il1r1 pe polyclonal Search Results


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Il 1r1 Pe, supplied by R&D Systems, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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P2Y 11 activation on human M2 macrophages causes IL-1R upregulation and CD39 downregulation as well as VEGF secretion. A–C The regulation of <t>IL-1R1</t> and the ecto-ATPase CD39 at the protein level was examined by flow cytometry. M2 macrophages were treated for 24 h with the P2Y 11 receptor agonist ATPγS (20 µM) in the presence or absence of the PDE4 inhibitor rolipram (10 µM). The antagonist NF340 (20 µM) was used to confirm that agonist-mediated responses were specific to P2Y 11 receptor stimulation. A Representative FACS histograms of IL-1R1 and CD39 expression from differentially treated M2 macrophages. Numbers represent mean fluorescence intensities (MFIs) of the respective staining after subtraction of isotype control MFIs. B, C Quantification of IL-1R1 ( B ) and CD39 ( C ) expression levels from differentially treated M2 macrophages ( n = 3). * p < 0.05, ** p < 0.01, **** p < 0.0001. D M2 macrophages were treated for 24 h with the P2Y 11 receptor agonist ATPγS (20 µM) in the presence or absence of the PDE4 inhibitor rolipram (10 µM). VEGF levels were measured in cell culture supernatants. NF340 (20 µM) was used to confirm that agonist-mediated responses were specific to P2Y 11 receptor stimulation ( n = 5). **** p < 0.0001
Goat Polyclonal Igg Antihuman Il 1r1, supplied by R&D Systems, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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R&D Systems polyclonal anti-il-1r1 phycoerythrin (pe)-conjugated antibody
P2Y 11 activation on human M2 macrophages causes IL-1R upregulation and CD39 downregulation as well as VEGF secretion. A–C The regulation of <t>IL-1R1</t> and the ecto-ATPase CD39 at the protein level was examined by flow cytometry. M2 macrophages were treated for 24 h with the P2Y 11 receptor agonist ATPγS (20 µM) in the presence or absence of the PDE4 inhibitor rolipram (10 µM). The antagonist NF340 (20 µM) was used to confirm that agonist-mediated responses were specific to P2Y 11 receptor stimulation. A Representative FACS histograms of IL-1R1 and CD39 expression from differentially treated M2 macrophages. Numbers represent mean fluorescence intensities (MFIs) of the respective staining after subtraction of isotype control MFIs. B, C Quantification of IL-1R1 ( B ) and CD39 ( C ) expression levels from differentially treated M2 macrophages ( n = 3). * p < 0.05, ** p < 0.01, **** p < 0.0001. D M2 macrophages were treated for 24 h with the P2Y 11 receptor agonist ATPγS (20 µM) in the presence or absence of the PDE4 inhibitor rolipram (10 µM). VEGF levels were measured in cell culture supernatants. NF340 (20 µM) was used to confirm that agonist-mediated responses were specific to P2Y 11 receptor stimulation ( n = 5). **** p < 0.0001
Polyclonal Anti Il 1r1 Phycoerythrin (Pe) Conjugated Antibody, supplied by R&D Systems, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Receptor for IL1A, IL1B and IL1RN. After binding to interleukin-1 associates with the corecptor IL1RAP to form the high affinity interleukin-1 receptor complex which mediates interleukin-1-dependent activation of NF-kappa-B, MAPK and other pathways. Signaling involves
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N/A
Receptor for IL1A, IL1B and IL1RN. After binding to interleukin-1 associates with the corecptor IL1RAP to form the high affinity interleukin-1 receptor complex which mediates interleukin-1-dependent activation of NF-kappa-B, MAPK and other pathways. Signaling involves
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N/A
Receptor for IL1A, IL1B and IL1RN. After binding to interleukin-1 associates with the corecptor IL1RAP to form the high affinity interleukin-1 receptor complex which mediates interleukin-1-dependent activation of NF-kappa-B, MAPK and other pathways. Signaling involves
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N/A
Galactose-specific lectin which binds IgE. May mediate with the alpha-3, beta-1 integrin the stimulation by CSPG4 of endothelial cells migration. Together with DMBT1, required for terminal differentiation of columnar epithelial cells during early embryogenesis. In
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N/A
Galactose-specific lectin which binds IgE. May mediate with the alpha-3, beta-1 integrin the stimulation by CSPG4 of endothelial cells migration. Together with DMBT1, required for terminal differentiation of columnar epithelial cells during early embryogenesis. In
  Buy from Supplier

