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  • 99
    Thermo Fisher celltracker orange cmra
    PI3Kδ D910A CD8 + T cells show functional defects. In vitro assays were conducted with 3 biological replicates. ( A ) CD8 + T cell cytotoxic capacity was measured in an in vitro killing assay, using tumor cells expressing ovalbumin (OVA) protein (stained with CMFDA <t>CellTracker</t> Green) as targets for in vitro–stimulated OT-I CD8 + T cells, and parental tumor cells (stained with <t>CMRA</t> CellTracker Orange) as controls. Representative FACS plots shows EL4-OVA and EL4 cells incubated with, from left to right, WT, PI3Kδ D910A , or no CD8 + T cells. ( B ) Cytotoxic efficiency measured in WT versus PI3Kδ D910A OT-I CD8 + cells using EL4-OVA, MC38-OVA, and LLC-OVA cells. ( C ) Cytotoxic efficiency measured in WT versus PI3Kδ D910A OT-I CD8 + cells using EL4 cells pulsed with SIINFEKL peptide, and single-amino-acid variants of decreasing binding affinity for the OT-I T cell receptor (TCR). ( D ) CD62L, granzyme A, and granzyme B expression measured in in vitro–stimulated WT versus PI3Kδ D910A OT-I CD8 + cells. MFI, median fluorescence intensity. ( E ) Granzyme A and B expression measured in tumor-infiltrating CD8 + T cells from WT vs PI3Kδ D910A mice ( n = 8). Statistical significance was determined by multiple t tests with Holm-Sidak correction ( B – D ) or the Mann-Whitney test ( E ). * P
    Celltracker Orange Cmra, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 99/100, based on 497 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/celltracker orange cmra/product/Thermo Fisher
    Average 99 stars, based on 497 article reviews
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    celltracker orange cmra - by Bioz Stars, 2020-09
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    93
    Thermo Fisher celltracer orange cmra
    FF interferes with the DCX-resistance of DU145 cells. ( A ) were cultivated in the presence of DCX (1.25–50 nM) and their proliferation was estimated after 48 h. ( B ) Comparison of the morphology, actin cytoskeleton architecture (left) and proliferation (right) of DU145, DU145_DCX20 and DU145_DCX50 cells in control conditions. ( C , D ) Motility (C) and trans-endothelial migration efficiency of DU145 and DCX-resistant DU145 cells (D) was estimated in actin/vinculin-stained specimens. DU145 cells were additionally stained with <t>CellTracer</t> Orange <t>CMRA.</t> Transmigration values show a percent of cancer cells that penetrated the adjacent endothelial barrier. ( E ) DU145 and DU145_DCX20 cells were subcutaneously injected into severe combined immunodeficient (SCID) mice (1.5 × 10 5 ) and the growth of tumors was estimated in the absence/presence of DCX (20 mg/kg b.w). Images show the structure of tumors visualized by hematoxilin/eosin staining. ( F ) The activity of efflux pumps in DCX-resistant DU145 cells was estimated with calcein efflux assay in control conditions (plotted as fluorescence intensity (a.u.)). ( G ) DU145_DCX20 cells were cultivated in the presence of DCX (0.3–5 nM) and/or FF (5–25 μM). Their proliferation was estimated after 48 h (plotted as % of control). ( H , I ) Naïve and DCX-resistant DU145 cells were treated with 2.5 nM DCX/25 μM FF and their motility was estimated with time-lapse videomicroscopy immediately afterwards (H) or (I) their viability (ATP levels (left)/proliferation (right)) were estimated after 48 h (calculated as % of control). Data representative of at least three independent experiments (N > 3). Statistical significance was analyzed with the t-Student ( A , B , D – G , I ) or with the non-parametric Mann-Whitney test ( C , H ) vs. non-treated control (* p ≤ 0.05), vs. DCX-treated variant ( # p ≤ 0.05; A ) or vs. the variant indicated by the brackets ( # p ≤ 0.05). Error bars represent SEM. Scale bar: 50 µm. Note the additive inhibitory effects of FF and DCX on the welfare and motility of DCX-resistant DU145 cells.
    Celltracer Orange Cmra, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 93/100, based on 39 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/celltracer orange cmra/product/Thermo Fisher
    Average 93 stars, based on 39 article reviews
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    celltracer orange cmra - by Bioz Stars, 2020-09
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    84
    Thermo Fisher celltracker orange cmra 185
