in Ang II-induced endothelial hyperpermeability in HUVECs. a Changes in the phosphorylation of VE-cadherin (Y731), Src (Tyr416), and β-catenin (Ser552) in HUVECs following transfection with RAGE siRNA and treatment with Ang II. Expression values were normalized to those of VE-cadherin, Src, and β-catenin ( n = 4 for each lane). b Immunocytochemistry of VE-cadherin (green) and DAPI (nuclei, blue), as examined under a confocal microscope (white scale bars: 50 μm in merged images and 20 μm in magnified images; ×400 magnification). The main images were selected from representative regions. c HUVECs transfected with siRNA targeting RAGE or with scrambled sequences were incubated for 72 h and were then stimulated with Ang II for 6 h. TEER was measured every 2 h. *** p
    Figure Legend Snippet: Importance of the AT1R-RAGE axis in Ang II-induced endothelial hyperpermeability in HUVECs. a Changes in the phosphorylation of VE-cadherin (Y731), Src (Tyr416), and β-catenin (Ser552) in HUVECs following transfection with RAGE siRNA and treatment with Ang II. Expression values were normalized to those of VE-cadherin, Src, and β-catenin ( n = 4 for each lane). b Immunocytochemistry of VE-cadherin (green) and DAPI (nuclei, blue), as examined under a confocal microscope (white scale bars: 50 μm in merged images and 20 μm in magnified images; ×400 magnification). The main images were selected from representative regions. c HUVECs transfected with siRNA targeting RAGE or with scrambled sequences were incubated for 72 h and were then stimulated with Ang II for 6 h. TEER was measured every 2 h. *** p

    Techniques Used: Transfection, Expressing, Immunocytochemistry, Microscopy, Incubation

    HMGB1 is an important mediator of AT1R-RAGE signaling. HUVECs were treated with Ang II in the absence or presence of losartan for 4 h. a HMGB1 release in supernatants was measured by ELISA and western blotting ( n = 4 for each lane). b , c HUVECs were incubated with Ang II in the presence or absence of anti-HMGB1-neutralizing antibody (50 ng/ml) for 4 h and analyzed by western blotting. The relative values of AT1R, RAGE, and mDia1 expression were normalized to that of GAPDH ( n = 4 for each lane). The relative values of phospho-VE-cadherin expression were normalized to that of VE-cadherin ( n = 3 for each lane). The values are presented as the means ± SEMs. * p
    Figure Legend Snippet: HMGB1 is an important mediator of AT1R-RAGE signaling. HUVECs were treated with Ang II in the absence or presence of losartan for 4 h. a HMGB1 release in supernatants was measured by ELISA and western blotting ( n = 4 for each lane). b , c HUVECs were incubated with Ang II in the presence or absence of anti-HMGB1-neutralizing antibody (50 ng/ml) for 4 h and analyzed by western blotting. The relative values of AT1R, RAGE, and mDia1 expression were normalized to that of GAPDH ( n = 4 for each lane). The relative values of phospho-VE-cadherin expression were normalized to that of VE-cadherin ( n = 3 for each lane). The values are presented as the means ± SEMs. * p

    Techniques Used: Enzyme-linked Immunosorbent Assay, Western Blot, Incubation, Expressing

