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anti human mouse cd11b apc cy7  (Cytek Biosciences)


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    Cytek Biosciences anti human mouse cd11b apc cy7
    Anti Human Mouse Cd11b Apc Cy7, supplied by Cytek Biosciences, used in various techniques. Bioz Stars score: 94/100, based on 30 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/anti human mouse cd11b apc cy7/product/Cytek Biosciences
    Average 94 stars, based on 30 article reviews
    anti human mouse cd11b apc cy7 - by Bioz Stars, 2026-03
    94/100 stars

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    (A) Representative plots and frequencies of splenic XCR1 + cDC1s, XCR1 − CD172a − merocytic DCs (mero), CLEC12A − cDC2A, and CLEC12A + cDC2B of total cDCs (Lin − MHCII + CD11c + CD26 + ) or of total cDC2s (CD172a + ) in female control (top) and Kdm5c ΔItgax (bottom) mice. (B) Representative plots, proportions, and counts of splenic Ly6C + pDCs and Ly6C − pDCs from female control and Kdm5c ΔItgax mice (parent gate: Lin(B220) + SiglecH + CD11c int <t>CD11b</t> − ). (C) BM chimeras were generated in CD45.1 + host mice by reconstituting their BM with a 1:1 mixture of CD45.1 + control and CD45.2 + Kdm5c ΔItgax BM or CD45.2 + Kdm5c ΔItgax BM alone. Proportions of splenic DC subsets are derived from CD45.1 + control and CD45.2 + Kdm5c ΔItgax cells 7 weeks post injection. (D) Proportions of splenic cDCs of mice administered α-IgG2b or α-PDCA1 to deplete pDCs. (E) Frequencies of splenic cDCs from control and Ifnar1 −/− mice. Each symbol represents an individual mouse. Data were pooled from 2–3 experiments of 9–11 mice per group. (A, B, D, and E) Statistical significance was determined by unpaired t test or (C) one-way ANOVA. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001. All error bars represent mean and SEM. See also .
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    Becton Dickinson apc-cy7 anti mouse-cd11b
    (A) Representative plots and frequencies of splenic XCR1 + cDC1s, XCR1 − CD172a − merocytic DCs (mero), CLEC12A − cDC2A, and CLEC12A + cDC2B of total cDCs (Lin − MHCII + CD11c + CD26 + ) or of total cDC2s (CD172a + ) in female control (top) and Kdm5c ΔItgax (bottom) mice. (B) Representative plots, proportions, and counts of splenic Ly6C + pDCs and Ly6C − pDCs from female control and Kdm5c ΔItgax mice (parent gate: Lin(B220) + SiglecH + CD11c int <t>CD11b</t> − ). (C) BM chimeras were generated in CD45.1 + host mice by reconstituting their BM with a 1:1 mixture of CD45.1 + control and CD45.2 + Kdm5c ΔItgax BM or CD45.2 + Kdm5c ΔItgax BM alone. Proportions of splenic DC subsets are derived from CD45.1 + control and CD45.2 + Kdm5c ΔItgax cells 7 weeks post injection. (D) Proportions of splenic cDCs of mice administered α-IgG2b or α-PDCA1 to deplete pDCs. (E) Frequencies of splenic cDCs from control and Ifnar1 −/− mice. Each symbol represents an individual mouse. Data were pooled from 2–3 experiments of 9–11 mice per group. (A, B, D, and E) Statistical significance was determined by unpaired t test or (C) one-way ANOVA. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001. All error bars represent mean and SEM. See also .
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    Cytek Biosciences cd11b apc cy7
    (A) Cell types, tissue origin, and biotin groups in SAMENT single-cell dataset. (B) GSVA analysis comparing biotin-positive NK cells to biotin-negative NK cells highlights potential regulations exerted by NK cells on macrophages. Biotin-positive NK cells appear to modulate the tumor microenvironment by enhancing chemotaxis and inhibiting both aging and apoptosis in macrophages. This suggests that upon encountering tumors, reprogrammed NK cells indirectly contribute to chronic inflammation and promote the survival of tumor-associated macrophages. (C) Top enriched pathways in biotin-positive immature B cells in bones compared with other tissues. (D) Top enriched pathways in monocyte and neutrophil precursors in lungs compared with other tissues. (E) Top enriched pathways in biotin-positive granulocyte-macrophage progenitors (GMPs) in bone compared with biotin-negative populations. (F) Validation of published tissue-specific macrophage signatures was conducted in the SAMENT dataset. Reported Microglia signatures include Tmem119 + , Trem2 + , Fcrls + , Slc2a5 + , P2ry12 + , and Cx3cr1 + . Alveolars signatures consist of Cd163 − , <t>Cd11b</t> − , Cd206 int , Spp1 + , SiglecF + and Cd11c + ; Osteoclasts signatures are characterized by Arg1 + , Spp1 + , Mmp9 + , and vacuolar [H+]-ATPase + ; Kupffers cell signatures include CD11b low , F4/80 high , and Clec4F + ; Monocyte-derived macrophage signatures , encompass CD11b + , F4/80 int , Ly6C + and CSF1R + . In our dataset, Mφ_c10 corresponds to Microglia, Mφ_c7 corresponds Alveolar macrophages, and Mφ_c5 corresponds to osteoclasts. Monocyte-derived macrophages are distributed across all macrophage subclusters, while we did not identify specific clusters for Kupffer cells. These findings support the observations depicted in .
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    Cytek Biosciences apc cy7 anti mouse 147 cd11b
    (A) Cell types, tissue origin, and biotin groups in SAMENT single-cell dataset. (B) GSVA analysis comparing biotin-positive NK cells to biotin-negative NK cells highlights potential regulations exerted by NK cells on macrophages. Biotin-positive NK cells appear to modulate the tumor microenvironment by enhancing chemotaxis and inhibiting both aging and apoptosis in macrophages. This suggests that upon encountering tumors, reprogrammed NK cells indirectly contribute to chronic inflammation and promote the survival of tumor-associated macrophages. (C) Top enriched pathways in biotin-positive immature B cells in bones compared with other tissues. (D) Top enriched pathways in monocyte and neutrophil precursors in lungs compared with other tissues. (E) Top enriched pathways in biotin-positive granulocyte-macrophage progenitors (GMPs) in bone compared with biotin-negative populations. (F) Validation of published tissue-specific macrophage signatures was conducted in the SAMENT dataset. Reported Microglia signatures include Tmem119 + , Trem2 + , Fcrls + , Slc2a5 + , P2ry12 + , and Cx3cr1 + . Alveolars signatures consist of Cd163 − , <t>Cd11b</t> − , Cd206 int , Spp1 + , SiglecF + and Cd11c + ; Osteoclasts signatures are characterized by Arg1 + , Spp1 + , Mmp9 + , and vacuolar [H+]-ATPase + ; Kupffers cell signatures include CD11b low , F4/80 high , and Clec4F + ; Monocyte-derived macrophage signatures , encompass CD11b + , F4/80 int , Ly6C + and CSF1R + . In our dataset, Mφ_c10 corresponds to Microglia, Mφ_c7 corresponds Alveolar macrophages, and Mφ_c5 corresponds to osteoclasts. Monocyte-derived macrophages are distributed across all macrophage subclusters, while we did not identify specific clusters for Kupffer cells. These findings support the observations depicted in .
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    Miltenyi Biotec reafinitytm mouse miltenyi biotec 130 117 692 cd11b pe cy7 mouse biolegend 301321 cd16 bv605 mouse biolegend 302040