    FF interferes with the DCX-resistance of DU145 cells. ( A ) were cultivated in the presence of DCX (1.25–50 nM) and their proliferation was estimated after 48 h. ( B ) Comparison of the morphology, actin cytoskeleton architecture (left) and proliferation (right) of DU145, DU145_DCX20 and DU145_DCX50 cells in control conditions. ( C , D ) Motility (C) and trans-endothelial migration efficiency of DU145 and DCX-resistant DU145 cells (D) was estimated in actin/vinculin-stained specimens. DU145 cells were additionally stained with <t>CellTracer</t> Orange <t>CMRA.</t> Transmigration values show a percent of cancer cells that penetrated the adjacent endothelial barrier. ( E ) DU145 and DU145_DCX20 cells were subcutaneously injected into severe combined immunodeficient (SCID) mice (1.5 × 10 5 ) and the growth of tumors was estimated in the absence/presence of DCX (20 mg/kg b.w). Images show the structure of tumors visualized by hematoxilin/eosin staining. ( F ) The activity of efflux pumps in DCX-resistant DU145 cells was estimated with calcein efflux assay in control conditions (plotted as fluorescence intensity (a.u.)). ( G ) DU145_DCX20 cells were cultivated in the presence of DCX (0.3–5 nM) and/or FF (5–25 μM). Their proliferation was estimated after 48 h (plotted as % of control). ( H , I ) Naïve and DCX-resistant DU145 cells were treated with 2.5 nM DCX/25 μM FF and their motility was estimated with time-lapse videomicroscopy immediately afterwards (H) or (I) their viability (ATP levels (left)/proliferation (right)) were estimated after 48 h (calculated as % of control). Data representative of at least three independent experiments (N > 3). Statistical significance was analyzed with the t-Student ( A , B , D – G , I ) or with the non-parametric Mann-Whitney test ( C , H ) vs. non-treated control (* p ≤ 0.05), vs. DCX-treated variant ( # p ≤ 0.05; A ) or vs. the variant indicated by the brackets ( # p ≤ 0.05). Error bars represent SEM. Scale bar: 50 µm. Note the additive inhibitory effects of FF and DCX on the welfare and motility of DCX-resistant DU145 cells.
    Celltracker Orange Cmra 185, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 84/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/celltracker orange cmra 185/product/Thermo Fisher
    Average 84 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    celltracker orange cmra 185 - by Bioz Stars, 2020-09
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    99
    Thermo Fisher celltracker orange cmra dye thermo fisher cat
    FF interferes with the DCX-resistance of DU145 cells. ( A ) were cultivated in the presence of DCX (1.25–50 nM) and their proliferation was estimated after 48 h. ( B ) Comparison of the morphology, actin cytoskeleton architecture (left) and proliferation (right) of DU145, DU145_DCX20 and DU145_DCX50 cells in control conditions. ( C , D ) Motility (C) and trans-endothelial migration efficiency of DU145 and DCX-resistant DU145 cells (D) was estimated in actin/vinculin-stained specimens. DU145 cells were additionally stained with <t>CellTracer</t> Orange <t>CMRA.</t> Transmigration values show a percent of cancer cells that penetrated the adjacent endothelial barrier. ( E ) DU145 and DU145_DCX20 cells were subcutaneously injected into severe combined immunodeficient (SCID) mice (1.5 × 10 5 ) and the growth of tumors was estimated in the absence/presence of DCX (20 mg/kg b.w). Images show the structure of tumors visualized by hematoxilin/eosin staining. ( F ) The activity of efflux pumps in DCX-resistant DU145 cells was estimated with calcein efflux assay in control conditions (plotted as fluorescence intensity (a.u.)). ( G ) DU145_DCX20 cells were cultivated in the presence of DCX (0.3–5 nM) and/or FF (5–25 μM). Their proliferation was estimated after 48 h (plotted as % of control). ( H , I ) Naïve and DCX-resistant DU145 cells were treated with 2.5 nM DCX/25 μM FF and their motility was estimated with time-lapse videomicroscopy immediately afterwards (H) or (I) their viability (ATP levels (left)/proliferation (right)) were estimated after 48 h (calculated as % of control). Data representative of at least three independent experiments (N > 3). Statistical significance was analyzed with the t-Student ( A , B , D – G , I ) or with the non-parametric Mann-Whitney test ( C , H ) vs. non-treated control (* p ≤ 0.05), vs. DCX-treated variant ( # p ≤ 0.05; A ) or vs. the variant indicated by the brackets ( # p ≤ 0.05). Error bars represent SEM. Scale bar: 50 µm. Note the additive inhibitory effects of FF and DCX on the welfare and motility of DCX-resistant DU145 cells.
    Celltracker Orange Cmra Dye Thermo Fisher Cat, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/celltracker orange cmra dye thermo fisher cat/product/Thermo Fisher
    Average 99 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    celltracker orange cmra dye thermo fisher cat - by Bioz Stars, 2020-09
    99/100 stars
      Buy from Supplier