    RAGE regulates Ang II-induced endothelial hyperpermeability via mDia1. a HUVECs were transfected with mDia1 siRNA and cultured in the presence of Ang II for an additional 4 h. Western blot analysis was performed to observe changes in phospho-Src, phospho-β-catenin, and phospho-VE-cadherin protein expression ( n = 4 for each lane). b Changes in mDia1 protein levels in HUVECs following transfection with RAGE siRNA, as determined by western blotting. Expression was normalized to that of GAPDH ( n = 3 for each lane). c Changes in mDia1 mRNA expression in HUVECs following transfection with RAGE siRNA, as determined by RT-PCR. Expression was normalized to that of the 18S rRNA gene ( n = 4 for each lane). d HUVECs were treated with Ang II and the NF-κB inhibitor (5 μg/ml) alone or in combination for 4 h. Protein levels of AT1R, RAGE, and mDia1 in cell lysates were determined by western blotting. Expression was normalized to that of GAPDH ( n = 4 for each lane). The values are presented as the means ± SEMs. * p
    Figure Legend Snippet: RAGE regulates Ang II-induced endothelial hyperpermeability via mDia1. a HUVECs were transfected with mDia1 siRNA and cultured in the presence of Ang II for an additional 4 h. Western blot analysis was performed to observe changes in phospho-Src, phospho-β-catenin, and phospho-VE-cadherin protein expression ( n = 4 for each lane). b Changes in mDia1 protein levels in HUVECs following transfection with RAGE siRNA, as determined by western blotting. Expression was normalized to that of GAPDH ( n = 3 for each lane). c Changes in mDia1 mRNA expression in HUVECs following transfection with RAGE siRNA, as determined by RT-PCR. Expression was normalized to that of the 18S rRNA gene ( n = 4 for each lane). d HUVECs were treated with Ang II and the NF-κB inhibitor (5 μg/ml) alone or in combination for 4 h. Protein levels of AT1R, RAGE, and mDia1 in cell lysates were determined by western blotting. Expression was normalized to that of GAPDH ( n = 4 for each lane). The values are presented as the means ± SEMs. * p

    Techniques Used: Transfection, Cell Culture, Western Blot, Expressing, Reverse Transcription Polymerase Chain Reaction

    Related Articles

    Western Blot:

    Article Title: Blunting of cardioprotective actions of estrogen in female rodent heart linked to altered expression of cardiac tissue chymase and ACE2
    Article Snippet: .. Immunoblots were probed using antibodies for AT1R (1:250; Alomone Labs, Jerusalem, Israel) and the Ang-(1-7) receptor, Mas (1:5000; Alomone Labs, Ltd, Jerusalem, Israel). ..

    Triple Immunostaining:

    Article Title: Kinin B1 Receptor Blockade Prevents Angiotensin II-induced Neuroinflammation and Oxidative Stress in Primary Hypothalamic Neurons
    Article Snippet: .. Triple immunostaining was performed with specific validated antibodies for detection of AT1R (#AAR-011, lot AN2002, Alomone labs, 1:200 dilution) and B1R (#ABR-011, lot An-01, Alomone labs, 1:200 dilution) coupled with MAP2 and DAPI staining. ..

    Staining:

    Article Title: Kinin B1 Receptor Blockade Prevents Angiotensin II-induced Neuroinflammation and Oxidative Stress in Primary Hypothalamic Neurons
    Article Snippet: .. Triple immunostaining was performed with specific validated antibodies for detection of AT1R (#AAR-011, lot AN2002, Alomone labs, 1:200 dilution) and B1R (#ABR-011, lot An-01, Alomone labs, 1:200 dilution) coupled with MAP2 and DAPI staining. ..

    Incubation:

    Article Title: Angiotensin-converting enzyme 2 inhibits high-mobility group box 1 and attenuates cardiac dysfunction post-myocardial ischemia
    Article Snippet: .. The membranes were blocked with 5 % nonfat milk solution in Tris-buffered saline (TBS) with 0.1 % Tween-20 for 1 h. Then the membranes were incubated either with primary antibody for multiple proteins including ACE2, ACE, AT1 R, AT2 R, MasR, HMGB1, and CD68 overnight at 4 °C [ACE2 goat polyclonal antibody (1:500; R & D systems), ACE rabbit polyclonal antibody (1:500; Santa Cruz Biotechnology), AT1 R rabbit polyclonal antibody (1:500; Alomone Labs), AT2 R rabbit polyclonal antibody (1:400; Alomone Labs), MasR rabbit polyclonal antibody (1:200; Alomone Labs); HMGB1 rabbit polyclonal antibody (1:1000; Abcam); CD68 mouse monoclonal antibody (1:1000; Biolegend)]. ..