N/A
Galactose-specific lectin which binds IgE. May mediate with the alpha-3, beta-1 integrin the stimulation by CSPG4 of endothelial cells migration. Together with DMBT1, required for terminal differentiation of columnar epithelial cells during early embryogenesis. In
  Buy from Supplier

N/A
Galactose-specific lectin which binds IgE. May mediate with the alpha-3, beta-1 integrin the stimulation by CSPG4 of endothelial cells migration. Together with DMBT1, required for terminal differentiation of columnar epithelial cells during early embryogenesis. In
  Buy from Supplier

N/A
Receptor for IL1A, IL1B and IL1RN. After binding to interleukin-1 associates with the corecptor IL1RAP to form the high affinity interleukin-1 receptor complex which mediates interleukin-1-dependent activation of NF-kappa-B, MAPK and other pathways. Signaling involves
  Buy from Supplier

N/A
Receptor for IL1A, IL1B and IL1RN. After binding to interleukin-1 associates with the corecptor IL1RAP to form the high affinity interleukin-1 receptor complex which mediates interleukin-1-dependent activation of NF-kappa-B, MAPK and other pathways. Signaling involves
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P2Y 11 activation on human M2 macrophages causes IL-1R upregulation and CD39 downregulation as well as VEGF secretion. A–C The regulation of IL-1R1 and the ecto-ATPase CD39 at the protein level was examined by flow cytometry. M2 macrophages were treated for 24 h with the P2Y 11 receptor agonist ATPγS (20 µM) in the presence or absence of the PDE4 inhibitor rolipram (10 µM). The antagonist NF340 (20 µM) was used to confirm that agonist-mediated responses were specific to P2Y 11 receptor stimulation. A Representative FACS histograms of IL-1R1 and CD39 expression from differentially treated M2 macrophages. Numbers represent mean fluorescence intensities (MFIs) of the respective staining after subtraction of isotype control MFIs. B, C Quantification of IL-1R1 ( B ) and CD39 ( C ) expression levels from differentially treated M2 macrophages ( n = 3). * p < 0.05, ** p < 0.01, **** p < 0.0001. D M2 macrophages were treated for 24 h with the P2Y 11 receptor agonist ATPγS (20 µM) in the presence or absence of the PDE4 inhibitor rolipram (10 µM). VEGF levels were measured in cell culture supernatants. NF340 (20 µM) was used to confirm that agonist-mediated responses were specific to P2Y 11 receptor stimulation ( n = 5). **** p < 0.0001

Journal: Cellular and Molecular Life Sciences

Article Title: The P2Y 11 receptor of human M2 macrophages activates canonical and IL-1 receptor signaling to translate the extracellular danger signal ATP into anti-inflammatory and pro-angiogenic responses

doi: 10.1007/s00018-022-04548-z

Figure Lengend Snippet: P2Y 11 activation on human M2 macrophages causes IL-1R upregulation and CD39 downregulation as well as VEGF secretion. A–C The regulation of IL-1R1 and the ecto-ATPase CD39 at the protein level was examined by flow cytometry. M2 macrophages were treated for 24 h with the P2Y 11 receptor agonist ATPγS (20 µM) in the presence or absence of the PDE4 inhibitor rolipram (10 µM). The antagonist NF340 (20 µM) was used to confirm that agonist-mediated responses were specific to P2Y 11 receptor stimulation. A Representative FACS histograms of IL-1R1 and CD39 expression from differentially treated M2 macrophages. Numbers represent mean fluorescence intensities (MFIs) of the respective staining after subtraction of isotype control MFIs. B, C Quantification of IL-1R1 ( B ) and CD39 ( C ) expression levels from differentially treated M2 macrophages ( n = 3). * p < 0.05, ** p < 0.01, **** p < 0.0001. D M2 macrophages were treated for 24 h with the P2Y 11 receptor agonist ATPγS (20 µM) in the presence or absence of the PDE4 inhibitor rolipram (10 µM). VEGF levels were measured in cell culture supernatants. NF340 (20 µM) was used to confirm that agonist-mediated responses were specific to P2Y 11 receptor stimulation ( n = 5). **** p < 0.0001