    Reafinitytm Mouse Miltenyi Biotec 130 117 692 Cd11b Pe Cy7 Mouse Biolegend 301321 Cd16 Bv605 Mouse Biolegend 302040, supplied by Miltenyi Biotec, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Image Search Results


    (A) Representative plots and frequencies of splenic XCR1 + cDC1s, XCR1 − CD172a − merocytic DCs (mero), CLEC12A − cDC2A, and CLEC12A + cDC2B of total cDCs (Lin − MHCII + CD11c + CD26 + ) or of total cDC2s (CD172a + ) in female control (top) and Kdm5c ΔItgax (bottom) mice. (B) Representative plots, proportions, and counts of splenic Ly6C + pDCs and Ly6C − pDCs from female control and Kdm5c ΔItgax mice (parent gate: Lin(B220) + SiglecH + CD11c int CD11b − ). (C) BM chimeras were generated in CD45.1 + host mice by reconstituting their BM with a 1:1 mixture of CD45.1 + control and CD45.2 + Kdm5c ΔItgax BM or CD45.2 + Kdm5c ΔItgax BM alone. Proportions of splenic DC subsets are derived from CD45.1 + control and CD45.2 + Kdm5c ΔItgax cells 7 weeks post injection. (D) Proportions of splenic cDCs of mice administered α-IgG2b or α-PDCA1 to deplete pDCs. (E) Frequencies of splenic cDCs from control and Ifnar1 −/− mice. Each symbol represents an individual mouse. Data were pooled from 2–3 experiments of 9–11 mice per group. (A, B, D, and E) Statistical significance was determined by unpaired t test or (C) one-way ANOVA. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001. All error bars represent mean and SEM. See also .

