anti mouse nk1 1 monoclonal antibody mab  (ATCC)


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    ATCC anti mouse nk1 1 monoclonal antibody mab
    A: a) B7-1 expression in the transfectants. B7-1 expression was determined by FACS assay using FITC-conjugated anti-mouse CD80 mAb; b, c and d) <t>NK1.1</t> population in mouse splenocytes were detected by anti-NK1.1 mAb. b) Normal mouse splenocytes, c) and d) the splenocytes from tumor-immunized and anti-NK1.1 mAb treated mouse (c: on the tumor cell challenge time and d: end of experiment). B and C: In vivo tumor growth assays. B: e) mice immunized with PBS (0), Lass5-peptide-pulsed and mitomycin-c-treated RMA-S/pUB (1) or RMA-S/B7-1 (2) cells. After immunization, the mice were challenged s.c with RMA-S/pUB or RMA-S/B7-1 cells. The insert indicates tumor growth during the time point of the initial tumor cell injection through two weeks. f) Mice immunized with Lass5-peptide-pulsed and mitomycin-c-treated RMA-S/pUB cells and followed by anti-NK1.1 mAb treatment. Afterwards, the mice were challenged s.c with RMA-S/pUB or RMA-S/B7-1 cells. Statistical analysis of tumor sizes indicated significant differences between RMA-S/pUB ‘ ’ and RMA-S/B7-1 ‘*’ cell challenge groups at relevant time points (P value≤0.05 or 0.01). C: Tumor sizes at the endpoint were shown in the mice immunized with Lass5-peptide-pulsed and mitomycin-c-treated RMA-S/pUB or RMA-S/B7-1 cells and followed by challenge with live RMA-S/pUB or RMA-S/B7-1 cells.
    Anti Mouse Nk1 1 Monoclonal Antibody Mab, supplied by ATCC, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/anti mouse nk1 1 monoclonal antibody mab/product/ATCC
    Average 93 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    anti mouse nk1 1 monoclonal antibody mab - by Bioz Stars, 2024-02
    93/100 stars

    Images

    1) Product Images from "Limited Density of an Antigen Presented by RMA-S Cells Requires B7-1/CD28 Signaling to Enhance T-Cell Immunity at the Effector Phase"

    Article Title: Limited Density of an Antigen Presented by RMA-S Cells Requires B7-1/CD28 Signaling to Enhance T-Cell Immunity at the Effector Phase