    Image Search Results


    PI3Kδ D910A CD8 + T cells show functional defects. In vitro assays were conducted with 3 biological replicates. ( A ) CD8 + T cell cytotoxic capacity was measured in an in vitro killing assay, using tumor cells expressing ovalbumin (OVA) protein (stained with CMFDA CellTracker Green) as targets for in vitro–stimulated OT-I CD8 + T cells, and parental tumor cells (stained with CMRA CellTracker Orange) as controls. Representative FACS plots shows EL4-OVA and EL4 cells incubated with, from left to right, WT, PI3Kδ D910A , or no CD8 + T cells. ( B ) Cytotoxic efficiency measured in WT versus PI3Kδ D910A OT-I CD8 + cells using EL4-OVA, MC38-OVA, and LLC-OVA cells. ( C ) Cytotoxic efficiency measured in WT versus PI3Kδ D910A OT-I CD8 + cells using EL4 cells pulsed with SIINFEKL peptide, and single-amino-acid variants of decreasing binding affinity for the OT-I T cell receptor (TCR). ( D ) CD62L, granzyme A, and granzyme B expression measured in in vitro–stimulated WT versus PI3Kδ D910A OT-I CD8 + cells. MFI, median fluorescence intensity. ( E ) Granzyme A and B expression measured in tumor-infiltrating CD8 + T cells from WT vs PI3Kδ D910A mice ( n = 8). Statistical significance was determined by multiple t tests with Holm-Sidak correction ( B – D ) or the Mann-Whitney test ( E ). * P

    Journal: JCI Insight

    Article Title: Phosphoinositide 3-kinase δ inhibition promotes antitumor responses but antagonizes checkpoint inhibitors

    doi: 10.1172/jci.insight.120626

    Figure Lengend Snippet: PI3Kδ D910A CD8 + T cells show functional defects. In vitro assays were conducted with 3 biological replicates. ( A ) CD8 + T cell cytotoxic capacity was measured in an in vitro killing assay, using tumor cells expressing ovalbumin (OVA) protein (stained with CMFDA CellTracker Green) as targets for in vitro–stimulated OT-I CD8 + T cells, and parental tumor cells (stained with CMRA CellTracker Orange) as controls. Representative FACS plots shows EL4-OVA and EL4 cells incubated with, from left to right, WT, PI3Kδ D910A , or no CD8 + T cells. ( B ) Cytotoxic efficiency measured in WT versus PI3Kδ D910A OT-I CD8 + cells using EL4-OVA, MC38-OVA, and LLC-OVA cells. ( C ) Cytotoxic efficiency measured in WT versus PI3Kδ D910A OT-I CD8 + cells using EL4 cells pulsed with SIINFEKL peptide, and single-amino-acid variants of decreasing binding affinity for the OT-I T cell receptor (TCR). ( D ) CD62L, granzyme A, and granzyme B expression measured in in vitro–stimulated WT versus PI3Kδ D910A OT-I CD8 + cells. MFI, median fluorescence intensity. ( E ) Granzyme A and B expression measured in tumor-infiltrating CD8 + T cells from WT vs PI3Kδ D910A mice ( n = 8). Statistical significance was determined by multiple t tests with Holm-Sidak correction ( B – D ) or the Mann-Whitney test ( E ). * P

    Article Snippet: Parental tumor cells and OVA-expressing derivatives were stained with, respectively, CellTracker Orange CMRA and CellTracker Green CMFDA (Molecular Probes).

    Techniques: Functional Assay, In Vitro, Expressing, Staining, FACS, Incubation, Binding Assay, Fluorescence, Mouse Assay, MANN-WHITNEY

