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rabbit anti cd11b primary antibody  (Boster Bio)


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    Structured Review

    Boster Bio rabbit anti cd11b primary antibody
    Daclatasvir treatment ameliorates liver damage and fibrosis in MCD diet-induced MASH mouse model. A: Schematic illustration of the experimental workflow for the daclatasvir treatment strategy in a methionine-choline deficient (MCD) diet-induced MASH mouse model. B: Liver weight, LW/BW, and LW/BMI were recorded for MCD diet-fed mice after 3 weeks of treatment with either vehicle or daclatasvir. C: Representative images of H&E, PSR, and <t>CD11b</t> staining of liver samples from vehicle or daclatasvir treated mice at 4 weeks of MCD diet administration. Scale bar, 200 μm for H&E and PSR; 100 μm for CD11b. D: Quantitative results for PSR and CD11b staining shown in (C). E: Enzyme activities of serum hepatic transaminases in MCD diet-fed mice after 3 weeks of treatment with either vehicle or daclatasvir. F–H: The mRNA expression of genes associated with lipid catabolism (F), inflammation (G), and fibrosis (H) in liver tissues from MCD diet-induced MASH mice following 3 weeks of daclatasvir or vehicle treatment. For (B–H), n = 6 mice per group. Data are presented as mean ± SD; ∗ P < 0.05, ∗∗ P < 0.01; Student’s t test for statistics.
    Rabbit Anti Cd11b Primary Antibody, supplied by Boster Bio, used in various techniques. Bioz Stars score: 93/100, based on 5 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/rabbit anti cd11b primary antibody/product/Boster Bio
    Average 93 stars, based on 5 article reviews
    rabbit anti cd11b primary antibody - by Bioz Stars, 2026-03
    93/100 stars

    Images

    1) Product Images from "Hepatoprotective drug screening identifies daclatasvir, a promising therapeutic candidate for MASLD by targeting PLIN2"

    Article Title: Hepatoprotective drug screening identifies daclatasvir, a promising therapeutic candidate for MASLD by targeting PLIN2

    Journal: Journal of Lipid Research

    doi: 10.1016/j.jlr.2025.100835

    Daclatasvir treatment ameliorates liver damage and fibrosis in MCD diet-induced MASH mouse model. A: Schematic illustration of the experimental workflow for the daclatasvir treatment strategy in a methionine-choline deficient (MCD) diet-induced MASH mouse model. B: Liver weight, LW/BW, and LW/BMI were recorded for MCD diet-fed mice after 3 weeks of treatment with either vehicle or daclatasvir. C: Representative images of H&E, PSR, and CD11b staining of liver samples from vehicle or daclatasvir treated mice at 4 weeks of MCD diet administration. Scale bar, 200 μm for H&E and PSR; 100 μm for CD11b. D: Quantitative results for PSR and CD11b staining shown in (C). E: Enzyme activities of serum hepatic transaminases in MCD diet-fed mice after 3 weeks of treatment with either vehicle or daclatasvir. F–H: The mRNA expression of genes associated with lipid catabolism (F), inflammation (G), and fibrosis (H) in liver tissues from MCD diet-induced MASH mice following 3 weeks of daclatasvir or vehicle treatment. For (B–H), n = 6 mice per group. Data are presented as mean ± SD; ∗ P < 0.05, ∗∗ P < 0.01; Student’s t test for statistics.
    Figure Legend Snippet: Daclatasvir treatment ameliorates liver damage and fibrosis in MCD diet-induced MASH mouse model. A: Schematic illustration of the experimental workflow for the daclatasvir treatment strategy in a methionine-choline deficient (MCD) diet-induced MASH mouse model. B: Liver weight, LW/BW, and LW/BMI were recorded for MCD diet-fed mice after 3 weeks of treatment with either vehicle or daclatasvir. C: Representative images of H&E, PSR, and CD11b staining of liver samples from vehicle or daclatasvir treated mice at 4 weeks of MCD diet administration. Scale bar, 200 μm for H&E and PSR; 100 μm for CD11b. D: Quantitative results for PSR and CD11b staining shown in (C). E: Enzyme activities of serum hepatic transaminases in MCD diet-fed mice after 3 weeks of treatment with either vehicle or daclatasvir. F–H: The mRNA expression of genes associated with lipid catabolism (F), inflammation (G), and fibrosis (H) in liver tissues from MCD diet-induced MASH mice following 3 weeks of daclatasvir or vehicle treatment. For (B–H), n = 6 mice per group. Data are presented as mean ± SD; ∗ P < 0.05, ∗∗ P < 0.01; Student’s t test for statistics.