    Journal: Cell reports

    Article Title: Transcriptional programming mediated by the histone demethylase KDM5C regulates dendritic cell population heterogeneity and function

    doi: 10.1016/j.celrep.2024.114506

    Figure Lengend Snippet: (A) Representative plots and frequencies of splenic XCR1 + cDC1s, XCR1 − CD172a − merocytic DCs (mero), CLEC12A − cDC2A, and CLEC12A + cDC2B of total cDCs (Lin − MHCII + CD11c + CD26 + ) or of total cDC2s (CD172a + ) in female control (top) and Kdm5c ΔItgax (bottom) mice. (B) Representative plots, proportions, and counts of splenic Ly6C + pDCs and Ly6C − pDCs from female control and Kdm5c ΔItgax mice (parent gate: Lin(B220) + SiglecH + CD11c int CD11b − ). (C) BM chimeras were generated in CD45.1 + host mice by reconstituting their BM with a 1:1 mixture of CD45.1 + control and CD45.2 + Kdm5c ΔItgax BM or CD45.2 + Kdm5c ΔItgax BM alone. Proportions of splenic DC subsets are derived from CD45.1 + control and CD45.2 + Kdm5c ΔItgax cells 7 weeks post injection. (D) Proportions of splenic cDCs of mice administered α-IgG2b or α-PDCA1 to deplete pDCs. (E) Frequencies of splenic cDCs from control and Ifnar1 −/− mice. Each symbol represents an individual mouse. Data were pooled from 2–3 experiments of 9–11 mice per group. (A, B, D, and E) Statistical significance was determined by unpaired t test or (C) one-way ANOVA. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001. All error bars represent mean and SEM. See also .

    Article Snippet: Anti-mouse CD11b APC/Cy7 (clone M1/70) , eBioscience , 47-0112-82; RRID:AB_1603193.

    Techniques: Control, Generated, Derivative Assay, Injection

    KEY RESOURCES TABLE

    Journal: Cell reports

    Article Title: Transcriptional programming mediated by the histone demethylase KDM5C regulates dendritic cell population heterogeneity and function

    doi: 10.1016/j.celrep.2024.114506

    Figure Lengend Snippet: KEY RESOURCES TABLE

    Article Snippet: Anti-mouse CD11b APC/Cy7 (clone M1/70) , eBioscience , 47-0112-82; RRID:AB_1603193.

    Techniques: Control, Blocking Assay, Virus, Recombinant, Protease Inhibitor, Lysis, Enzyme-linked Immunosorbent Assay, Staining, Cell Isolation, DNA Library Preparation, Purification, RNA HS Assay, Mutagenesis, Software

    (A) Cell types, tissue origin, and biotin groups in SAMENT single-cell dataset. (B) GSVA analysis comparing biotin-positive NK cells to biotin-negative NK cells highlights potential regulations exerted by NK cells on macrophages. Biotin-positive NK cells appear to modulate the tumor microenvironment by enhancing chemotaxis and inhibiting both aging and apoptosis in macrophages. This suggests that upon encountering tumors, reprogrammed NK cells indirectly contribute to chronic inflammation and promote the survival of tumor-associated macrophages. (C) Top enriched pathways in biotin-positive immature B cells in bones compared with other tissues. (D) Top enriched pathways in monocyte and neutrophil precursors in lungs compared with other tissues. (E) Top enriched pathways in biotin-positive granulocyte-macrophage progenitors (GMPs) in bone compared with biotin-negative populations. (F) Validation of published tissue-specific macrophage signatures was conducted in the SAMENT dataset. Reported Microglia signatures include Tmem119 + , Trem2 + , Fcrls + , Slc2a5 + , P2ry12 + , and Cx3cr1 + . Alveolars signatures consist of Cd163 − , Cd11b − , Cd206 int , Spp1 + , SiglecF + and Cd11c + ; Osteoclasts signatures are characterized by Arg1 + , Spp1 + , Mmp9 + , and vacuolar [H+]-ATPase + ; Kupffers cell signatures include CD11b low , F4/80 high , and Clec4F + ; Monocyte-derived macrophage signatures , encompass CD11b + , F4/80 int , Ly6C + and CSF1R + . In our dataset, Mφ_c10 corresponds to Microglia, Mφ_c7 corresponds Alveolar macrophages, and Mφ_c5 corresponds to osteoclasts. Monocyte-derived macrophages are distributed across all macrophage subclusters, while we did not identify specific clusters for Kupffer cells. These findings support the observations depicted in .

