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cd14 primary ab conjugates antibody  (Bangs Laboratories)

 
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    Structured Review

    Bangs Laboratories cd14 primary ab conjugates antibody
    Integrin expression is elevated on monocytes from blood samples of cardiac patients compared with healthy age-matched subjects. (A) Gating strategy for the monocyte subsets based on expression of HLA-DR, <t>CCR2,</t> CD14, and CD16 applied to each patient cohort to define monocyte subsets, as indicated via representative images (CD14, green; CD16, red). Blood was collected from age-matched healthy controls (n = 6) and compared with CAD (n = 16) and NSTEMI (n = 27) on the day of percutaneous intervention for assessment of integrin expression on (B) cMo, (C) iMo, and (D) ncMo via FACS. Data are represented as mean receptor number ± SD (two-way ANOVA with Tukey posttest, *p < 0.05 between healthy age-matched subject cohorts).
    Cd14 Primary Ab Conjugates Antibody, supplied by Bangs Laboratories, 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/cd14+primary+ab+conjugates+antibody/pmc07653512-122-15-24?v=Bangs+Laboratories
    Average 90 stars, based on 1 article reviews
    cd14 primary ab conjugates antibody - by Bioz Stars, 2026-07
    90/100 stars

    Images

    1) Product Images from "An Allosteric shift in CD11c affinity activates a pro-atherogenic state in arrested intermediate monocytes"

    Article Title: An Allosteric shift in CD11c affinity activates a pro-atherogenic state in arrested intermediate monocytes

    Journal: Journal of immunology (Baltimore, Md. : 1950)

    doi: 10.4049/jimmunol.2000485

    Integrin expression is elevated on monocytes from blood samples of cardiac patients compared with healthy age-matched subjects. (A) Gating strategy for the monocyte subsets based on expression of HLA-DR, CCR2, CD14, and CD16 applied to each patient cohort to define monocyte subsets, as indicated via representative images (CD14, green; CD16, red). Blood was collected from age-matched healthy controls (n = 6) and compared with CAD (n = 16) and NSTEMI (n = 27) on the day of percutaneous intervention for assessment of integrin expression on (B) cMo, (C) iMo, and (D) ncMo via FACS. Data are represented as mean receptor number ± SD (two-way ANOVA with Tukey posttest, *p < 0.05 between healthy age-matched subject cohorts).
    Figure Legend Snippet: Integrin expression is elevated on monocytes from blood samples of cardiac patients compared with healthy age-matched subjects. (A) Gating strategy for the monocyte subsets based on expression of HLA-DR, CCR2, CD14, and CD16 applied to each patient cohort to define monocyte subsets, as indicated via representative images (CD14, green; CD16, red). Blood was collected from age-matched healthy controls (n = 6) and compared with CAD (n = 16) and NSTEMI (n = 27) on the day of percutaneous intervention for assessment of integrin expression on (B) cMo, (C) iMo, and (D) ncMo via FACS. Data are represented as mean receptor number ± SD (two-way ANOVA with Tukey posttest, *p < 0.05 between healthy age-matched subject cohorts).