Article Snippet: The following antibodies were used: rabbit polyclonal IgG antihuman P2Y 11 receptor (bs-12071R-A-488; Bioss, Woburn, MA, USA), mouse monoclonal IgG2b antihuman CD14 (clone MϕP9, 345787-APC; BD Biosciences, Franklin Lakes, NJ, USA), mouse monoclonal IgG1 antihuman CD163 (clone GHI/61, 556018-PE; BD Biosciences), goat polyclonal IgG antihuman IL-1R1 (FAB269P-PE; R&D Systems) and mouse monoclonal IgG2b antihuman CD39 (clone TU66, 561444-FITC; BD Biosciences).

Techniques: Activation Assay, Flow Cytometry, Expressing, Fluorescence, Staining, Control, Cell Culture

P2Y 11 -mediated sTNFR2 release and VEGF secretion as well as IL-1R upregulation depend on Ca 2+ and protein kinase C, but are differentially regulated by cAMP elevation. A M2 macrophages were treated for 24 h with the P2Y 11 receptor agonist ATPγS (20 µM) in the presence or absence of the PDE4 inhibitor rolipram (10 µM). In addition, cells were treated either with the PDE4 inhibitor rolipram (10 µM), the direct AC activator forskolin (10 µM) or with the combination of both. sTNFR2 and VEGF were measured in cell culture supernatants and IL-1R1 MFIs were determined by flow cytometry. Mean IL-1R1 MFI values are shown ( n = 3). B M2 macrophages were treated for 24 h with the P2Y 11 receptor agonist ATPγS (20 µM) in the presence or absence of the PDE4 inhibitor rolipram (10 µM), either with or without the Ca 2+ chelator BAPTA-AM (10 µM) or the protein kinase C inhibitor calphostin C (250 nM). sTNFR2 and VEGF were measured in cell culture supernatants and IL-1R1 MFIs were determined by flow cytometry. Mean IL-1R1 MFI values are shown ( n = 3). * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001, ## p < 0.01, ### p < 0.001

Journal: Cellular and Molecular Life Sciences

Article Title: The P2Y 11 receptor of human M2 macrophages activates canonical and IL-1 receptor signaling to translate the extracellular danger signal ATP into anti-inflammatory and pro-angiogenic responses

doi: 10.1007/s00018-022-04548-z

Figure Lengend Snippet: P2Y 11 -mediated sTNFR2 release and VEGF secretion as well as IL-1R upregulation depend on Ca 2+ and protein kinase C, but are differentially regulated by cAMP elevation. A M2 macrophages were treated for 24 h with the P2Y 11 receptor agonist ATPγS (20 µM) in the presence or absence of the PDE4 inhibitor rolipram (10 µM). In addition, cells were treated either with the PDE4 inhibitor rolipram (10 µM), the direct AC activator forskolin (10 µM) or with the combination of both. sTNFR2 and VEGF were measured in cell culture supernatants and IL-1R1 MFIs were determined by flow cytometry. Mean IL-1R1 MFI values are shown ( n = 3). B M2 macrophages were treated for 24 h with the P2Y 11 receptor agonist ATPγS (20 µM) in the presence or absence of the PDE4 inhibitor rolipram (10 µM), either with or without the Ca 2+ chelator BAPTA-AM (10 µM) or the protein kinase C inhibitor calphostin C (250 nM). sTNFR2 and VEGF were measured in cell culture supernatants and IL-1R1 MFIs were determined by flow cytometry. Mean IL-1R1 MFI values are shown ( n = 3). * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001, ## p < 0.01, ### p < 0.001

Article Snippet: The following antibodies were used: rabbit polyclonal IgG antihuman P2Y 11 receptor (bs-12071R-A-488; Bioss, Woburn, MA, USA), mouse monoclonal IgG2b antihuman CD14 (clone MϕP9, 345787-APC; BD Biosciences, Franklin Lakes, NJ, USA), mouse monoclonal IgG1 antihuman CD163 (clone GHI/61, 556018-PE; BD Biosciences), goat polyclonal IgG antihuman IL-1R1 (FAB269P-PE; R&D Systems) and mouse monoclonal IgG2b antihuman CD39 (clone TU66, 561444-FITC; BD Biosciences).

Techniques: Cell Culture, Flow Cytometry