    Article Title: Connexin37‐Dependent Mechanisms Selectively Contribute to Modulate Angiotensin II‐Mediated Hypertension
    Article Snippet: .. The membranes were then incubated overnight at 4°C with 1 of the following primary antibodies: rabbit polyclonal antibodies against AT1R (Alomone labs, AAR‐011, 1:1000), AT2R (Alomone labs, AAR‐012, 1:1000), MLC2 (Cell Signaling, 3672, 1:1000), P‐MLC2 (Cell Signaling, 3674, 1:1000), ERK (Cell Signaling, 4695, 1:1000), P‐ERK (Cell Signaling, 9101, 1:1000), AKT (Cell Signaling, 9272S, 1:1000), Cx40 (Chemicon, AB1726; 1:250), Cx37 (Biotrend Chemikalien, Cx37A11‐A; 1:500), Cx43 (Cell Signaling, 3512S, 1:500) or Cx45 (Millipore, AB1745, 1:500); mouse monoclonal antibodies against eNOS (BD Biosciences, 610297, 1:500), PeNOS (BD Biosciences, 612392, 1:500), P‐AKT (Cell Signaling, 4051, 1:500), and α‐tubulin (Sigma‐Aldrich, T5168; 1:2500). ..

    Article Title: Angiotensin-converting enzyme 2 inhibits high-mobility group box 1 and attenuates cardiac dysfunction post-myocardial ischemia
    Article Snippet: .. The membranes were blocked with 5 % nonfat milk solution in Tris-buffered saline (TBS) with 0.1 % Tween-20 for 1 h. Then the membranes were incubated either with primary antibody for multiple proteins including ACE2, ACE, AT1 R, AT2 R, MasR, HMGB1, and CD68 overnight at 4 °C [ACE2 goat polyclonal antibody (1:500; R & D systems), ACE rabbit polyclonal antibody (1:500; Santa Cruz Biotechnology), AT1 R rabbit polyclonal antibody (1:500; Alomone Labs), AT2R rabbit polyclonal antibody (1:400; Alomone Labs), MasR rabbit polyclonal antibody (1:200; Alomone Labs); HMGB1 rabbit polyclonal antibody (1:1000; Abcam); CD68 mouse monoclonal antibody (1:1000; Biolegend)]. ..

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    Alomone Labs anti at1r antibody
    Schematic diagram of signal transduction pathways involved in Ang II-induced endothelial hyperpermeability via <t>AT1R/RAGE/mDia1/Src/β-catenin/VE-cadherin.</t> a As Ang II binds to and stimulates AT1R, the expression and secretion of HMGB1 can be increased by NF-κB activation. NF-κB-mediated expression of proinflammatory molecules, including RAGE itself, can occur. HMGB1 binds to RAGE, which can induce RAGE-mediated activation of Src/β-catenin/VE-cadherin via mDia1. b Blockade of RAGE activation by sRAGE attenuates the Ang II-induced increase in endothelial hyperpermeability by inhibiting RAGE-mediated signaling pathways
    Anti At1r Antibody, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/anti at1r antibody/product/Alomone Labs
    Average 93 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    anti at1r antibody - by Bioz Stars, 2021-10
    93/100 stars
      Buy from Supplier

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    Schematic diagram of signal transduction pathways involved in Ang II-induced endothelial hyperpermeability via AT1R/RAGE/mDia1/Src/β-catenin/VE-cadherin. a As Ang II binds to and stimulates AT1R, the expression and secretion of HMGB1 can be increased by NF-κB activation. NF-κB-mediated expression of proinflammatory molecules, including RAGE itself, can occur. HMGB1 binds to RAGE, which can induce RAGE-mediated activation of Src/β-catenin/VE-cadherin via mDia1. b Blockade of RAGE activation by sRAGE attenuates the Ang II-induced increase in endothelial hyperpermeability by inhibiting RAGE-mediated signaling pathways