    Techniques Used: Expressing

    Monocyte recruitment to inflamed endothelium under shear stress is β1- and β2-integrin–dependent on binding to VCAM-1. (A) Monocytes were perfused into the A-Chip onto TNF-α–stimulated HAEC in the presence of blocking Abs to CD11c, CD11b, VLA-4, or a nonspecific isotype IgG (Control) and TEM of adherent cells (white arrows) assessed by phase-contrast imaging after 10 min of shear at 2 dynes/cm2. Images display a time course of monocyte arrest and transmigration (phase dark) over 2 min. Scale bar, 10 μm. Monocyte subsets were determined based upon on-chip analysis of relative fluorescence intensity of Abs to CD14, CD16, and CCR2, which enabled the assessment of the number of arrested per field of view (FOV) at original magnification ×40. (B) Quantification of arrested iMo (filled bars) and the number of those arrested cells that have transmigrated (open bars) over 10 min of constant shear (2 dynes/cm2). Data are represented as mean arrested or transmigrated cells per FOV ± SD (n = 4–5 per group) (two-way ANOVA with Tukey posttest *p < 0.05 between isotype control within each cohort TEM color, #p < 0.05 compared with healthy, $p < 0.05 between CAD and NSTEMI cohorts for each Ab blocking treatment).(C) Monocyte subset arrest frequency on rVCAM-1 on the A-Chip. Data are represented as mean ± SD monocyte subset fraction of total arrested measured on the day of percutaneous coronary intervention or venous blood draw from healthy (n = 6), CAD (n = 8), and NSTEMI (n = 20) analyzed via two-way ANOVA with Tukey posttest. *p < 0.05 between healthy age-matched subject groups.
    Figure Legend Snippet: Monocyte recruitment to inflamed endothelium under shear stress is β1- and β2-integrin–dependent on binding to VCAM-1. (A) Monocytes were perfused into the A-Chip onto TNF-α–stimulated HAEC in the presence of blocking Abs to CD11c, CD11b, VLA-4, or a nonspecific isotype IgG (Control) and TEM of adherent cells (white arrows) assessed by phase-contrast imaging after 10 min of shear at 2 dynes/cm2. Images display a time course of monocyte arrest and transmigration (phase dark) over 2 min. Scale bar, 10 μm. Monocyte subsets were determined based upon on-chip analysis of relative fluorescence intensity of Abs to CD14, CD16, and CCR2, which enabled the assessment of the number of arrested per field of view (FOV) at original magnification ×40. (B) Quantification of arrested iMo (filled bars) and the number of those arrested cells that have transmigrated (open bars) over 10 min of constant shear (2 dynes/cm2). Data are represented as mean arrested or transmigrated cells per FOV ± SD (n = 4–5 per group) (two-way ANOVA with Tukey posttest *p < 0.05 between isotype control within each cohort TEM color, #p < 0.05 compared with healthy, $p < 0.05 between CAD and NSTEMI cohorts for each Ab blocking treatment).(C) Monocyte subset arrest frequency on rVCAM-1 on the A-Chip. Data are represented as mean ± SD monocyte subset fraction of total arrested measured on the day of percutaneous coronary intervention or venous blood draw from healthy (n = 6), CAD (n = 8), and NSTEMI (n = 20) analyzed via two-way ANOVA with Tukey posttest. *p < 0.05 between healthy age-matched subject groups.

    Techniques Used: Shear, Binding Assay, Blocking Assay, Control, Imaging, Transmigration Assay, Fluorescence



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    Integrin expression is elevated on monocytes from blood samples of cardiac patients compared with healthy age-matched subjects. (A) Gating strategy for the monocyte subsets based on expression of HLA-DR, <t>CCR2,</t> CD14, and CD16 applied to each patient cohort to define monocyte subsets, as indicated via representative images (CD14, green; CD16, red). Blood was collected from age-matched healthy controls (n = 6) and compared with CAD (n = 16) and NSTEMI (n = 27) on the day of percutaneous intervention for assessment of integrin expression on (B) cMo, (C) iMo, and (D) ncMo via FACS. Data are represented as mean receptor number ± SD (two-way ANOVA with Tukey posttest, *p < 0.05 between healthy age-matched subject cohorts).
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    Integrin expression is elevated on monocytes from blood samples of cardiac patients compared with healthy age-matched subjects. (A) Gating strategy for the monocyte subsets based on expression of HLA-DR, <t>CCR2,</t> CD14, and CD16 applied to each patient cohort to define monocyte subsets, as indicated via representative images (CD14, green; CD16, red). Blood was collected from age-matched healthy controls (n = 6) and compared with CAD (n = 16) and NSTEMI (n = 27) on the day of percutaneous intervention for assessment of integrin expression on (B) cMo, (C) iMo, and (D) ncMo via FACS. Data are represented as mean receptor number ± SD (two-way ANOVA with Tukey posttest, *p < 0.05 between healthy age-matched subject cohorts).
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    Image Search Results


    Integrin expression is elevated on monocytes from blood samples of cardiac patients compared with healthy age-matched subjects. (A) Gating strategy for the monocyte subsets based on expression of HLA-DR, CCR2, CD14, and CD16 applied to each patient cohort to define monocyte subsets, as indicated via representative images (CD14, green; CD16, red). Blood was collected from age-matched healthy controls (n = 6) and compared with CAD (n = 16) and NSTEMI (n = 27) on the day of percutaneous intervention for assessment of integrin expression on (B) cMo, (C) iMo, and (D) ncMo via FACS. Data are represented as mean receptor number ± SD (two-way ANOVA with Tukey posttest, *p < 0.05 between healthy age-matched subject cohorts).

    Journal: Journal of immunology (Baltimore, Md. : 1950)

    Article Title: An Allosteric shift in CD11c affinity activates a pro-atherogenic state in arrested intermediate monocytes

    doi: 10.4049/jimmunol.2000485

    Figure Lengend Snippet: Integrin expression is elevated on monocytes from blood samples of cardiac patients compared with healthy age-matched subjects. (A) Gating strategy for the monocyte subsets based on expression of HLA-DR, CCR2, CD14, and CD16 applied to each patient cohort to define monocyte subsets, as indicated via representative images (CD14, green; CD16, red). Blood was collected from age-matched healthy controls (n = 6) and compared with CAD (n = 16) and NSTEMI (n = 27) on the day of percutaneous intervention for assessment of integrin expression on (B) cMo, (C) iMo, and (D) ncMo via FACS. Data are represented as mean receptor number ± SD (two-way ANOVA with Tukey posttest, *p < 0.05 between healthy age-matched subject cohorts).

