nk92 egfp cd16 pta 8836 cell lines  (ATCC)


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    ATCC nk92 egfp cd16 pta 8836 cell lines
    Neuroblastoma-derived sEVs modulate NK cell maturation in vivo and NK cell-mediated ADCC in vitro. (A) Schematic of NK cell subpopulations. Created with BioRender.com. (B) Representative flow cytometry plots of splenic NK cell subpopulations isolated from 9464D-GD2 tumor-bearing mice receiving the indicated treatments as described in . (C) Quantification of the percentage of immature splenic NK cell (CD27 +CD11b-; left panel) and mature NK cell (CD27- CD11b+; right panel) subpopulations in 9464D-GD2 tumor-bearing mice treated as described in . Mean±SEM, n=7 per group. Student’s t-test. *p<0.05; **p<0.01; ***p<0.001. (D–G) Human (IMR32) or murine (9464D-GD2) neuroblastoma cells treated as indicated in the presence or absence of <t>NK92-CD16-EGFP</t> cells (NK) and monitored for viability utilizing cell impermeant nucleic acid stain YOYO-3 with the IncuCyte S3 Live-Cell Analysis System. The cell-by-cell analysis module was used to quantify viable tumor cells (YOYO3- EGFP-). (D) Kinetic analysis of the IMR32 in vitro NK-cell-mediated ADCC assay. Mean±SEM, n=6. Viable cells calculated as percentage of viable cells in each treatment condition divided by viable cells in untreated control group. (E) Percentage of viable IMR32 cells at 24 hours, n=6. Mean±SD. One-way ANOVA with Tukey’s/Sidak’s post hoc tests. **p<0.01; ***p<0.001. (F) Kinetic analysis of the 9464D-GD2 in vitro NK-cell-mediated ADCC assay. Mean±SEM, n=4. Viable cells calculated as percentage of viable cells in each treatment condition divided by viable cells in untreated control group. (G) Percentage of viable 9464D-GD2 cells at 24 hours, n=4. Mean±SD. One-way ANOVA with Tukey’s/Sidak’s post hoc tests. *p<0.05; **p<0.01; ***p<0.001. ADCC, antibody-dependent cell-mediated cytotoxicity; ANOVA, analysis of variance; DN, double negative; DP, double positive; sEV, small extracellular vesicle.
    Nk92 Egfp Cd16 Pta 8836 Cell Lines, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Average 99 stars, based on 1 article reviews
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    1) Product Images from "Small extracellular vesicles induce resistance to anti-GD2 immunotherapy unveiling tipifarnib as an adjunct to neuroblastoma immunotherapy"

    Article Title: Small extracellular vesicles induce resistance to anti-GD2 immunotherapy unveiling tipifarnib as an adjunct to neuroblastoma immunotherapy