    Journal: Experimental & Molecular Medicine

    Article Title: Soluble RAGE attenuates AngII-induced endothelial hyperpermeability by disrupting HMGB1-mediated crosstalk between AT1R and RAGE

    doi: 10.1038/s12276-019-0312-5

    Figure Lengend Snippet: Schematic diagram of signal transduction pathways involved in Ang II-induced endothelial hyperpermeability via AT1R/RAGE/mDia1/Src/β-catenin/VE-cadherin. a As Ang II binds to and stimulates AT1R, the expression and secretion of HMGB1 can be increased by NF-κB activation. NF-κB-mediated expression of proinflammatory molecules, including RAGE itself, can occur. HMGB1 binds to RAGE, which can induce RAGE-mediated activation of Src/β-catenin/VE-cadherin via mDia1. b Blockade of RAGE activation by sRAGE attenuates the Ang II-induced increase in endothelial hyperpermeability by inhibiting RAGE-mediated signaling pathways

    Article Snippet: Anti-AT1R antibody (AAR-011) was purchased from Alomone Labs (Hadassah Ein Kerem, Israel).

    Techniques: Transduction, Expressing, Activation Assay

    Importance of the AT1R-RAGE axis in Ang II-induced endothelial hyperpermeability in HUVECs. a Changes in the phosphorylation of VE-cadherin (Y731), Src (Tyr416), and β-catenin (Ser552) in HUVECs following transfection with RAGE siRNA and treatment with Ang II. Expression values were normalized to those of VE-cadherin, Src, and β-catenin ( n = 4 for each lane). b Immunocytochemistry of VE-cadherin (green) and DAPI (nuclei, blue), as examined under a confocal microscope (white scale bars: 50 μm in merged images and 20 μm in magnified images; ×400 magnification). The main images were selected from representative regions. c HUVECs transfected with siRNA targeting RAGE or with scrambled sequences were incubated for 72 h and were then stimulated with Ang II for 6 h. TEER was measured every 2 h. *** p

    Journal: Experimental & Molecular Medicine

    Article Title: Soluble RAGE attenuates AngII-induced endothelial hyperpermeability by disrupting HMGB1-mediated crosstalk between AT1R and RAGE

    doi: 10.1038/s12276-019-0312-5

    Figure Lengend Snippet: Importance of the AT1R-RAGE axis in Ang II-induced endothelial hyperpermeability in HUVECs. a Changes in the phosphorylation of VE-cadherin (Y731), Src (Tyr416), and β-catenin (Ser552) in HUVECs following transfection with RAGE siRNA and treatment with Ang II. Expression values were normalized to those of VE-cadherin, Src, and β-catenin ( n = 4 for each lane). b Immunocytochemistry of VE-cadherin (green) and DAPI (nuclei, blue), as examined under a confocal microscope (white scale bars: 50 μm in merged images and 20 μm in magnified images; ×400 magnification). The main images were selected from representative regions. c HUVECs transfected with siRNA targeting RAGE or with scrambled sequences were incubated for 72 h and were then stimulated with Ang II for 6 h. TEER was measured every 2 h. *** p

    Article Snippet: Anti-AT1R antibody (AAR-011) was purchased from Alomone Labs (Hadassah Ein Kerem, Israel).