    Techniques Used: Staining, Expressing



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    Image Search Results


    Daclatasvir treatment ameliorates liver damage and fibrosis in MCD diet-induced MASH mouse model. A: Schematic illustration of the experimental workflow for the daclatasvir treatment strategy in a methionine-choline deficient (MCD) diet-induced MASH mouse model. B: Liver weight, LW/BW, and LW/BMI were recorded for MCD diet-fed mice after 3 weeks of treatment with either vehicle or daclatasvir. C: Representative images of H&E, PSR, and CD11b staining of liver samples from vehicle or daclatasvir treated mice at 4 weeks of MCD diet administration. Scale bar, 200 μm for H&E and PSR; 100 μm for CD11b. D: Quantitative results for PSR and CD11b staining shown in (C). E: Enzyme activities of serum hepatic transaminases in MCD diet-fed mice after 3 weeks of treatment with either vehicle or daclatasvir. F–H: The mRNA expression of genes associated with lipid catabolism (F), inflammation (G), and fibrosis (H) in liver tissues from MCD diet-induced MASH mice following 3 weeks of daclatasvir or vehicle treatment. For (B–H), n = 6 mice per group. Data are presented as mean ± SD; ∗ P < 0.05, ∗∗ P < 0.01; Student’s t test for statistics.

    Journal: Journal of Lipid Research

    Article Title: Hepatoprotective drug screening identifies daclatasvir, a promising therapeutic candidate for MASLD by targeting PLIN2

    doi: 10.1016/j.jlr.2025.100835

    Figure Lengend Snippet: Daclatasvir treatment ameliorates liver damage and fibrosis in MCD diet-induced MASH mouse model. A: Schematic illustration of the experimental workflow for the daclatasvir treatment strategy in a methionine-choline deficient (MCD) diet-induced MASH mouse model. B: Liver weight, LW/BW, and LW/BMI were recorded for MCD diet-fed mice after 3 weeks of treatment with either vehicle or daclatasvir. C: Representative images of H&E, PSR, and CD11b staining of liver samples from vehicle or daclatasvir treated mice at 4 weeks of MCD diet administration. Scale bar, 200 μm for H&E and PSR; 100 μm for CD11b. D: Quantitative results for PSR and CD11b staining shown in (C). E: Enzyme activities of serum hepatic transaminases in MCD diet-fed mice after 3 weeks of treatment with either vehicle or daclatasvir. F–H: The mRNA expression of genes associated with lipid catabolism (F), inflammation (G), and fibrosis (H) in liver tissues from MCD diet-induced MASH mice following 3 weeks of daclatasvir or vehicle treatment. For (B–H), n = 6 mice per group. Data are presented as mean ± SD; ∗ P < 0.05, ∗∗ P < 0.01; Student’s t test for statistics.

    Article Snippet: The sections were incubated with a rabbit anti-CD11b primary antibody (BM3925, Boster) overnight at 4°C, followed by incubation with a goat anti-rabbit fluorophore-conjugated secondary antibody (A-11036, Invitrogen).

    Techniques: Staining, Expressing

    Expression of ATX in CD11b + myeloid cells in primary and metastatic human melanomas T-distributed stochastic neighbor embedding (t-SNE) plots of ENPP2 (ATX) and ITGAM (CD11b) expression, and corresponding immune cell populations in (A) human melanoma tumors and (B) melanoma tumors treated with checkpoint inhibitors. T-SNE plots were generated using the Single Cell Portal ( https://singlecell.broadinstitute.org/single_cell ). NK, natural killer cells; CAF, cancer associated fibroblasts. (C) Representative immunofluorescence staining of ATX and CD11b in human primary (TriMetis #111889 634A1; #111699 594A1) and metastatic (TriMetis #109960 335B2; #111850 618A3) melanoma sections. Nuclei were counterstained for DAPI (blue), and cells were stained for CD11b (red; TRITC channel) and ATX (green; FITC channel). Merged images of all three stains are shown in the fourth panel (left). White scale bars represent 1000 μm.

