at1r  (Alomone Labs)


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    Alomone Labs at1r
    At1r, 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/at1r/product/Alomone Labs
    Average 93 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    at1r - by Bioz Stars, 2022-07
    93/100 stars

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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, 2022-07
    93/100 stars
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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

    Expression of AT1-R and AT2-R in the peri-implantation endometrium. Representative micrographs of immunohistochemical stain of (a) AT1-R in fertile control, (b) AT1-R in RM, (c) AT2-R in fertile control, (d) AT2-R in RM. Magnification ×200. Scale bar = 200 μm. AT1-R, angiotensin type 1 receptor; AT2-R, angiotensin type 2 receptor; BV, blood vessels; GE, glandular epithelium; LE, luminal epithelium; RM, recurrent miscarriage; ST, stroma.

    Journal: Therapeutic Advances in Endocrinology and Metabolism

    Article Title: The role of the renin–angiotensin system in regulating endometrial neovascularization during the peri-implantation period: literature review and preliminary data

    doi: 10.1177/2042018820920560

    Figure Lengend Snippet: Expression of AT1-R and AT2-R in the peri-implantation endometrium. Representative micrographs of immunohistochemical stain of (a) AT1-R in fertile control, (b) AT1-R in RM, (c) AT2-R in fertile control, (d) AT2-R in RM. Magnification ×200. Scale bar = 200 μm. AT1-R, angiotensin type 1 receptor; AT2-R, angiotensin type 2 receptor; BV, blood vessels; GE, glandular epithelium; LE, luminal epithelium; RM, recurrent miscarriage; ST, stroma.

    Article Snippet: The primary antibodies were rabbit anti-human angiotensin II receptor type-1 polyclonal antibody (AAR-011, Alomone Labs, Jerusalem, Israel) at a dilution of 1:100 and rabbit anti-human angiotensin II type 2 receptor antibody (ab19134, AbCam, UK) at a dilution of 1:100.

    Techniques: Expressing, Immunohistochemistry, Staining

    The possible pathways of Ang II-mediated angiogenesis. ANG II stimulates the generation of ROS through membrane NAD(P)H oxidases in VSMCs after binding to AT1-R. ROS are involved in many Ang II mediated effects, including production of HIF-1α in vascular cells, activation of p38MAPK, and transcription factor NF-kB. Interactions between Ang II and ROS are critical in vascular physiology and pathology in terms of regulating vascular structure and functions. Ang-Tie could also trigger the production of ROS through NADPH oxidase. Ang II, angiotensin II; Ang-Tie, angiopoietin-Tie; AT1-R, angiotensin II type 1 (AT1) receptor; HIF-1α, hypoxia inducible factor-1α; NF-kB, nuclear factor kappa AB; ROS, reactive oxygen species; VSMCs, vascular smooth muscle cells.

    Journal: Therapeutic Advances in Endocrinology and Metabolism

    Article Title: The role of the renin–angiotensin system in regulating endometrial neovascularization during the peri-implantation period: literature review and preliminary data

    doi: 10.1177/2042018820920560

    Figure Lengend Snippet: The possible pathways of Ang II-mediated angiogenesis. ANG II stimulates the generation of ROS through membrane NAD(P)H oxidases in VSMCs after binding to AT1-R. ROS are involved in many Ang II mediated effects, including production of HIF-1α in vascular cells, activation of p38MAPK, and transcription factor NF-kB. Interactions between Ang II and ROS are critical in vascular physiology and pathology in terms of regulating vascular structure and functions. Ang-Tie could also trigger the production of ROS through NADPH oxidase. Ang II, angiotensin II; Ang-Tie, angiopoietin-Tie; AT1-R, angiotensin II type 1 (AT1) receptor; HIF-1α, hypoxia inducible factor-1α; NF-kB, nuclear factor kappa AB; ROS, reactive oxygen species; VSMCs, vascular smooth muscle cells.

    Article Snippet: The primary antibodies were rabbit anti-human angiotensin II receptor type-1 polyclonal antibody (AAR-011, Alomone Labs, Jerusalem, Israel) at a dilution of 1:100 and rabbit anti-human angiotensin II type 2 receptor antibody (ab19134, AbCam, UK) at a dilution of 1:100.

    Techniques: Binding Assay, Activation Assay

    Expression of the AT1 receptor ( A ), AT2 receptor ( B ), and NOS3 ( C ) in kidney vessels from male and female mice on a normal sodium diet (all n = 5).

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

    Article Title: Sex differences in acute ANG II-mediated hemodynamic responses in mice

    doi: 10.1152/ajpregu.00638.2009

    Figure Lengend Snippet: Expression of the AT1 receptor ( A ), AT2 receptor ( B ), and NOS3 ( C ) in kidney vessels from male and female mice on a normal sodium diet (all n = 5).

    Article Snippet: All blots were incubated overnight with the following primary antibodies: anti-AT1 receptor (Alomone Labs, Jerusalem, Israel), anti-AT2 receptor antibody (Alomone Labs), and anti-endothelial nitric oxide synthase 3 (NOS3) (BD Biosciences, San Jose, CA).

    Techniques: Expressing, Mouse Assay

    Expression of the AT1 receptor ( A ), AT2 receptor ( B ), and NOS3 ( C ), in kidney vessels from male and female mice on a low-sodium diet (all n = 5).

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

    Article Title: Sex differences in acute ANG II-mediated hemodynamic responses in mice

    doi: 10.1152/ajpregu.00638.2009

    Figure Lengend Snippet: Expression of the AT1 receptor ( A ), AT2 receptor ( B ), and NOS3 ( C ), in kidney vessels from male and female mice on a low-sodium diet (all n = 5).

    Article Snippet: All blots were incubated overnight with the following primary antibodies: anti-AT1 receptor (Alomone Labs, Jerusalem, Israel), anti-AT2 receptor antibody (Alomone Labs), and anti-endothelial nitric oxide synthase 3 (NOS3) (BD Biosciences, San Jose, CA).

    Techniques: Expressing, Mouse Assay

    Expression of the AT1 receptor ( A ), AT2 receptor ( B ), and NOS3 ( C ) in kidney vessels from male and female mice on a high-sodium diet (all n = 5).

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

    Article Title: Sex differences in acute ANG II-mediated hemodynamic responses in mice

    doi: 10.1152/ajpregu.00638.2009

    Figure Lengend Snippet: Expression of the AT1 receptor ( A ), AT2 receptor ( B ), and NOS3 ( C ) in kidney vessels from male and female mice on a high-sodium diet (all n = 5).

    Article Snippet: All blots were incubated overnight with the following primary antibodies: anti-AT1 receptor (Alomone Labs, Jerusalem, Israel), anti-AT2 receptor antibody (Alomone Labs), and anti-endothelial nitric oxide synthase 3 (NOS3) (BD Biosciences, San Jose, CA).

    Techniques: Expressing, Mouse Assay