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0108192

    A: a) B7-1 expression in the transfectants. B7-1 expression was determined by FACS assay using FITC-conjugated anti-mouse CD80 mAb; b, c and d) NK1.1 population in mouse splenocytes were detected by anti-NK1.1 mAb. b) Normal mouse splenocytes, c) and d) the splenocytes from tumor-immunized and anti-NK1.1 mAb treated mouse (c: on the tumor cell challenge time and d: end of experiment). B and C: In vivo tumor growth assays. B: e) mice immunized with PBS (0), Lass5-peptide-pulsed and mitomycin-c-treated RMA-S/pUB (1) or RMA-S/B7-1 (2) cells. After immunization, the mice were challenged s.c with RMA-S/pUB or RMA-S/B7-1 cells. The insert indicates tumor growth during the time point of the initial tumor cell injection through two weeks. f) Mice immunized with Lass5-peptide-pulsed and mitomycin-c-treated RMA-S/pUB cells and followed by anti-NK1.1 mAb treatment. Afterwards, the mice were challenged s.c with RMA-S/pUB or RMA-S/B7-1 cells. Statistical analysis of tumor sizes indicated significant differences between RMA-S/pUB ‘ ’ and RMA-S/B7-1 ‘*’ cell challenge groups at relevant time points (P value≤0.05 or 0.01). C: Tumor sizes at the endpoint were shown in the mice immunized with Lass5-peptide-pulsed and mitomycin-c-treated RMA-S/pUB or RMA-S/B7-1 cells and followed by challenge with live RMA-S/pUB or RMA-S/B7-1 cells.
    Figure Legend Snippet: A: a) B7-1 expression in the transfectants. B7-1 expression was determined by FACS assay using FITC-conjugated anti-mouse CD80 mAb; b, c and d) NK1.1 population in mouse splenocytes were detected by anti-NK1.1 mAb. b) Normal mouse splenocytes, c) and d) the splenocytes from tumor-immunized and anti-NK1.1 mAb treated mouse (c: on the tumor cell challenge time and d: end of experiment). B and C: In vivo tumor growth assays. B: e) mice immunized with PBS (0), Lass5-peptide-pulsed and mitomycin-c-treated RMA-S/pUB (1) or RMA-S/B7-1 (2) cells. After immunization, the mice were challenged s.c with RMA-S/pUB or RMA-S/B7-1 cells. The insert indicates tumor growth during the time point of the initial tumor cell injection through two weeks. f) Mice immunized with Lass5-peptide-pulsed and mitomycin-c-treated RMA-S/pUB cells and followed by anti-NK1.1 mAb treatment. Afterwards, the mice were challenged s.c with RMA-S/pUB or RMA-S/B7-1 cells. Statistical analysis of tumor sizes indicated significant differences between RMA-S/pUB ‘ ’ and RMA-S/B7-1 ‘*’ cell challenge groups at relevant time points (P value≤0.05 or 0.01). C: Tumor sizes at the endpoint were shown in the mice immunized with Lass5-peptide-pulsed and mitomycin-c-treated RMA-S/pUB or RMA-S/B7-1 cells and followed by challenge with live RMA-S/pUB or RMA-S/B7-1 cells.

    Techniques Used: Expressing, In Vivo, Injection

    anti mouse nk1 1 monoclonal antibody mab  (ATCC)


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    ATCC anti mouse nk1 1 monoclonal antibody mab
    A: a) B7-1 expression in the transfectants. B7-1 expression was determined by FACS assay using FITC-conjugated anti-mouse CD80 mAb; b, c and d) <t>NK1.1</t> population in mouse splenocytes were detected by anti-NK1.1 mAb. b) Normal mouse splenocytes, c) and d) the splenocytes from tumor-immunized and anti-NK1.1 mAb treated mouse (c: on the tumor cell challenge time and d: end of experiment). B and C: In vivo tumor growth assays. B: e) mice immunized with PBS (0), Lass5-peptide-pulsed and mitomycin-c-treated RMA-S/pUB (1) or RMA-S/B7-1 (2) cells. After immunization, the mice were challenged s.c with RMA-S/pUB or RMA-S/B7-1 cells. The insert indicates tumor growth during the time point of the initial tumor cell injection through two weeks. f) Mice immunized with Lass5-peptide-pulsed and mitomycin-c-treated RMA-S/pUB cells and followed by anti-NK1.1 mAb treatment. Afterwards, the mice were challenged s.c with RMA-S/pUB or RMA-S/B7-1 cells. Statistical analysis of tumor sizes indicated significant differences between RMA-S/pUB ‘ ’ and RMA-S/B7-1 ‘*’ cell challenge groups at relevant time points (P value≤0.05 or 0.01). C: Tumor sizes at the endpoint were shown in the mice immunized with Lass5-peptide-pulsed and mitomycin-c-treated RMA-S/pUB or RMA-S/B7-1 cells and followed by challenge with live RMA-S/pUB or RMA-S/B7-1 cells.
    Anti Mouse Nk1 1 Monoclonal Antibody Mab, supplied by ATCC, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/anti mouse nk1 1 monoclonal antibody mab/product/ATCC
    Average 93 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    anti mouse nk1 1 monoclonal antibody mab - by Bioz Stars, 2024-02
    93/100 stars

