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10 ng/100 µl sample anti-ulbp-2/5/6 pe-conjugated antibody  (R&D Systems)


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    R&D Systems 10 ng/100 µl sample anti-ulbp-2/5/6 pe-conjugated antibody
    10 Ng/100 µl Sample Anti Ulbp 2/5/6 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
    https://www.bioz.com/product/ng+2+pe/Human+ULBP-2%2F5%2F6+PE-conjugated+Antibody/pmc07601115-89-16-19
    Average 90 stars, based on 1 article reviews
    10 ng/100 µl sample anti-ulbp-2/5/6 pe-conjugated antibody - by Bioz Stars, 2026-10
    90/100 stars

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    Article Title: Activation of the Wnt/Planar Cell Polarity Pathway Is Required for Pericyte Recruitment during Pulmonary Angiogenesis
    Article Snippet: .. Immunophenotyping of cell surface molecules was performed by labeling cells with directly conjugated antibodies: NG-2-PE (FAB2585P; R&D Systems Inc., Minneapolis, MN), thymus cell antigen 1 (catalog number 562685; BD Biosciences), CD146-PE-Cy7 (catalog number 562135; BD Biosciences), platelet-derived growth factor receptor (PDGFR) β−PerCPC Y5.5 (catalog number 562714; BD Biosciences), CD31 PerCP-eFlow 710 (catalog number 46-0319-41; eBioscience, Inc., San Diego, CA), CD45-APC CY7 (catalog number 47-0459-41; eBioscience, Inc.), and 3G5 IgG. .. For assessing intracellular protein expression, cells were fixed and permeabilized with Cytofix/Cytoperm Plus (BD Biosciences) and incubated with the primary antibodies: α-smooth muscle actin (SMA)–fluorescein isothiocyanate (ab8211; Abcam plc, Cambridge, UK), calponin (ab700; Abcam plc), smooth muscle 22-α (SM22α; ab10135; Abcam plc), and smooth muscle myosin heavy chain (IC4470A; R&D Systems Inc.).



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    Image Search Results


    Sepsis induces pericyte loss, vascular hyporeactivity and leakage in rats. a Mesenteric microvascular networks from CLP and LPS (10 mg/kg)-induced sepsis at 6, 12 and 24 h were stained for NG-2 (pericyte marker; green), PDGFR-β (pericyte marker; green), and CD31 (VEC marker; red). Pericyte coverage rate of endothelium was quantified by analyzing percentage of CD31 + capillaries opposed to NG-2 + and PDGFR-β + PCs ( n = 8 rats). Scale bars: 100 μm. b TEM observation of ultrastructural changes of pericyte in mesenteric venules at 24 h after CLP and LPS administration (yellow arrowheads indicate pericyte loss and swelling, *indicate erythrocyte diapedesis). Scale bars: 2 μm. c Changes in vascular response of mesenteric arterioles to NE and Ach in vivo ( n = 8 rats). d Vascular leakage of mesenteric venules measured by the appearance of intravenously injected FITC–BSA and quantitation of FITC–BSA + vessel ( n = 8 rats). Scale bars: 50 μm. e Representative TEM images of tight junctions in mesenteric venules after CLP and LPS administration at 24 h (green arrow indicate the tight junction, red arrowheads indicate the endothelial fragments and disrupted VEC junctions). Scale bars: 1 μm. PC pericyte, CLP cecal ligation and puncture, LPS lipopolysaccharides, NG-2 nerve/glial antigen 2, PDGFR-β platelet-derived growth factor receptor beta, VEC vascular endothelial cell, RBC red blood cell, L lumen, NE norepinephrine, Ach acetylcholine, MA mesenteric arteriole, TJ tight junction, TEM transmission electron microscopy. Data shown as mean ± SD. * P < 0.05, ** P < 0.01, *** P < 0.001 vs. Sham (one-way ANOVA)

    Journal: Military Medical Research

    Article Title: Pericytes protect rats and mice from sepsis-induced injuries by maintaining vascular reactivity and barrier function: implication of miRNAs and microvesicles

    doi: 10.1186/s40779-023-00442-2

    Figure Lengend Snippet: Sepsis induces pericyte loss, vascular hyporeactivity and leakage in rats. a Mesenteric microvascular networks from CLP and LPS (10 mg/kg)-induced sepsis at 6, 12 and 24 h were stained for NG-2 (pericyte marker; green), PDGFR-β (pericyte marker; green), and CD31 (VEC marker; red). Pericyte coverage rate of endothelium was quantified by analyzing percentage of CD31 + capillaries opposed to NG-2 + and PDGFR-β + PCs ( n = 8 rats). Scale bars: 100 μm. b TEM observation of ultrastructural changes of pericyte in mesenteric venules at 24 h after CLP and LPS administration (yellow arrowheads indicate pericyte loss and swelling, *indicate erythrocyte diapedesis). Scale bars: 2 μm. c Changes in vascular response of mesenteric arterioles to NE and Ach in vivo ( n = 8 rats). d Vascular leakage of mesenteric venules measured by the appearance of intravenously injected FITC–BSA and quantitation of FITC–BSA + vessel ( n = 8 rats). Scale bars: 50 μm. e Representative TEM images of tight junctions in mesenteric venules after CLP and LPS administration at 24 h (green arrow indicate the tight junction, red arrowheads indicate the endothelial fragments and disrupted VEC junctions). Scale bars: 1 μm. PC pericyte, CLP cecal ligation and puncture, LPS lipopolysaccharides, NG-2 nerve/glial antigen 2, PDGFR-β platelet-derived growth factor receptor beta, VEC vascular endothelial cell, RBC red blood cell, L lumen, NE norepinephrine, Ach acetylcholine, MA mesenteric arteriole, TJ tight junction, TEM transmission electron microscopy. Data shown as mean ± SD. * P < 0.05, ** P < 0.01, *** P < 0.001 vs. Sham (one-way ANOVA)

    Article Snippet: For flow cytometry, cells were labeled with directly conjugated antibodies, including NG-2-PE, CD146-PE, PDGFR-β-PE, CD31-PE and IgG-PE (all from BD Biosciences, Franklin Lakes, NJ, USA).