    Techniques: Transfection, Expressing, Immunocytochemistry, Microscopy, Incubation

    HMGB1 is an important mediator of AT1R-RAGE signaling. HUVECs were treated with Ang II in the absence or presence of losartan for 4 h. a HMGB1 release in supernatants was measured by ELISA and western blotting ( n = 4 for each lane). b , c HUVECs were incubated with Ang II in the presence or absence of anti-HMGB1-neutralizing antibody (50 ng/ml) for 4 h and analyzed by western blotting. The relative values of AT1R, RAGE, and mDia1 expression were normalized to that of GAPDH ( n = 4 for each lane). The relative values of phospho-VE-cadherin expression were normalized to that of VE-cadherin ( n = 3 for each lane). The values are presented as the means ± SEMs. * p

    Journal: Experimental & Molecular Medicine

    Article Title: Soluble RAGE attenuates AngII-induced endothelial hyperpermeability by disrupting HMGB1-mediated crosstalk between AT1R and RAGE

    doi: 10.1038/s12276-019-0312-5

    Figure Lengend Snippet: HMGB1 is an important mediator of AT1R-RAGE signaling. HUVECs were treated with Ang II in the absence or presence of losartan for 4 h. a HMGB1 release in supernatants was measured by ELISA and western blotting ( n = 4 for each lane). b , c HUVECs were incubated with Ang II in the presence or absence of anti-HMGB1-neutralizing antibody (50 ng/ml) for 4 h and analyzed by western blotting. The relative values of AT1R, RAGE, and mDia1 expression were normalized to that of GAPDH ( n = 4 for each lane). The relative values of phospho-VE-cadherin expression were normalized to that of VE-cadherin ( n = 3 for each lane). The values are presented as the means ± SEMs. * p

    Article Snippet: Anti-AT1R antibody (AAR-011) was purchased from Alomone Labs (Hadassah Ein Kerem, Israel).

    Techniques: Enzyme-linked Immunosorbent Assay, Western Blot, Incubation, Expressing

    RAGE regulates Ang II-induced endothelial hyperpermeability via mDia1. a HUVECs were transfected with mDia1 siRNA and cultured in the presence of Ang II for an additional 4 h. Western blot analysis was performed to observe changes in phospho-Src, phospho-β-catenin, and phospho-VE-cadherin protein expression ( n = 4 for each lane). b Changes in mDia1 protein levels in HUVECs following transfection with RAGE siRNA, as determined by western blotting. Expression was normalized to that of GAPDH ( n = 3 for each lane). c Changes in mDia1 mRNA expression in HUVECs following transfection with RAGE siRNA, as determined by RT-PCR. Expression was normalized to that of the 18S rRNA gene ( n = 4 for each lane). d HUVECs were treated with Ang II and the NF-κB inhibitor (5 μg/ml) alone or in combination for 4 h. Protein levels of AT1R, RAGE, and mDia1 in cell lysates were determined by western blotting. Expression was normalized to that of GAPDH ( n = 4 for each lane). The values are presented as the means ± SEMs. * p

    Journal: Experimental & Molecular Medicine

    Article Title: Soluble RAGE attenuates AngII-induced endothelial hyperpermeability by disrupting HMGB1-mediated crosstalk between AT1R and RAGE

    doi: 10.1038/s12276-019-0312-5

    Figure Lengend Snippet: RAGE regulates Ang II-induced endothelial hyperpermeability via mDia1. a HUVECs were transfected with mDia1 siRNA and cultured in the presence of Ang II for an additional 4 h. Western blot analysis was performed to observe changes in phospho-Src, phospho-β-catenin, and phospho-VE-cadherin protein expression ( n = 4 for each lane). b Changes in mDia1 protein levels in HUVECs following transfection with RAGE siRNA, as determined by western blotting. Expression was normalized to that of GAPDH ( n = 3 for each lane). c Changes in mDia1 mRNA expression in HUVECs following transfection with RAGE siRNA, as determined by RT-PCR. Expression was normalized to that of the 18S rRNA gene ( n = 4 for each lane). d HUVECs were treated with Ang II and the NF-κB inhibitor (5 μg/ml) alone or in combination for 4 h. Protein levels of AT1R, RAGE, and mDia1 in cell lysates were determined by western blotting. Expression was normalized to that of GAPDH ( n = 4 for each lane). The values are presented as the means ± SEMs. * p

    Article Snippet: Anti-AT1R antibody (AAR-011) was purchased from Alomone Labs (Hadassah Ein Kerem, Israel).

