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recombinant bmi1 igg1 rea438 apc miltenyi biotec 130 124 301 isotype control mouse igg1κ  (Miltenyi Biotec)


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    Miltenyi Biotec recombinant bmi1 igg1 rea438 apc miltenyi biotec 130 124 301 isotype control mouse igg1κ
    Recombinant Bmi1 Igg1 Rea438 Apc Miltenyi Biotec 130 124 301 Isotype Control Mouse Igg1κ, supplied by Miltenyi Biotec, used in various techniques. Bioz Stars score: 93/100, based on 4 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/human+igg+isotype+control+antibodies/BMI-1+Antibody%2C+anti-human%2C+REAfinity/pm41991735-194-0-5
    Average 93 stars, based on 4 article reviews
    recombinant bmi1 igg1 rea438 apc miltenyi biotec 130 124 301 isotype control mouse igg1κ - by Bioz Stars, 2026-11
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    Staining:

    Article Title: Systemic Inflammation Modulates Clearance and drives Extra-Hepatic Distribution of Extracellular Vesicles
    Article Snippet: For the analysis of EV at the single vesicle level, high resolution Imaging Flow Cytometry (IFCM) on a Cell stream instrument (Cytek/Amnis) based on previously optimized settings and protocols established on an Amnis Cellstream instrument (Amnis/Luminex).EVs from plasma were diluted in PBS-HAT buffer (ref 4) in all steps. .. In brief, 2.5 ×10 8 EVs (NTA-based particles) were stained in a total volume of 25 μl with 8 nM of fluorescent antibodies against human CD63 or human IgG isotype control antibodies (Miltenyi Biotec). ..

    Article Title: Systemic Inflammation Modulates Clearance and Drives Extra‐Hepatic Distribution of Extracellular Vesicles
    Article Snippet: .. In brief, 2.5 × 10 8 EVs (NTA‐based particles) were stained in a total volume of 25 μL with 8 nM of fluorescent antibodies against human CD63 or human IgG isotype control antibodies (Miltenyi Biotec). ..

    Article Title: Systemic Inflammation Modulates Clearance and Drives Extra-Hepatic Distribution of Extracellular Vesicles.
    Article Snippet: .. In brief, 2.5 × 108 EVs (NTA-based particles) were stained in a total volume of 25 μL with 8 nM of fluorescent antibodies against human CD63 or human IgG isotype control antibodies (Miltenyi Biotec). ..

    Control:

    Article Title: Systemic Inflammation Modulates Clearance and drives Extra-Hepatic Distribution of Extracellular Vesicles
    Article Snippet: For the analysis of EV at the single vesicle level, high resolution Imaging Flow Cytometry (IFCM) on a Cell stream instrument (Cytek/Amnis) based on previously optimized settings and protocols established on an Amnis Cellstream instrument (Amnis/Luminex).EVs from plasma were diluted in PBS-HAT buffer (ref 4) in all steps. .. In brief, 2.5 ×10 8 EVs (NTA-based particles) were stained in a total volume of 25 μl with 8 nM of fluorescent antibodies against human CD63 or human IgG isotype control antibodies (Miltenyi Biotec). ..

    Article Title: Systemic Inflammation Modulates Clearance and Drives Extra‐Hepatic Distribution of Extracellular Vesicles
    Article Snippet: .. In brief, 2.5 × 10 8 EVs (NTA‐based particles) were stained in a total volume of 25 μL with 8 nM of fluorescent antibodies against human CD63 or human IgG isotype control antibodies (Miltenyi Biotec). ..

    Article Title: Systemic Inflammation Modulates Clearance and Drives Extra-Hepatic Distribution of Extracellular Vesicles.
    Article Snippet: .. In brief, 2.5 × 108 EVs (NTA-based particles) were stained in a total volume of 25 μL with 8 nM of fluorescent antibodies against human CD63 or human IgG isotype control antibodies (Miltenyi Biotec). ..