    FF interferes with the DCX-resistance of DU145 cells. ( A ) were cultivated in the presence of DCX (1.25–50 nM) and their proliferation was estimated after 48 h. ( B ) Comparison of the morphology, actin cytoskeleton architecture (left) and proliferation (right) of DU145, DU145_DCX20 and DU145_DCX50 cells in control conditions. ( C , D ) Motility (C) and trans-endothelial migration efficiency of DU145 and DCX-resistant DU145 cells (D) was estimated in actin/vinculin-stained specimens. DU145 cells were additionally stained with CellTracer Orange CMRA. Transmigration values show a percent of cancer cells that penetrated the adjacent endothelial barrier. ( E ) DU145 and DU145_DCX20 cells were subcutaneously injected into severe combined immunodeficient (SCID) mice (1.5 × 10 5 ) and the growth of tumors was estimated in the absence/presence of DCX (20 mg/kg b.w). Images show the structure of tumors visualized by hematoxilin/eosin staining. ( F ) The activity of efflux pumps in DCX-resistant DU145 cells was estimated with calcein efflux assay in control conditions (plotted as fluorescence intensity (a.u.)). ( G ) DU145_DCX20 cells were cultivated in the presence of DCX (0.3–5 nM) and/or FF (5–25 μM). Their proliferation was estimated after 48 h (plotted as % of control). ( H , I ) Naïve and DCX-resistant DU145 cells were treated with 2.5 nM DCX/25 μM FF and their motility was estimated with time-lapse videomicroscopy immediately afterwards (H) or (I) their viability (ATP levels (left)/proliferation (right)) were estimated after 48 h (calculated as % of control). Data representative of at least three independent experiments (N > 3). Statistical significance was analyzed with the t-Student ( A , B , D – G , I ) or with the non-parametric Mann-Whitney test ( C , H ) vs. non-treated control (* p ≤ 0.05), vs. DCX-treated variant ( # p ≤ 0.05; A ) or vs. the variant indicated by the brackets ( # p ≤ 0.05). Error bars represent SEM. Scale bar: 50 µm. Note the additive inhibitory effects of FF and DCX on the welfare and motility of DCX-resistant DU145 cells.

    Journal: Cancers

    Article Title: Fenofibrate Augments the Sensitivity of Drug-Resistant Prostate Cancer Cells to Docetaxel

    doi: 10.3390/cancers11010077

    Figure Lengend Snippet: FF interferes with the DCX-resistance of DU145 cells. ( A ) were cultivated in the presence of DCX (1.25–50 nM) and their proliferation was estimated after 48 h. ( B ) Comparison of the morphology, actin cytoskeleton architecture (left) and proliferation (right) of DU145, DU145_DCX20 and DU145_DCX50 cells in control conditions. ( C , D ) Motility (C) and trans-endothelial migration efficiency of DU145 and DCX-resistant DU145 cells (D) was estimated in actin/vinculin-stained specimens. DU145 cells were additionally stained with CellTracer Orange CMRA. Transmigration values show a percent of cancer cells that penetrated the adjacent endothelial barrier. ( E ) DU145 and DU145_DCX20 cells were subcutaneously injected into severe combined immunodeficient (SCID) mice (1.5 × 10 5 ) and the growth of tumors was estimated in the absence/presence of DCX (20 mg/kg b.w). Images show the structure of tumors visualized by hematoxilin/eosin staining. ( F ) The activity of efflux pumps in DCX-resistant DU145 cells was estimated with calcein efflux assay in control conditions (plotted as fluorescence intensity (a.u.)). ( G ) DU145_DCX20 cells were cultivated in the presence of DCX (0.3–5 nM) and/or FF (5–25 μM). Their proliferation was estimated after 48 h (plotted as % of control). ( H , I ) Naïve and DCX-resistant DU145 cells were treated with 2.5 nM DCX/25 μM FF and their motility was estimated with time-lapse videomicroscopy immediately afterwards (H) or (I) their viability (ATP levels (left)/proliferation (right)) were estimated after 48 h (calculated as % of control). Data representative of at least three independent experiments (N > 3). Statistical significance was analyzed with the t-Student ( A , B , D – G , I ) or with the non-parametric Mann-Whitney test ( C , H ) vs. non-treated control (* p ≤ 0.05), vs. DCX-treated variant ( # p ≤ 0.05; A ) or vs. the variant indicated by the brackets ( # p ≤ 0.05). Error bars represent SEM. Scale bar: 50 µm. Note the additive inhibitory effects of FF and DCX on the welfare and motility of DCX-resistant DU145 cells.

    Article Snippet: For transmigration assays, human umbilical vein endothelial cells (HUVEC) were seeded on coverslips at 2 × 104 cells/well and grown to confluence for 72 h. Thereafter, CellTracer Orange CMRA (10 μM, Life Technologies)-stained cancer cells were seeded (1300/cm2 ) on HUVEC monolayers and incubated for 1 and 6 h [ ].

    Techniques: Migration, Staining, Transmigration Assay, Injection, Mouse Assay, Activity Assay, Fluorescence, MANN-WHITNEY, Variant Assay