    Article Snippet: Monocyte subset abundance was quantified by calibrating fluorescent signals derived from the CD14, CD16, and CCR2 primary Ab conjugates to receptor expression calculated using Bangs Laboratories beads with a known number of binding sites/area.

    Techniques: Expressing

    Monocyte recruitment to inflamed endothelium under shear stress is β1- and β2-integrin–dependent on binding to VCAM-1. (A) Monocytes were perfused into the A-Chip onto TNF-α–stimulated HAEC in the presence of blocking Abs to CD11c, CD11b, VLA-4, or a nonspecific isotype IgG (Control) and TEM of adherent cells (white arrows) assessed by phase-contrast imaging after 10 min of shear at 2 dynes/cm2. Images display a time course of monocyte arrest and transmigration (phase dark) over 2 min. Scale bar, 10 μm. Monocyte subsets were determined based upon on-chip analysis of relative fluorescence intensity of Abs to CD14, CD16, and CCR2, which enabled the assessment of the number of arrested per field of view (FOV) at original magnification ×40. (B) Quantification of arrested iMo (filled bars) and the number of those arrested cells that have transmigrated (open bars) over 10 min of constant shear (2 dynes/cm2). Data are represented as mean arrested or transmigrated cells per FOV ± SD (n = 4–5 per group) (two-way ANOVA with Tukey posttest *p < 0.05 between isotype control within each cohort TEM color, #p < 0.05 compared with healthy, $p < 0.05 between CAD and NSTEMI cohorts for each Ab blocking treatment).(C) Monocyte subset arrest frequency on rVCAM-1 on the A-Chip. Data are represented as mean ± SD monocyte subset fraction of total arrested measured on the day of percutaneous coronary intervention or venous blood draw from healthy (n = 6), CAD (n = 8), and NSTEMI (n = 20) analyzed via two-way ANOVA with Tukey posttest. *p < 0.05 between healthy age-matched subject groups.

    Journal: Journal of immunology (Baltimore, Md. : 1950)

    Article Title: An Allosteric shift in CD11c affinity activates a pro-atherogenic state in arrested intermediate monocytes

    doi: 10.4049/jimmunol.2000485

    Figure Lengend Snippet: Monocyte recruitment to inflamed endothelium under shear stress is β1- and β2-integrin–dependent on binding to VCAM-1. (A) Monocytes were perfused into the A-Chip onto TNF-α–stimulated HAEC in the presence of blocking Abs to CD11c, CD11b, VLA-4, or a nonspecific isotype IgG (Control) and TEM of adherent cells (white arrows) assessed by phase-contrast imaging after 10 min of shear at 2 dynes/cm2. Images display a time course of monocyte arrest and transmigration (phase dark) over 2 min. Scale bar, 10 μm. Monocyte subsets were determined based upon on-chip analysis of relative fluorescence intensity of Abs to CD14, CD16, and CCR2, which enabled the assessment of the number of arrested per field of view (FOV) at original magnification ×40. (B) Quantification of arrested iMo (filled bars) and the number of those arrested cells that have transmigrated (open bars) over 10 min of constant shear (2 dynes/cm2). Data are represented as mean arrested or transmigrated cells per FOV ± SD (n = 4–5 per group) (two-way ANOVA with Tukey posttest *p < 0.05 between isotype control within each cohort TEM color, #p < 0.05 compared with healthy, $p < 0.05 between CAD and NSTEMI cohorts for each Ab blocking treatment).(C) Monocyte subset arrest frequency on rVCAM-1 on the A-Chip. Data are represented as mean ± SD monocyte subset fraction of total arrested measured on the day of percutaneous coronary intervention or venous blood draw from healthy (n = 6), CAD (n = 8), and NSTEMI (n = 20) analyzed via two-way ANOVA with Tukey posttest. *p < 0.05 between healthy age-matched subject groups.

    Article Snippet: Monocyte subset abundance was quantified by calibrating fluorescent signals derived from the CD14, CD16, and CCR2 primary Ab conjugates to receptor expression calculated using Bangs Laboratories beads with a known number of binding sites/area.

    Techniques: Shear, Binding Assay, Blocking Assay, Control, Imaging, Transmigration Assay, Fluorescence