    Journal: Journal for Immunotherapy of Cancer

    doi: 10.1136/jitc-2021-004399

    Neuroblastoma-derived sEVs modulate NK cell maturation in vivo and NK cell-mediated ADCC in vitro. (A) Schematic of NK cell subpopulations. Created with BioRender.com. (B) Representative flow cytometry plots of splenic NK cell subpopulations isolated from 9464D-GD2 tumor-bearing mice receiving the indicated treatments as described in . (C) Quantification of the percentage of immature splenic NK cell (CD27 +CD11b-; left panel) and mature NK cell (CD27- CD11b+; right panel) subpopulations in 9464D-GD2 tumor-bearing mice treated as described in . Mean±SEM, n=7 per group. Student’s t-test. *p<0.05; **p<0.01; ***p<0.001. (D–G) Human (IMR32) or murine (9464D-GD2) neuroblastoma cells treated as indicated in the presence or absence of NK92-CD16-EGFP cells (NK) and monitored for viability utilizing cell impermeant nucleic acid stain YOYO-3 with the IncuCyte S3 Live-Cell Analysis System. The cell-by-cell analysis module was used to quantify viable tumor cells (YOYO3- EGFP-). (D) Kinetic analysis of the IMR32 in vitro NK-cell-mediated ADCC assay. Mean±SEM, n=6. Viable cells calculated as percentage of viable cells in each treatment condition divided by viable cells in untreated control group. (E) Percentage of viable IMR32 cells at 24 hours, n=6. Mean±SD. One-way ANOVA with Tukey’s/Sidak’s post hoc tests. **p<0.01; ***p<0.001. (F) Kinetic analysis of the 9464D-GD2 in vitro NK-cell-mediated ADCC assay. Mean±SEM, n=4. Viable cells calculated as percentage of viable cells in each treatment condition divided by viable cells in untreated control group. (G) Percentage of viable 9464D-GD2 cells at 24 hours, n=4. Mean±SD. One-way ANOVA with Tukey’s/Sidak’s post hoc tests. *p<0.05; **p<0.01; ***p<0.001. ADCC, antibody-dependent cell-mediated cytotoxicity; ANOVA, analysis of variance; DN, double negative; DP, double positive; sEV, small extracellular vesicle.
    Figure Legend Snippet: Neuroblastoma-derived sEVs modulate NK cell maturation in vivo and NK cell-mediated ADCC in vitro. (A) Schematic of NK cell subpopulations. Created with BioRender.com. (B) Representative flow cytometry plots of splenic NK cell subpopulations isolated from 9464D-GD2 tumor-bearing mice receiving the indicated treatments as described in . (C) Quantification of the percentage of immature splenic NK cell (CD27 +CD11b-; left panel) and mature NK cell (CD27- CD11b+; right panel) subpopulations in 9464D-GD2 tumor-bearing mice treated as described in . Mean±SEM, n=7 per group. Student’s t-test. *p<0.05; **p<0.01; ***p<0.001. (D–G) Human (IMR32) or murine (9464D-GD2) neuroblastoma cells treated as indicated in the presence or absence of NK92-CD16-EGFP cells (NK) and monitored for viability utilizing cell impermeant nucleic acid stain YOYO-3 with the IncuCyte S3 Live-Cell Analysis System. The cell-by-cell analysis module was used to quantify viable tumor cells (YOYO3- EGFP-). (D) Kinetic analysis of the IMR32 in vitro NK-cell-mediated ADCC assay. Mean±SEM, n=6. Viable cells calculated as percentage of viable cells in each treatment condition divided by viable cells in untreated control group. (E) Percentage of viable IMR32 cells at 24 hours, n=6. Mean±SD. One-way ANOVA with Tukey’s/Sidak’s post hoc tests. **p<0.01; ***p<0.001. (F) Kinetic analysis of the 9464D-GD2 in vitro NK-cell-mediated ADCC assay. Mean±SEM, n=4. Viable cells calculated as percentage of viable cells in each treatment condition divided by viable cells in untreated control group. (G) Percentage of viable 9464D-GD2 cells at 24 hours, n=4. Mean±SD. One-way ANOVA with Tukey’s/Sidak’s post hoc tests. *p<0.05; **p<0.01; ***p<0.001. ADCC, antibody-dependent cell-mediated cytotoxicity; ANOVA, analysis of variance; DN, double negative; DP, double positive; sEV, small extracellular vesicle.

    Techniques Used: Derivative Assay, In Vivo, In Vitro, Flow Cytometry, Isolation, Staining, ADCC Assay

    cd16 nk 92  (ATCC)


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    ATCC cd16 nk 92
    Cd16 Nk 92, supplied by ATCC, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    nk92 egfp cd16 pta 8836 cell lines  (ATCC)


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    ATCC nk92 egfp cd16 pta 8836 cell lines
    Neuroblastoma-derived sEVs modulate NK cell maturation in vivo and NK cell-mediated ADCC in vitro. (A) Schematic of NK cell subpopulations. Created with BioRender.com. (B) Representative flow cytometry plots of splenic NK cell subpopulations isolated from 9464D-GD2 tumor-bearing mice receiving the indicated treatments as described in . (C) Quantification of the percentage of immature splenic NK cell (CD27 +CD11b-; left panel) and mature NK cell (CD27- CD11b+; right panel) subpopulations in 9464D-GD2 tumor-bearing mice treated as described in . Mean±SEM, n=7 per group. Student’s t-test. *p<0.05; **p<0.01; ***p<0.001. (D–G) Human (IMR32) or murine (9464D-GD2) neuroblastoma cells treated as indicated in the presence or absence of <t>NK92-CD16-EGFP</t> cells (NK) and monitored for viability utilizing cell impermeant nucleic acid stain YOYO-3 with the IncuCyte S3 Live-Cell Analysis System. The cell-by-cell analysis module was used to quantify viable tumor cells (YOYO3- EGFP-). (D) Kinetic analysis of the IMR32 in vitro NK-cell-mediated ADCC assay. Mean±SEM, n=6. Viable cells calculated as percentage of viable cells in each treatment condition divided by viable cells in untreated control group. (E) Percentage of viable IMR32 cells at 24 hours, n=6. Mean±SD. One-way ANOVA with Tukey’s/Sidak’s post hoc tests. **p<0.01; ***p<0.001. (F) Kinetic analysis of the 9464D-GD2 in vitro NK-cell-mediated ADCC assay. Mean±SEM, n=4. Viable cells calculated as percentage of viable cells in each treatment condition divided by viable cells in untreated control group. (G) Percentage of viable 9464D-GD2 cells at 24 hours, n=4. Mean±SD. One-way ANOVA with Tukey’s/Sidak’s post hoc tests. *p<0.05; **p<0.01; ***p<0.001. ADCC, antibody-dependent cell-mediated cytotoxicity; ANOVA, analysis of variance; DN, double negative; DP, double positive; sEV, small extracellular vesicle.
    Nk92 Egfp Cd16 Pta 8836 Cell Lines, supplied by ATCC, 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/nk92 egfp cd16 pta 8836 cell lines/product/ATCC
    Average 99 stars, based on 1 article reviews
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    nk92 egfp cd16 pta 8836 cell lines - by Bioz Stars, 2024-02
    99/100 stars