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    The effect of PTPN2/PTPN1 inhibition on T cells activation and synapse formation. Peripheral blood CLL cells were treated with the indicated concentration of AC484 for 2 hours. DMSO treated cells served as controls (NT ). Following treatment, the cells were stimulated with Dynabeads ® Human T Cells-Activator CD3/CD28 for 24 hours at 37 °C. After incubation, the cells were stained with Pacific Blue Anti-Human CD8 or CD4 and PE Anti-Human CD69 or CD25. Samples were acquired by FACSCanto II (BD) and analyzed using BD FACSDiva software. (A) Quantification of %CD25+ cells in CD4 + population (n=10) (B) Quantification of %CD69+ cells in CD4 + population (n=10). (C) Quantification of %CD25+ cells in CD8 + population (n=10). (D) Quantification of %CD69+ cells in CD8 + population (n=10). (E–H) Subgroup analysis of CD25 or CD69 expression in CD8 + or CD4 + T cells population according to IGHV mutation status, (E, F) M-CLL (n=5) or (G, H) U-CLL (n=5), *p<0.05, **p<0.01, ***p<0.001. Data shown as mean+SD. (I–K) CLL cells were seeded on poly-L-lysine coated glass, then treated with 1µM AC484 for 2 hours. Then the cells were incubated with 1μg/mL of mosunetuzumab or human IgG kappa isotype control for 72 hours. The cells were fixed and permeabilized, followed by staining for CD8 (white), granzyme B (red), IgM (green) and DAPI (blue). Representative confocal images showing synapse formation between B cells (green) and CD8 + T cells (white). (I) Representative image of cells treated with the isotype control. (J) Representative image of cells treated with mosunetuzumab. (K) Representative image of cells treated with mosunetuzumab and the PTPN2/PTPN1 inhibitor AC484. Scale bar, 5 µm.

    Journal: Frontiers in Immunology

    Article Title: PTPN2/PTPN1 inhibition enhances ex vivo T- cell responses and potentiates mosunetuzumab activity in chronic lymphocytic leukemia

    doi: 10.3389/fimmu.2026.1948967

    Figure Lengend Snippet: The effect of PTPN2/PTPN1 inhibition on T cells activation and synapse formation. Peripheral blood CLL cells were treated with the indicated concentration of AC484 for 2 hours. DMSO treated cells served as controls (NT ). Following treatment, the cells were stimulated with Dynabeads ® Human T Cells-Activator CD3/CD28 for 24 hours at 37 °C. After incubation, the cells were stained with Pacific Blue Anti-Human CD8 or CD4 and PE Anti-Human CD69 or CD25. Samples were acquired by FACSCanto II (BD) and analyzed using BD FACSDiva software. (A) Quantification of %CD25+ cells in CD4 + population (n=10) (B) Quantification of %CD69+ cells in CD4 + population (n=10). (C) Quantification of %CD25+ cells in CD8 + population (n=10). (D) Quantification of %CD69+ cells in CD8 + population (n=10). (E–H) Subgroup analysis of CD25 or CD69 expression in CD8 + or CD4 + T cells population according to IGHV mutation status, (E, F) M-CLL (n=5) or (G, H) U-CLL (n=5), *p<0.05, **p<0.01, ***p<0.001. Data shown as mean+SD. (I–K) CLL cells were seeded on poly-L-lysine coated glass, then treated with 1µM AC484 for 2 hours. Then the cells were incubated with 1μg/mL of mosunetuzumab or human IgG kappa isotype control for 72 hours. The cells were fixed and permeabilized, followed by staining for CD8 (white), granzyme B (red), IgM (green) and DAPI (blue). Representative confocal images showing synapse formation between B cells (green) and CD8 + T cells (white). (I) Representative image of cells treated with the isotype control. (J) Representative image of cells treated with mosunetuzumab. (K) Representative image of cells treated with mosunetuzumab and the PTPN2/PTPN1 inhibitor AC484. Scale bar, 5 µm.

    Article Snippet: PTPN2/PTPN1 inhibitor ABBV-CLS-484 (AC484,Osunprotafib,HY-145923), mosunetuzumab (HY-P99033) and human IgG kappa isotype control (HY-P99001) were from MedChemExpress (USA).

    Techniques: Inhibition, Activation Assay, Concentration Assay, Incubation, Staining, Software, Analysis, Expressing, Mutagenesis, Glass, Control, Confocal

    ( A ) Interleukin-2 (IL-2) and interferon gamma (IFN-γ) inhibition in CD3 + cells during allogeneic one-way MLR measured at day 2 and day 5, respectively, treated with 50 nM combination pharmacological inhibitors of TNF/TNFR targets of interest. Monotreatment groups included 50 nM of human IgG1. Cytokine inhibition was calculated as percent reduction from IgG1 control treatment. Ill denotes P <0.05 in student t-test for monotreatments vs. IgG1 control, # denotes P <0.05 in student t-tests for combination treatment groups vs. IgG1 controls and both constituent monotreatments. ( B ) Normalized IL-2 and IFN-γ expression in four promising combinations of TNF/TNFR inhibitors. ( C-D ) Proliferation in CD3 + cells during allogeneic one-way MLR measured at day 5 in the presence of combination pharmacological inhibition of TNF/TNFR targets of interest.* denotes P <0.05 in student t-test. Data from three unique stimulator-responder MLR pairs, mean ± SEM plotted. Large-molecule pharmacological TNF/TNFR inhibitors used: Adalimumab (abbr. Ada, α-TNF), Pateclizumab (α-LTA), Baminercept (abbr. Bam, LTβR decoy), Dapirolizumab (abbr. Dapiro, α-CD40L), Amlitelimab (abbr. Amlite, α-OX40L), CD30Li (α-CD30L), 4-1BB-Fc (4-1BB decoy), Quisovalimab (α-LIGHT), Duvakitug (α-TL1A), and GITRi (α-GITR).