    Journal: bioRxiv

    Article Title: Unbiased metastatic niche-labeling identifies estrogen receptor-positive macrophages as a barrier of T cell infiltration during bone colonization

    doi: 10.1101/2024.05.07.593016

    Figure Lengend Snippet: (A) Cell types, tissue origin, and biotin groups in SAMENT single-cell dataset. (B) GSVA analysis comparing biotin-positive NK cells to biotin-negative NK cells highlights potential regulations exerted by NK cells on macrophages. Biotin-positive NK cells appear to modulate the tumor microenvironment by enhancing chemotaxis and inhibiting both aging and apoptosis in macrophages. This suggests that upon encountering tumors, reprogrammed NK cells indirectly contribute to chronic inflammation and promote the survival of tumor-associated macrophages. (C) Top enriched pathways in biotin-positive immature B cells in bones compared with other tissues. (D) Top enriched pathways in monocyte and neutrophil precursors in lungs compared with other tissues. (E) Top enriched pathways in biotin-positive granulocyte-macrophage progenitors (GMPs) in bone compared with biotin-negative populations. (F) Validation of published tissue-specific macrophage signatures was conducted in the SAMENT dataset. Reported Microglia signatures include Tmem119 + , Trem2 + , Fcrls + , Slc2a5 + , P2ry12 + , and Cx3cr1 + . Alveolars signatures consist of Cd163 − , Cd11b − , Cd206 int , Spp1 + , SiglecF + and Cd11c + ; Osteoclasts signatures are characterized by Arg1 + , Spp1 + , Mmp9 + , and vacuolar [H+]-ATPase + ; Kupffers cell signatures include CD11b low , F4/80 high , and Clec4F + ; Monocyte-derived macrophage signatures , encompass CD11b + , F4/80 int , Ly6C + and CSF1R + . In our dataset, Mφ_c10 corresponds to Microglia, Mφ_c7 corresponds Alveolar macrophages, and Mφ_c5 corresponds to osteoclasts. Monocyte-derived macrophages are distributed across all macrophage subclusters, while we did not identify specific clusters for Kupffer cells. These findings support the observations depicted in .

    Article Snippet: The antibodies used in this study included: Immune cell panel, CD45-VF450 (Cytek® Biosciences,75–0451), CD11b-APC/Cy7 (Cytek® Biosciences, 25–0112), Ly6G-Percp/Cy5.5 (Cytek® Biosciences, 65–1276), Ly6C-PE/Cy7 (BioLegend,128018), F4/80-BV510 (BioLegend,123135), B220-APC/Cy7 (Cytek® Biosciences, 25-0452), CD3e-Percp/Cy5.5 (Cytek® Biosciences,65-0031), CD4-PE/Cy7 (Cytek® Biosciences,60-0041), CD8a-BV711 (BD Biosciences,752634), PD-1-BV605 (BioLegend,135219), Biotin-APC (Miltenyi Biotec,130-113-288) or Biotin-PE(Miltenyi Biotec,130-113-291); Stromal cell panel, CD45-BV605 (BioLegend,103140), Ter119-BV605 (BioLegend,116239), CD31-APC/Cy7 (BioLegend,102440), Sca-1-Percp/Cy5.5 (eBioscience,45–5981-82), CD51-BV421 (BD Biosciences, 740062), CD140α-PE/Cy7 (BioLegend, 135912), Biotin-APC (Miltenyi Biotec,130-113-288) or Biotin-PE(Miltenyi Biotec,130-113-291) Flow cytometry analysis was conducted using a BD LSRFortessa flow cytometer and data were further analyzed with FlowJo software.

    Techniques: Chemotaxis Assay, Biomarker Discovery, Derivative Assay

    Journal: iScience

    Article Title: Engraftment of adult hematopoietic stem and progenitor cells in a novel model of humanized mice

    doi: 10.1016/j.isci.2024.109238

    Figure Lengend Snippet:

    Article Snippet: Mouse CD11b-APC/Cy7 (M1/70) , TONBO , 25-0112-U100; RRID: AB_3094465.

    Techniques: Recombinant, Staining, Red Blood Cell Lysis, Enzyme-linked Immunosorbent Assay, Software