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    1) Product Images from "Small extracellular vesicles induce resistance to anti-GD2 immunotherapy unveiling tipifarnib as an adjunct to neuroblastoma immunotherapy"

    Article Title: Small extracellular vesicles induce resistance to anti-GD2 immunotherapy unveiling tipifarnib as an adjunct to neuroblastoma immunotherapy

    Journal: Journal for Immunotherapy of Cancer

    doi: 10.1136/jitc-2021-004399

    Neuroblastoma-derived sEVs modulate NK cell maturation in vivo and NK cell-mediated ADCC in vitro. (A) Schematic of NK cell subpopulations. Created with BioRender.com. (B) Representative flow cytometry plots of splenic NK cell subpopulations isolated from 9464D-GD2 tumor-bearing mice receiving the indicated treatments as described in . (C) Quantification of the percentage of immature splenic NK cell (CD27 +CD11b-; left panel) and mature NK cell (CD27- CD11b+; right panel) subpopulations in 9464D-GD2 tumor-bearing mice treated as described in . Mean±SEM, n=7 per group. Student’s t-test. *p<0.05; **p<0.01; ***p<0.001. (D–G) Human (IMR32) or murine (9464D-GD2) neuroblastoma cells treated as indicated in the presence or absence of NK92-CD16-EGFP cells (NK) and monitored for viability utilizing cell impermeant nucleic acid stain YOYO-3 with the IncuCyte S3 Live-Cell Analysis System. The cell-by-cell analysis module was used to quantify viable tumor cells (YOYO3- EGFP-). (D) Kinetic analysis of the IMR32 in vitro NK-cell-mediated ADCC assay. Mean±SEM, n=6. Viable cells calculated as percentage of viable cells in each treatment condition divided by viable cells in untreated control group. (E) Percentage of viable IMR32 cells at 24 hours, n=6. Mean±SD. One-way ANOVA with Tukey’s/Sidak’s post hoc tests. **p<0.01; ***p<0.001. (F) Kinetic analysis of the 9464D-GD2 in vitro NK-cell-mediated ADCC assay. Mean±SEM, n=4. Viable cells calculated as percentage of viable cells in each treatment condition divided by viable cells in untreated control group. (G) Percentage of viable 9464D-GD2 cells at 24 hours, n=4. Mean±SD. One-way ANOVA with Tukey’s/Sidak’s post hoc tests. *p<0.05; **p<0.01; ***p<0.001. ADCC, antibody-dependent cell-mediated cytotoxicity; ANOVA, analysis of variance; DN, double negative; DP, double positive; sEV, small extracellular vesicle.
    Figure Legend Snippet: Neuroblastoma-derived sEVs modulate NK cell maturation in vivo and NK cell-mediated ADCC in vitro. (A) Schematic of NK cell subpopulations. Created with BioRender.com. (B) Representative flow cytometry plots of splenic NK cell subpopulations isolated from 9464D-GD2 tumor-bearing mice receiving the indicated treatments as described in . (C) Quantification of the percentage of immature splenic NK cell (CD27 +CD11b-; left panel) and mature NK cell (CD27- CD11b+; right panel) subpopulations in 9464D-GD2 tumor-bearing mice treated as described in . Mean±SEM, n=7 per group. Student’s t-test. *p<0.05; **p<0.01; ***p<0.001. (D–G) Human (IMR32) or murine (9464D-GD2) neuroblastoma cells treated as indicated in the presence or absence of NK92-CD16-EGFP cells (NK) and monitored for viability utilizing cell impermeant nucleic acid stain YOYO-3 with the IncuCyte S3 Live-Cell Analysis System. The cell-by-cell analysis module was used to quantify viable tumor cells (YOYO3- EGFP-). (D) Kinetic analysis of the IMR32 in vitro NK-cell-mediated ADCC assay. Mean±SEM, n=6. Viable cells calculated as percentage of viable cells in each treatment condition divided by viable cells in untreated control group. (E) Percentage of viable IMR32 cells at 24 hours, n=6. Mean±SD. One-way ANOVA with Tukey’s/Sidak’s post hoc tests. **p<0.01; ***p<0.001. (F) Kinetic analysis of the 9464D-GD2 in vitro NK-cell-mediated ADCC assay. Mean±SEM, n=4. Viable cells calculated as percentage of viable cells in each treatment condition divided by viable cells in untreated control group. (G) Percentage of viable 9464D-GD2 cells at 24 hours, n=4. Mean±SD. One-way ANOVA with Tukey’s/Sidak’s post hoc tests. *p<0.05; **p<0.01; ***p<0.001. ADCC, antibody-dependent cell-mediated cytotoxicity; ANOVA, analysis of variance; DN, double negative; DP, double positive; sEV, small extracellular vesicle.