    Images

    1) Product Images from "Limited Density of an Antigen Presented by RMA-S Cells Requires B7-1/CD28 Signaling to Enhance T-Cell Immunity at the Effector Phase"

    Article Title: Limited Density of an Antigen Presented by RMA-S Cells Requires B7-1/CD28 Signaling to Enhance T-Cell Immunity at the Effector Phase

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0108192

    A: a) B7-1 expression in the transfectants. B7-1 expression was determined by FACS assay using FITC-conjugated anti-mouse CD80 mAb; b, c and d) NK1.1 population in mouse splenocytes were detected by anti-NK1.1 mAb. b) Normal mouse splenocytes, c) and d) the splenocytes from tumor-immunized and anti-NK1.1 mAb treated mouse (c: on the tumor cell challenge time and d: end of experiment). B and C: In vivo tumor growth assays. B: e) mice immunized with PBS (0), Lass5-peptide-pulsed and mitomycin-c-treated RMA-S/pUB (1) or RMA-S/B7-1 (2) cells. After immunization, the mice were challenged s.c with RMA-S/pUB or RMA-S/B7-1 cells. The insert indicates tumor growth during the time point of the initial tumor cell injection through two weeks. f) Mice immunized with Lass5-peptide-pulsed and mitomycin-c-treated RMA-S/pUB cells and followed by anti-NK1.1 mAb treatment. Afterwards, the mice were challenged s.c with RMA-S/pUB or RMA-S/B7-1 cells. Statistical analysis of tumor sizes indicated significant differences between RMA-S/pUB ‘ ’ and RMA-S/B7-1 ‘*’ cell challenge groups at relevant time points (P value≤0.05 or 0.01). C: Tumor sizes at the endpoint were shown in the mice immunized with Lass5-peptide-pulsed and mitomycin-c-treated RMA-S/pUB or RMA-S/B7-1 cells and followed by challenge with live RMA-S/pUB or RMA-S/B7-1 cells.
    Figure Legend Snippet: A: a) B7-1 expression in the transfectants. B7-1 expression was determined by FACS assay using FITC-conjugated anti-mouse CD80 mAb; b, c and d) NK1.1 population in mouse splenocytes were detected by anti-NK1.1 mAb. b) Normal mouse splenocytes, c) and d) the splenocytes from tumor-immunized and anti-NK1.1 mAb treated mouse (c: on the tumor cell challenge time and d: end of experiment). B and C: In vivo tumor growth assays. B: e) mice immunized with PBS (0), Lass5-peptide-pulsed and mitomycin-c-treated RMA-S/pUB (1) or RMA-S/B7-1 (2) cells. After immunization, the mice were challenged s.c with RMA-S/pUB or RMA-S/B7-1 cells. The insert indicates tumor growth during the time point of the initial tumor cell injection through two weeks. f) Mice immunized with Lass5-peptide-pulsed and mitomycin-c-treated RMA-S/pUB cells and followed by anti-NK1.1 mAb treatment. Afterwards, the mice were challenged s.c with RMA-S/pUB or RMA-S/B7-1 cells. Statistical analysis of tumor sizes indicated significant differences between RMA-S/pUB ‘ ’ and RMA-S/B7-1 ‘*’ cell challenge groups at relevant time points (P value≤0.05 or 0.01). C: Tumor sizes at the endpoint were shown in the mice immunized with Lass5-peptide-pulsed and mitomycin-c-treated RMA-S/pUB or RMA-S/B7-1 cells and followed by challenge with live RMA-S/pUB or RMA-S/B7-1 cells.