    Techniques: Transfection, Cell Culture, Western Blot, Expressing, Reverse Transcription Polymerase Chain Reaction

    Angiotensin II-induced neuroinflammation and oxidative stress are mediated by kinin B1R. Mouse neonatal primary hypothermic neurons express both B1R and AT1R. Ang II stimulation of neurons increased expression of B1R, which in turn increased resulted in upregulation of Nox2 and Nox4 expression, and NF-κB activation, and ultimately leading to expression of pro-inflammatory cytokine production. Treatment with R715, the specific B1R antagonist blunted angiotensin II-induced neuroinflammation and oxidative stress by reducing Nox gene expression and attenuating NF-κB activation.

    Journal: Cellular and molecular neurobiology

    Article Title: Kinin B1 Receptor Blockade Prevents Angiotensin II-induced Neuroinflammation and Oxidative Stress in Primary Hypothalamic Neurons

    doi: 10.1007/s10571-019-00778-1

    Figure Lengend Snippet: Angiotensin II-induced neuroinflammation and oxidative stress are mediated by kinin B1R. Mouse neonatal primary hypothermic neurons express both B1R and AT1R. Ang II stimulation of neurons increased expression of B1R, which in turn increased resulted in upregulation of Nox2 and Nox4 expression, and NF-κB activation, and ultimately leading to expression of pro-inflammatory cytokine production. Treatment with R715, the specific B1R antagonist blunted angiotensin II-induced neuroinflammation and oxidative stress by reducing Nox gene expression and attenuating NF-κB activation.

    Article Snippet: Triple immunostaining was performed with specific validated antibodies for detection of AT1R (#AAR-011, lot AN2002, Alomone labs, 1:200 dilution) and B1R (#ABR-011, lot An-01, Alomone labs, 1:200 dilution) coupled with MAP2 and DAPI staining.

    Techniques: Expressing, Activation Assay

    Kinin B1 receptor gene expression is induced by angiotensin II in primary hypothalamic neurons. Brightfield photomicrograph showing primary mouse hypothalamic neuron cultures grown for 5 days (A). Representative photomicrographs showing immunofluorescence staining for neuron specific marker microtubule associated protein 2, MAP-2 (Red) and glial cell specific marker glial fibrillary acidic protein, GFAP (Green) in primary neurons cultured for 10 days without Ara-C (B) and with Ara-C (C) treatment. Treatment with Ara-C for 14 days resulted in primarily predominant neuronal population as stained for neuronal marker MAP-2 (D). Triple immunostaining revealed that Kinin B1R (E) and AT1R (F) are expressed in primary hypothalamic neurons. Treatment with angiotensin II (300 nM) induced increase in B1R mRNA levels in cultured neurons, measured by real time PCR (G). (n=4 independent cultures/group). Statistical significance: One-way ANOVA followed by Tukey’s multiple comparisons test. * p

    Journal: Cellular and molecular neurobiology

    Article Title: Kinin B1 Receptor Blockade Prevents Angiotensin II-induced Neuroinflammation and Oxidative Stress in Primary Hypothalamic Neurons

    doi: 10.1007/s10571-019-00778-1

    Figure Lengend Snippet: Kinin B1 receptor gene expression is induced by angiotensin II in primary hypothalamic neurons. Brightfield photomicrograph showing primary mouse hypothalamic neuron cultures grown for 5 days (A). Representative photomicrographs showing immunofluorescence staining for neuron specific marker microtubule associated protein 2, MAP-2 (Red) and glial cell specific marker glial fibrillary acidic protein, GFAP (Green) in primary neurons cultured for 10 days without Ara-C (B) and with Ara-C (C) treatment. Treatment with Ara-C for 14 days resulted in primarily predominant neuronal population as stained for neuronal marker MAP-2 (D). Triple immunostaining revealed that Kinin B1R (E) and AT1R (F) are expressed in primary hypothalamic neurons. Treatment with angiotensin II (300 nM) induced increase in B1R mRNA levels in cultured neurons, measured by real time PCR (G). (n=4 independent cultures/group). Statistical significance: One-way ANOVA followed by Tukey’s multiple comparisons test. * p