    Techniques Used: Derivative Assay, In Vivo, In Vitro, Flow Cytometry, Isolation, Staining, ADCC Assay

    human nk cell line  (ATCC)


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    ATCC human nk cell line
    Human Nk Cell Line, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    human nk 92 cell line  (ATCC)


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    ATCC human nk 92 cell line
    Human Nk 92 Cell Line, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    natural killer nk 92 lineages  (ATCC)


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    ATCC natural killer nk 92 lineages
    Natural Killer Nk 92 Lineages, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    natural killer cell line nk  (ATCC)


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    ATCC natural killer cell line nk
    VPA enhances the sensitivity of pancreatic cancer cells to NK cell-mediated lysis via a NKG2D-dependent mechanism. (A) VPA sensitized pancreatic cancer cells to NK cell-mediated lysis; * P < 0.05; ** P < 0.01. (B) Blockade of NKG2D attenuated the ability of VPA to sensitize pancreatic cancer cells to NK cell-mediated lysis; * P < 0.05 for VPA + IgG vs. VPA + NKG2D; ** P < 0.01 for VPA + IgG vs. VPA + NKG2D. Data are mean ± SD of a single experiment performed in triplicate, all results were reproducible in three independent experiments. E:T, effector/ target ratio.
    Natural Killer Cell Line Nk, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Average 99 stars, based on 1 article reviews
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    natural killer cell line nk - by Bioz Stars, 2024-02
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    1) Product Images from "Valproic acid sensitizes pancreatic cancer cells to natural killer cell-mediated lysis by upregulating MICA and MICB via the PI3K/Akt signaling pathway"

    Article Title: Valproic acid sensitizes pancreatic cancer cells to natural killer cell-mediated lysis by upregulating MICA and MICB via the PI3K/Akt signaling pathway

    Journal: BMC Cancer

    doi: 10.1186/1471-2407-14-370

    VPA enhances the sensitivity of pancreatic cancer cells to NK cell-mediated lysis via a NKG2D-dependent mechanism. (A) VPA sensitized pancreatic cancer cells to NK cell-mediated lysis; * P < 0.05; ** P < 0.01. (B) Blockade of NKG2D attenuated the ability of VPA to sensitize pancreatic cancer cells to NK cell-mediated lysis; * P < 0.05 for VPA + IgG vs. VPA + NKG2D; ** P < 0.01 for VPA + IgG vs. VPA + NKG2D. Data are mean ± SD of a single experiment performed in triplicate, all results were reproducible in three independent experiments. E:T, effector/ target ratio.
    Figure Legend Snippet: VPA enhances the sensitivity of pancreatic cancer cells to NK cell-mediated lysis via a NKG2D-dependent mechanism. (A) VPA sensitized pancreatic cancer cells to NK cell-mediated lysis; * P < 0.05; ** P < 0.01. (B) Blockade of NKG2D attenuated the ability of VPA to sensitize pancreatic cancer cells to NK cell-mediated lysis; * P < 0.05 for VPA + IgG vs. VPA + NKG2D; ** P < 0.01 for VPA + IgG vs. VPA + NKG2D. Data are mean ± SD of a single experiment performed in triplicate, all results were reproducible in three independent experiments. E:T, effector/ target ratio.