    Techniques Used: Expressing, In Vivo, Injection

    mouse monoclonal anti human igg antibody  (ATCC)


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    ATCC mouse monoclonal anti human igg antibody
    Mouse Monoclonal Anti Human Igg Antibody, supplied by ATCC, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    93/100 stars

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    mouse monoclonal hybridoma supernatant anti hnk  (ATCC)


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    ATCC mouse monoclonal hybridoma supernatant anti hnk
    Mouse Monoclonal Hybridoma Supernatant Anti Hnk, supplied by ATCC, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    mouse monoclonal anti human igg antibody  (ATCC)


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    ATCC mouse monoclonal anti human igg antibody
    Mouse Monoclonal Anti Human Igg Antibody, supplied by ATCC, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/mouse monoclonal anti human igg antibody/product/ATCC
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    e specific monoclonal antibody  (ATCC)


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    ATCC e specific monoclonal antibody
    E Specific Monoclonal Antibody, supplied by ATCC, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    mouse monoclonal anti human immunoglobulin g igg antibody  (ATCC)


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    ATCC mouse monoclonal anti human immunoglobulin g igg antibody
    Mouse Monoclonal Anti Human Immunoglobulin G Igg Antibody, supplied by ATCC, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    anti human col11a1 mouse monoclonal antibody  (ATCC)


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    ATCC anti human col11a1 mouse monoclonal antibody
    Anti Human Col11a1 Mouse Monoclonal Antibody, supplied by ATCC, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    mouse monoclonal anti human intercellular adhesion molecule 1  (ATCC)


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    ATCC mouse monoclonal anti human intercellular adhesion molecule 1
    Effect of δ-tocopherol on receptor-mediated uptake in diseased endothelial cells. (A) Microscopy quantification of the uptake (2-hour) of fluorescent ligands of individual endocytic pathways in imipramine-diseased endothelial cells (Dis) vs. control (Ctrl) cells. (B) Uptake of fluorescent ligands (3-hour) in imiprimine-diseased cells treated for 48 hours with 40 µM δ-tocopherol under noninflammatory or (C) inflammatory-like conditions (overnight incubation with TNFα). Ligands were CTB (caveolae-mediated endocytosis), Tf (clathrin-mediated endocytosis), 200 nm polymer nanocarriers targeted to <t>ICAM-1</t> (anti-ICAM NCs; CAM-mediated endocytosis), and 1 µm IgG-coated microparticles (phagocytosis; Phag.). (A–C) After ligand incubation, cells were washed and fixed, and cell surface–bound ligands were immunostained with antibodies fluorescently labeled in a different color to distinguish internalized vs. surface-bound localization (see Materials and Methods). Data are mean ± S.E.M. (n ≥ 4 independent wells), normalized to conditions shown in the horizontal solid lines. *Comparison with untreated diseased cells; †comparison with untreated diseased cells; #comparison with the CAM pathway; $comparison with the clathrin pathway (P < 0.05 by Student’s t test).
    Mouse Monoclonal Anti Human Intercellular Adhesion Molecule 1, supplied by ATCC, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    1) Product Images from "δ -Tocopherol Effect on Endocytosis and Its Combination with Enzyme Replacement Therapy for Lysosomal Disorders: A New Type of Drug Interaction? "

    Article Title: δ -Tocopherol Effect on Endocytosis and Its Combination with Enzyme Replacement Therapy for Lysosomal Disorders: A New Type of Drug Interaction?