    Journal: iScience

    Article Title: Deleting autotaxin in LysM+ myeloid cells impairs innate tumor immunity in models of metastatic melanoma

    doi: 10.1016/j.isci.2024.110971

    Figure Lengend Snippet: Expression of ATX in CD11b + myeloid cells in primary and metastatic human melanomas T-distributed stochastic neighbor embedding (t-SNE) plots of ENPP2 (ATX) and ITGAM (CD11b) expression, and corresponding immune cell populations in (A) human melanoma tumors and (B) melanoma tumors treated with checkpoint inhibitors. T-SNE plots were generated using the Single Cell Portal ( https://singlecell.broadinstitute.org/single_cell ). NK, natural killer cells; CAF, cancer associated fibroblasts. (C) Representative immunofluorescence staining of ATX and CD11b in human primary (TriMetis #111889 634A1; #111699 594A1) and metastatic (TriMetis #109960 335B2; #111850 618A3) melanoma sections. Nuclei were counterstained for DAPI (blue), and cells were stained for CD11b (red; TRITC channel) and ATX (green; FITC channel). Merged images of all three stains are shown in the fourth panel (left). White scale bars represent 1000 μm.

    Article Snippet: Rabbit anti-CD11b primary antibody , Thermo Fisher Scientific , Cat#PA5-90724, RRID: AB_2806205.

    Techniques: Expressing, Generated, Immunofluorescence, Staining

    Accumulation of MAM population at D18 (EMM) in LysM-WT mice After collection and digestion of the lungs, red blood cells were lysed, and the remaining cells were stained and fixed in PBS 2% formalin. Flow cytometry was performed using a 10-color antibody-panel. Dead cells were excluded and live single cells (Zombie Green-) were analyzed for surface expression of CD45. MAM population (red boxes) was identified using the following markers F480 + Ly6G − CD11b +++ Ly6C −/lo . MAM population at D14 (Top panel), D10 (Mid panel), and D18 (Bottom panel). Left panels: representative flow cytometry gating of MAM population. Right panels: MAMs shown as percentages of CD45 + cells and absolute cell number (per 200,000 total viable cells). N number of mice is represented by individual black (WT) and red (KO) dots in the graphs. Each group has a minimum of 9 mice per genotype. Statistical analysis performed with unpaired t-test. Data shown as mean ± SEM where ∗ p < 0.05 is considered statistically significant.

    Journal: iScience

    Article Title: Deleting autotaxin in LysM+ myeloid cells impairs innate tumor immunity in models of metastatic melanoma

    doi: 10.1016/j.isci.2024.110971

    Figure Lengend Snippet: Accumulation of MAM population at D18 (EMM) in LysM-WT mice After collection and digestion of the lungs, red blood cells were lysed, and the remaining cells were stained and fixed in PBS 2% formalin. Flow cytometry was performed using a 10-color antibody-panel. Dead cells were excluded and live single cells (Zombie Green-) were analyzed for surface expression of CD45. MAM population (red boxes) was identified using the following markers F480 + Ly6G − CD11b +++ Ly6C −/lo . MAM population at D14 (Top panel), D10 (Mid panel), and D18 (Bottom panel). Left panels: representative flow cytometry gating of MAM population. Right panels: MAMs shown as percentages of CD45 + cells and absolute cell number (per 200,000 total viable cells). N number of mice is represented by individual black (WT) and red (KO) dots in the graphs. Each group has a minimum of 9 mice per genotype. Statistical analysis performed with unpaired t-test. Data shown as mean ± SEM where ∗ p < 0.05 is considered statistically significant.

    Article Snippet: Rabbit anti-CD11b primary antibody , Thermo Fisher Scientific , Cat#PA5-90724, RRID: AB_2806205.

    Techniques: Staining, Flow Cytometry, Expressing

    Journal: iScience

    Article Title: Deleting autotaxin in LysM+ myeloid cells impairs innate tumor immunity in models of metastatic melanoma

    doi: 10.1016/j.isci.2024.110971

    Figure Lengend Snippet:

    Article Snippet: Rabbit anti-CD11b primary antibody , Thermo Fisher Scientific , Cat#PA5-90724, RRID: AB_2806205.

    Techniques: Recombinant, Purification, Staining, Plasmid Preparation, RNA Extraction, Reverse Transcription, Software