    Techniques Used: Lysis

    PI3K/Akt signaling is required for VPA-induced upregulation of MICA and MICB in pancreatic cancer cells. (A, B) Quantitative real-time RT-PCR analysis. The VPA-induced upregulation of MICA and MICB mRNA expression were inhibited by the HER2/HER3 inhibitor lapatinib and the PI3K inhibitor LY294002, but not by the ATM/ATR inhibitor caffeine. Data are mean ± SD of a single experiment performed in triplicate, all results were reproducible in three independent experiments. * P < 0.05; ** P < 0.01; ns P > 0.05. (C) Flow cytometry analysis. The VPA-induced upregulation of MICA and MICB protein expression on the cell surface were inhibited by the PI3K inhibitor LY294002. MFI, mean fluorescence intensity; * P < 0.05. (D) Western blotting analysis. Transfection of the PI3KCA siRNA inhibited PI3KCA protein expression at 48 h post-transfection. NC, negative control; siR1-3, PI3KCA_siR sequence 1-3; ** P < 0.01. (E) Quantitative real-time RT-PCR analysis. VPA-induced upregulation of MICA and MICB mRNA expression were attenuated in PI3KCA-knockdown cells; Data are mean ± SD of a single experiment performed in triplicate, all results were reproducible in three independent experiments. ** P < 0.01. (F) Flow cytometric analysis. VPA-induced upregulation of MICA and MICB protein expression on the cell surface were attenuated in PI3KCA-knockdown cells. MFI, mean fluorescence intensity; * P < 0.05; ** P < 0.01. (G) LDH release assay. The VPA-induced susceptibility of cancer cells to NK cell-mediated cell lysis was reduced in PI3KCA-knockdown cells. Data are mean ± SD of a single experiment performed in triplicate, all results were reproducible in three independent experiments. ** P < 0.01 and * P < 0.05 for NC vs. siR2; ▲▲ P < 0.01 and ▲ P < 0.05 for NC vs. siR3. siR2, PI3KCA siR sequence 2; siR3, PI3KCA siR sequence 3.
    Figure Legend Snippet: PI3K/Akt signaling is required for VPA-induced upregulation of MICA and MICB in pancreatic cancer cells. (A, B) Quantitative real-time RT-PCR analysis. The VPA-induced upregulation of MICA and MICB mRNA expression were inhibited by the HER2/HER3 inhibitor lapatinib and the PI3K inhibitor LY294002, but not by the ATM/ATR inhibitor caffeine. Data are mean ± SD of a single experiment performed in triplicate, all results were reproducible in three independent experiments. * P < 0.05; ** P < 0.01; ns P > 0.05. (C) Flow cytometry analysis. The VPA-induced upregulation of MICA and MICB protein expression on the cell surface were inhibited by the PI3K inhibitor LY294002. MFI, mean fluorescence intensity; * P < 0.05. (D) Western blotting analysis. Transfection of the PI3KCA siRNA inhibited PI3KCA protein expression at 48 h post-transfection. NC, negative control; siR1-3, PI3KCA_siR sequence 1-3; ** P < 0.01. (E) Quantitative real-time RT-PCR analysis. VPA-induced upregulation of MICA and MICB mRNA expression were attenuated in PI3KCA-knockdown cells; Data are mean ± SD of a single experiment performed in triplicate, all results were reproducible in three independent experiments. ** P < 0.01. (F) Flow cytometric analysis. VPA-induced upregulation of MICA and MICB protein expression on the cell surface were attenuated in PI3KCA-knockdown cells. MFI, mean fluorescence intensity; * P < 0.05; ** P < 0.01. (G) LDH release assay. The VPA-induced susceptibility of cancer cells to NK cell-mediated cell lysis was reduced in PI3KCA-knockdown cells. Data are mean ± SD of a single experiment performed in triplicate, all results were reproducible in three independent experiments. ** P < 0.01 and * P < 0.05 for NC vs. siR2; ▲▲ P < 0.01 and ▲ P < 0.05 for NC vs. siR3. siR2, PI3KCA siR sequence 2; siR3, PI3KCA siR sequence 3.