    Journal: The Journal of Pharmacology and Experimental Therapeutics

    doi: 10.1124/jpet.119.257345

    Effect of δ-tocopherol on receptor-mediated uptake in diseased endothelial cells. (A) Microscopy quantification of the uptake (2-hour) of fluorescent ligands of individual endocytic pathways in imipramine-diseased endothelial cells (Dis) vs. control (Ctrl) cells. (B) Uptake of fluorescent ligands (3-hour) in imiprimine-diseased cells treated for 48 hours with 40 µM δ-tocopherol under noninflammatory or (C) inflammatory-like conditions (overnight incubation with TNFα). Ligands were CTB (caveolae-mediated endocytosis), Tf (clathrin-mediated endocytosis), 200 nm polymer nanocarriers targeted to ICAM-1 (anti-ICAM NCs; CAM-mediated endocytosis), and 1 µm IgG-coated microparticles (phagocytosis; Phag.). (A–C) After ligand incubation, cells were washed and fixed, and cell surface–bound ligands were immunostained with antibodies fluorescently labeled in a different color to distinguish internalized vs. surface-bound localization (see Materials and Methods). Data are mean ± S.E.M. (n ≥ 4 independent wells), normalized to conditions shown in the horizontal solid lines. *Comparison with untreated diseased cells; †comparison with untreated diseased cells; #comparison with the CAM pathway; $comparison with the clathrin pathway (P < 0.05 by Student’s t test).
    Figure Legend Snippet: Effect of δ-tocopherol on receptor-mediated uptake in diseased endothelial cells. (A) Microscopy quantification of the uptake (2-hour) of fluorescent ligands of individual endocytic pathways in imipramine-diseased endothelial cells (Dis) vs. control (Ctrl) cells. (B) Uptake of fluorescent ligands (3-hour) in imiprimine-diseased cells treated for 48 hours with 40 µM δ-tocopherol under noninflammatory or (C) inflammatory-like conditions (overnight incubation with TNFα). Ligands were CTB (caveolae-mediated endocytosis), Tf (clathrin-mediated endocytosis), 200 nm polymer nanocarriers targeted to ICAM-1 (anti-ICAM NCs; CAM-mediated endocytosis), and 1 µm IgG-coated microparticles (phagocytosis; Phag.). (A–C) After ligand incubation, cells were washed and fixed, and cell surface–bound ligands were immunostained with antibodies fluorescently labeled in a different color to distinguish internalized vs. surface-bound localization (see Materials and Methods). Data are mean ± S.E.M. (n ≥ 4 independent wells), normalized to conditions shown in the horizontal solid lines. *Comparison with untreated diseased cells; †comparison with untreated diseased cells; #comparison with the CAM pathway; $comparison with the clathrin pathway (P < 0.05 by Student’s t test).

    Techniques Used: Microscopy, Incubation, Labeling

    mouse monoclonal anti human intercellular adhesion molecule 1  (ATCC)


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    ATCC mouse monoclonal anti human intercellular adhesion molecule 1
    Effect of δ-tocopherol on receptor-mediated uptake in diseased endothelial cells. (A) Microscopy quantification of the uptake (2-hour) of fluorescent ligands of individual endocytic pathways in imipramine-diseased endothelial cells (Dis) vs. control (Ctrl) cells. (B) Uptake of fluorescent ligands (3-hour) in imiprimine-diseased cells treated for 48 hours with 40 µM δ-tocopherol under noninflammatory or (C) inflammatory-like conditions (overnight incubation with TNFα). Ligands were CTB (caveolae-mediated endocytosis), Tf (clathrin-mediated endocytosis), 200 nm polymer nanocarriers targeted to <t>ICAM-1</t> (anti-ICAM NCs; CAM-mediated endocytosis), and 1 µm IgG-coated microparticles (phagocytosis; Phag.). (A–C) After ligand incubation, cells were washed and fixed, and cell surface–bound ligands were immunostained with antibodies fluorescently labeled in a different color to distinguish internalized vs. surface-bound localization (see Materials and Methods). Data are mean ± S.E.M. (n ≥ 4 independent wells), normalized to conditions shown in the horizontal solid lines. *Comparison with untreated diseased cells; †comparison with untreated diseased cells; #comparison with the CAM pathway; $comparison with the clathrin pathway (P < 0.05 by Student’s t test).
    Mouse Monoclonal Anti Human Intercellular Adhesion Molecule 1, supplied by ATCC, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/mouse monoclonal anti human intercellular adhesion molecule 1/product/ATCC
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    1) Product Images from "δ -Tocopherol Effect on Endocytosis and Its Combination with Enzyme Replacement Therapy for Lysosomal Disorders: A New Type of Drug Interaction? "

    Article Title: δ -Tocopherol Effect on Endocytosis and Its Combination with Enzyme Replacement Therapy for Lysosomal Disorders: A New Type of Drug Interaction?