    Techniques: Staining, Marker, In Vivo, Injection, Quantitation Assay, Ligation, Derivative Assay, Transmission Assay, Electron Microscopy

    The transplanted pericytes improve the vascular hyporeactivity and leakage after sepsis. a Effects of transplanting different amount of exogenous pericytes on animal survival ( n = 16 rats). Intravital microscopy ( b , red arrows indicate GFP-PC) and immunofluorescence ( c ) by CLSM were used to monitor the GFP-PC location on mesenteric venules at 24 h after transplantation of exogenous pericytes (10 6 ). Scale bars: 50 μm. d Mesenteric microvascular networks were stained for NG-2, PDGFR-β, and CD31 at 24 h after resuscitation ( n = 8 rats). Scale bars: 100 μm. e Changes in vascular response of mesenteric arterioles to NE and Ach in vivo after sepsis in rats ( n = 8). f Vascular leakage of mesenteric venules measured by the appearance of intravenously injected FITC–BSA and quantitation of FITC–BSA + vessel ( n = 8 rats). Scale bars: 50 μm. g Immunohistochemistry for ZO-1 and VE-cadherin in mesenteric venules. Scale bars: 20 μm. h Representative TEM images of tight junctions in mesenteric venules (green arrows indicate the tight junction, *indicate the erythrocyte diapedesis). Scale bars: 1 μm. NG-2 nerve/glial antigen 2, PDGFR-β platelet-derived growth factor receptor beta, CT conventional treatment, CLSM confocal laser scanning microscopy, PC pericyte, Poly(I:C)PC polyinosine-polycytidylic acid pre-treatment pericyte, NE norepinephrine, Ach acetylcholine, MA mesenteric arteriole, ZO-1 zonula occludens-1, VE-cadherin vascular endothelial cadherin, VEC vascular endothelial cell, RBC red blood cell, TJ tight junction, L lumen, TEM transmission electron microscopy. Data shown as mean ± SD. ** P < 0.01, *** P < 0.001 vs. Sham; ## P < 0.01, ### P < 0.001 vs. Sepsis; && P < 0.01, &&& P < 0.001 vs. Sepsis + CT (one-way ANOVA)

    Journal: Military Medical Research

    Article Title: Pericytes protect rats and mice from sepsis-induced injuries by maintaining vascular reactivity and barrier function: implication of miRNAs and microvesicles

    doi: 10.1186/s40779-023-00442-2

    Figure Lengend Snippet: The transplanted pericytes improve the vascular hyporeactivity and leakage after sepsis. a Effects of transplanting different amount of exogenous pericytes on animal survival ( n = 16 rats). Intravital microscopy ( b , red arrows indicate GFP-PC) and immunofluorescence ( c ) by CLSM were used to monitor the GFP-PC location on mesenteric venules at 24 h after transplantation of exogenous pericytes (10 6 ). Scale bars: 50 μm. d Mesenteric microvascular networks were stained for NG-2, PDGFR-β, and CD31 at 24 h after resuscitation ( n = 8 rats). Scale bars: 100 μm. e Changes in vascular response of mesenteric arterioles to NE and Ach in vivo after sepsis in rats ( n = 8). f Vascular leakage of mesenteric venules measured by the appearance of intravenously injected FITC–BSA and quantitation of FITC–BSA + vessel ( n = 8 rats). Scale bars: 50 μm. g Immunohistochemistry for ZO-1 and VE-cadherin in mesenteric venules. Scale bars: 20 μm. h Representative TEM images of tight junctions in mesenteric venules (green arrows indicate the tight junction, *indicate the erythrocyte diapedesis). Scale bars: 1 μm. NG-2 nerve/glial antigen 2, PDGFR-β platelet-derived growth factor receptor beta, CT conventional treatment, CLSM confocal laser scanning microscopy, PC pericyte, Poly(I:C)PC polyinosine-polycytidylic acid pre-treatment pericyte, NE norepinephrine, Ach acetylcholine, MA mesenteric arteriole, ZO-1 zonula occludens-1, VE-cadherin vascular endothelial cadherin, VEC vascular endothelial cell, RBC red blood cell, TJ tight junction, L lumen, TEM transmission electron microscopy. Data shown as mean ± SD. ** P < 0.01, *** P < 0.001 vs. Sham; ## P < 0.01, ### P < 0.001 vs. Sepsis; && P < 0.01, &&& P < 0.001 vs. Sepsis + CT (one-way ANOVA)

    Article Snippet: For flow cytometry, cells were labeled with directly conjugated antibodies, including NG-2-PE, CD146-PE, PDGFR-β-PE, CD31-PE and IgG-PE (all from BD Biosciences, Franklin Lakes, NJ, USA).

    Techniques: Intravital Microscopy, Immunofluorescence, Transplantation Assay, Staining, In Vivo, Injection, Quantitation Assay, Immunohistochemistry, Derivative Assay, Confocal Laser Scanning Microscopy, Transmission Assay, Electron Microscopy