    Article Snippet: Triple immunostaining was performed with specific validated antibodies for detection of AT1R (#AAR-011, lot AN2002, Alomone labs, 1:200 dilution) and B1R (#ABR-011, lot An-01, Alomone labs, 1:200 dilution) coupled with MAP2 and DAPI staining.

    Techniques: Expressing, Immunofluorescence, Staining, Marker, Cell Culture, Acetylene Reduction Assay, Triple Immunostaining, Real-time Polymerase Chain Reaction

    Renal cortical expression of angiotensin type 1 receptors (AT1R). A : mRNA expression of the AT1R is reduced in the renal cortex of SLE mice compared with controls, measured by real-time quantitative PCR (SLE: n = 10, control: n = 11 ). B : AT1R protein

    Journal: American Journal of Physiology - Regulatory, Integrative and Comparative Physiology

    Article Title: Blood pressure and renal hemodynamic responses to acute angiotensin II infusion are enhanced in a female mouse model of systemic lupus erythematosus

    doi: 10.1152/ajpregu.00079.2011

    Figure Lengend Snippet: Renal cortical expression of angiotensin type 1 receptors (AT1R). A : mRNA expression of the AT1R is reduced in the renal cortex of SLE mice compared with controls, measured by real-time quantitative PCR (SLE: n = 10, control: n = 11 ). B : AT1R protein

    Article Snippet: Rabbit polyclonal anti-AT1R antibody (1:500; Alomone Laboratories, Jerusalem, Israel), rabbit polyclonal anti-AT2R antibody (1:500; Alomone Laboratories), goat polyclonal anti-renin (1:250; Santa Cruz Biotechnology, Santa Cruz, CA) and mouse anti-β-actin (1:5,000; Abcam, Cambridge, MA) were used.

    Techniques: Expressing, Mouse Assay, Real-time Polymerase Chain Reaction

    Expression of Ang II receptors in satellite cells. A , AT1R expression in satellite cells. CD45 − /Sca-1 − /CD11b − /CD31 − /CD34 + /Integrin α7 + cells were sorted from gastrocnemius muscles, and AT1R expression on these cells

    Journal: The Journal of Biological Chemistry

    Article Title: Angiotensin II Inhibits Satellite Cell Proliferation and Prevents Skeletal Muscle Regeneration *

    doi: 10.1074/jbc.M112.449074

    Figure Lengend Snippet: Expression of Ang II receptors in satellite cells. A , AT1R expression in satellite cells. CD45 − /Sca-1 − /CD11b − /CD31 − /CD34 + /Integrin α7 + cells were sorted from gastrocnemius muscles, and AT1R expression on these cells

    Article Snippet: Antibodies used for flow cytometry included anti-mouse CD45 (clone 30-F11, APC conjugate, eBioscience, 1:1600), anti-mouse Sca-1 (clone D7, APC conjugate, eBioscience, 1:800), anti-mouse CD11b (clone M1/70, APC-conjugate, eBioscience, 1:800), anti-mouse CD31 (clone MEC 13.3, APC-conjugate, BD Biosciences, 1:200), anti-mouse CD34 (clone RAM34, PE-conjugate or Alexa Fluor 700 conjugate, BD Biosciences or eBioscience, respectively, 1:50), anti-mouse integrinα7 (clone 3C12, FITC conjugate, MBL, 1:20), and anti-mouse AT1R (rabbit polyclonal, Alomone Labs, 1:100).

    Techniques: Expressing