    Journal: The Journal of Pharmacology and Experimental Therapeutics

    doi: 10.1124/jpet.119.257345

    Effect of δ-tocopherol on receptor-mediated uptake in diseased endothelial cells. (A) Microscopy quantification of the uptake (2-hour) of fluorescent ligands of individual endocytic pathways in imipramine-diseased endothelial cells (Dis) vs. control (Ctrl) cells. (B) Uptake of fluorescent ligands (3-hour) in imiprimine-diseased cells treated for 48 hours with 40 µM δ-tocopherol under noninflammatory or (C) inflammatory-like conditions (overnight incubation with TNFα). Ligands were CTB (caveolae-mediated endocytosis), Tf (clathrin-mediated endocytosis), 200 nm polymer nanocarriers targeted to ICAM-1 (anti-ICAM NCs; CAM-mediated endocytosis), and 1 µm IgG-coated microparticles (phagocytosis; Phag.). (A–C) After ligand incubation, cells were washed and fixed, and cell surface–bound ligands were immunostained with antibodies fluorescently labeled in a different color to distinguish internalized vs. surface-bound localization (see Materials and Methods). Data are mean ± S.E.M. (n ≥ 4 independent wells), normalized to conditions shown in the horizontal solid lines. *Comparison with untreated diseased cells; †comparison with untreated diseased cells; #comparison with the CAM pathway; $comparison with the clathrin pathway (P < 0.05 by Student’s t test).
    Figure Legend Snippet: Effect of δ-tocopherol on receptor-mediated uptake in diseased endothelial cells. (A) Microscopy quantification of the uptake (2-hour) of fluorescent ligands of individual endocytic pathways in imipramine-diseased endothelial cells (Dis) vs. control (Ctrl) cells. (B) Uptake of fluorescent ligands (3-hour) in imiprimine-diseased cells treated for 48 hours with 40 µM δ-tocopherol under noninflammatory or (C) inflammatory-like conditions (overnight incubation with TNFα). Ligands were CTB (caveolae-mediated endocytosis), Tf (clathrin-mediated endocytosis), 200 nm polymer nanocarriers targeted to ICAM-1 (anti-ICAM NCs; CAM-mediated endocytosis), and 1 µm IgG-coated microparticles (phagocytosis; Phag.). (A–C) After ligand incubation, cells were washed and fixed, and cell surface–bound ligands were immunostained with antibodies fluorescently labeled in a different color to distinguish internalized vs. surface-bound localization (see Materials and Methods). Data are mean ± S.E.M. (n ≥ 4 independent wells), normalized to conditions shown in the horizontal solid lines. *Comparison with untreated diseased cells; †comparison with untreated diseased cells; #comparison with the CAM pathway; $comparison with the clathrin pathway (P < 0.05 by Student’s t test).

    Techniques Used: Microscopy, Incubation, Labeling

    mouse monoclonal anti human intercellular adhesion molecule 1  (ATCC)