    Journal: bioRxiv

    Article Title: Combination antagonism of TNF superfamily signaling for T cell immunosuppression

    doi: 10.64898/2026.04.27.721101

    Figure Lengend Snippet: ( A ) Interleukin-2 (IL-2) and interferon gamma (IFN-γ) inhibition in CD3 + cells during allogeneic one-way MLR measured at day 2 and day 5, respectively, treated with 50 nM combination pharmacological inhibitors of TNF/TNFR targets of interest. Monotreatment groups included 50 nM of human IgG1. Cytokine inhibition was calculated as percent reduction from IgG1 control treatment. Ill denotes P <0.05 in student t-test for monotreatments vs. IgG1 control, # denotes P <0.05 in student t-tests for combination treatment groups vs. IgG1 controls and both constituent monotreatments. ( B ) Normalized IL-2 and IFN-γ expression in four promising combinations of TNF/TNFR inhibitors. ( C-D ) Proliferation in CD3 + cells during allogeneic one-way MLR measured at day 5 in the presence of combination pharmacological inhibition of TNF/TNFR targets of interest.* denotes P <0.05 in student t-test. Data from three unique stimulator-responder MLR pairs, mean ± SEM plotted. Large-molecule pharmacological TNF/TNFR inhibitors used: Adalimumab (abbr. Ada, α-TNF), Pateclizumab (α-LTA), Baminercept (abbr. Bam, LTβR decoy), Dapirolizumab (abbr. Dapiro, α-CD40L), Amlitelimab (abbr. Amlite, α-OX40L), CD30Li (α-CD30L), 4-1BB-Fc (4-1BB decoy), Quisovalimab (α-LIGHT), Duvakitug (α-TL1A), and GITRi (α-GITR).

    Article Snippet: Adalimumab (Cat. HY-P9908), Pateclizumab (Cat. HY-P990034), Baminercept (Cat. HY-P99459), Amlitelimab (Cat. HY-P99434), Dapirolizumab (Cat. HY-P99842A), Quisovalimab (Cat. HY-P99810), Duvakitug (Cat. HY-P99842A), human IgG1 (Cat. HY-P99001) and human IgG4 (Cat. HY-P99003) were purchased from MedChemExpress.

    Techniques: Inhibition, Control, Expressing

    ( A-B ) Interleukin-2 (IL-2) and interferon gamma (IFN-γ) inhibition in CD3 + cells during allogeneic one-way MLR measured at day 2 and day 5, respectively, treated with 50 nM combination pharmacological inhibitors of TNF/TNFR targets of interest. Monotreatment groups included 50 nM of human IgG1. Cytokine expression normalized to IgG1 control treatment. * denotes P <0.05 in student t-test for monotreatments vs. IgG1 control. Data from three individual stimulator-responder MLR pairs, mean ± SEM plotted.

    Journal: bioRxiv

    Article Title: Combination antagonism of TNF superfamily signaling for T cell immunosuppression

    doi: 10.64898/2026.04.27.721101

    Figure Lengend Snippet: ( A-B ) Interleukin-2 (IL-2) and interferon gamma (IFN-γ) inhibition in CD3 + cells during allogeneic one-way MLR measured at day 2 and day 5, respectively, treated with 50 nM combination pharmacological inhibitors of TNF/TNFR targets of interest. Monotreatment groups included 50 nM of human IgG1. Cytokine expression normalized to IgG1 control treatment. * denotes P <0.05 in student t-test for monotreatments vs. IgG1 control. Data from three individual stimulator-responder MLR pairs, mean ± SEM plotted.

    Article Snippet: Adalimumab (Cat. HY-P9908), Pateclizumab (Cat. HY-P990034), Baminercept (Cat. HY-P99459), Amlitelimab (Cat. HY-P99434), Dapirolizumab (Cat. HY-P99842A), Quisovalimab (Cat. HY-P99810), Duvakitug (Cat. HY-P99842A), human IgG1 (Cat. HY-P99001) and human IgG4 (Cat. HY-P99003) were purchased from MedChemExpress.

    Techniques: Inhibition, Expressing, Control