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    ATCC mouse monoclonal anti human intercellular adhesion molecule 1
    Effect of δ-tocopherol on receptor-mediated uptake in diseased endothelial cells. (A) Microscopy quantification of the uptake (2-hour) of fluorescent ligands of individual endocytic pathways in imipramine-diseased endothelial cells (Dis) vs. control (Ctrl) cells. (B) Uptake of fluorescent ligands (3-hour) in imiprimine-diseased cells treated for 48 hours with 40 µM δ-tocopherol under noninflammatory or (C) inflammatory-like conditions (overnight incubation with TNFα). Ligands were CTB (caveolae-mediated endocytosis), Tf (clathrin-mediated endocytosis), 200 nm polymer nanocarriers targeted to <t>ICAM-1</t> (anti-ICAM NCs; CAM-mediated endocytosis), and 1 µm IgG-coated microparticles (phagocytosis; Phag.). (A–C) After ligand incubation, cells were washed and fixed, and cell surface–bound ligands were immunostained with antibodies fluorescently labeled in a different color to distinguish internalized vs. surface-bound localization (see Materials and Methods). Data are mean ± S.E.M. (n ≥ 4 independent wells), normalized to conditions shown in the horizontal solid lines. *Comparison with untreated diseased cells; †comparison with untreated diseased cells; #comparison with the CAM pathway; $comparison with the clathrin pathway (P < 0.05 by Student’s t test).
    Mouse Monoclonal Anti Human Intercellular Adhesion Molecule 1, supplied by ATCC, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    1) Product Images from "δ -Tocopherol Effect on Endocytosis and Its Combination with Enzyme Replacement Therapy for Lysosomal Disorders: A New Type of Drug Interaction? "

    Article Title: δ -Tocopherol Effect on Endocytosis and Its Combination with Enzyme Replacement Therapy for Lysosomal Disorders: A New Type of Drug Interaction?

    Journal: The Journal of Pharmacology and Experimental Therapeutics

    doi: 10.1124/jpet.119.257345

    Effect of δ-tocopherol on receptor-mediated uptake in diseased endothelial cells. (A) Microscopy quantification of the uptake (2-hour) of fluorescent ligands of individual endocytic pathways in imipramine-diseased endothelial cells (Dis) vs. control (Ctrl) cells. (B) Uptake of fluorescent ligands (3-hour) in imiprimine-diseased cells treated for 48 hours with 40 µM δ-tocopherol under noninflammatory or (C) inflammatory-like conditions (overnight incubation with TNFα). Ligands were CTB (caveolae-mediated endocytosis), Tf (clathrin-mediated endocytosis), 200 nm polymer nanocarriers targeted to ICAM-1 (anti-ICAM NCs; CAM-mediated endocytosis), and 1 µm IgG-coated microparticles (phagocytosis; Phag.). (A–C) After ligand incubation, cells were washed and fixed, and cell surface–bound ligands were immunostained with antibodies fluorescently labeled in a different color to distinguish internalized vs. surface-bound localization (see Materials and Methods). Data are mean ± S.E.M. (n ≥ 4 independent wells), normalized to conditions shown in the horizontal solid lines. *Comparison with untreated diseased cells; †comparison with untreated diseased cells; #comparison with the CAM pathway; $comparison with the clathrin pathway (P < 0.05 by Student’s t test).
    Figure Legend Snippet: Effect of δ-tocopherol on receptor-mediated uptake in diseased endothelial cells. (A) Microscopy quantification of the uptake (2-hour) of fluorescent ligands of individual endocytic pathways in imipramine-diseased endothelial cells (Dis) vs. control (Ctrl) cells. (B) Uptake of fluorescent ligands (3-hour) in imiprimine-diseased cells treated for 48 hours with 40 µM δ-tocopherol under noninflammatory or (C) inflammatory-like conditions (overnight incubation with TNFα). Ligands were CTB (caveolae-mediated endocytosis), Tf (clathrin-mediated endocytosis), 200 nm polymer nanocarriers targeted to ICAM-1 (anti-ICAM NCs; CAM-mediated endocytosis), and 1 µm IgG-coated microparticles (phagocytosis; Phag.). (A–C) After ligand incubation, cells were washed and fixed, and cell surface–bound ligands were immunostained with antibodies fluorescently labeled in a different color to distinguish internalized vs. surface-bound localization (see Materials and Methods). Data are mean ± S.E.M. (n ≥ 4 independent wells), normalized to conditions shown in the horizontal solid lines. *Comparison with untreated diseased cells; †comparison with untreated diseased cells; #comparison with the CAM pathway; $comparison with the clathrin pathway (P < 0.05 by Student’s t test).

    Techniques Used: Microscopy, Incubation, Labeling