    Techniques Used: Quantitative RT-PCR, Expressing, Flow Cytometry, Fluorescence, Western Blot, Transfection, Negative Control, Sequencing, Lactate Dehydrogenase Assay, Lysis

    VPA sensitizes pancreatic cancer cells to NK cell-mediated lysis in vivo by upregulating the expression of MICA and MICB. (A, B) Excised xenograft tumors and growth curves for the xenografts; VPA enhanced the growth inhibitory effect of NK cells in vivo ; this effect was attenuated by the PI3K inhibitor LY294002. Data are mean ± SD of five mice per group; * P < 0.05 for NK-92 vs. NK-92 + VPA; Δ P < 0.05 for NK-92 + VPA + LY294002 vs. NK-92 + VPA. (C) Immunohistochemical staining and quantification of MICA and MICB expression in the xenograft tumors; VPA significantly upregulated the expression of MICA and MICB in the pancreatic cancer xenograft tumors in vivo , this effect was attenuated by the PI3K inhibitor LY294002.
    Figure Legend Snippet: VPA sensitizes pancreatic cancer cells to NK cell-mediated lysis in vivo by upregulating the expression of MICA and MICB. (A, B) Excised xenograft tumors and growth curves for the xenografts; VPA enhanced the growth inhibitory effect of NK cells in vivo ; this effect was attenuated by the PI3K inhibitor LY294002. Data are mean ± SD of five mice per group; * P < 0.05 for NK-92 vs. NK-92 + VPA; Δ P < 0.05 for NK-92 + VPA + LY294002 vs. NK-92 + VPA. (C) Immunohistochemical staining and quantification of MICA and MICB expression in the xenograft tumors; VPA significantly upregulated the expression of MICA and MICB in the pancreatic cancer xenograft tumors in vivo , this effect was attenuated by the PI3K inhibitor LY294002.

    Techniques Used: Lysis, In Vivo, Expressing, Immunohistochemical staining, Staining

    human nk cell line nk  (ATCC)


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    ATCC human nk cell line nk
    Intratumoral infiltration of <t>NK</t> <t>cells,</t> induced by miR-124 EVs in a tri-culture system. (A) U373MG and microglia were embedded in a collagen gel at a ratio of 2:1, 2 days before seeding of NK cells. Representative images of NK cells on ( B ) day 2 and ( C ) day 4 in the microfluidic device treated with miR-NC EVs or miR-124 EVs. Live NK cells were immunostained with PE-conjugated CD 45 (red). (D) Maximum infiltration distance, ( E ) average infiltration distance, and ( F ) infiltration area of NK cells were investigated. N indicates the total number of ROI. Box-and-whisker plots show all individual points on the box.** p < 0.01, *** p < 0.001. Scale bar represents 200 µm.
    Human Nk Cell Line Nk, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Average 99 stars, based on 1 article reviews
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    human nk cell line nk - by Bioz Stars, 2024-02
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    1) Product Images from "Inhibition of tumor progression and M2 microglial polarization by extracellular vesicle-mediated microRNA-124 in a 3D microfluidic glioblastoma microenvironment"

    Article Title: Inhibition of tumor progression and M2 microglial polarization by extracellular vesicle-mediated microRNA-124 in a 3D microfluidic glioblastoma microenvironment

    Journal: Theranostics

    doi: 10.7150/thno.60851

    Intratumoral infiltration of NK cells, induced by miR-124 EVs in a tri-culture system. (A) U373MG and microglia were embedded in a collagen gel at a ratio of 2:1, 2 days before seeding of NK cells. Representative images of NK cells on ( B ) day 2 and ( C ) day 4 in the microfluidic device treated with miR-NC EVs or miR-124 EVs. Live NK cells were immunostained with PE-conjugated CD 45 (red). (D) Maximum infiltration distance, ( E ) average infiltration distance, and ( F ) infiltration area of NK cells were investigated. N indicates the total number of ROI. Box-and-whisker plots show all individual points on the box.** p < 0.01, *** p < 0.001. Scale bar represents 200 µm.
    Figure Legend Snippet: Intratumoral infiltration of NK cells, induced by miR-124 EVs in a tri-culture system. (A) U373MG and microglia were embedded in a collagen gel at a ratio of 2:1, 2 days before seeding of NK cells. Representative images of NK cells on ( B ) day 2 and ( C ) day 4 in the microfluidic device treated with miR-NC EVs or miR-124 EVs. Live NK cells were immunostained with PE-conjugated CD 45 (red). (D) Maximum infiltration distance, ( E ) average infiltration distance, and ( F ) infiltration area of NK cells were investigated. N indicates the total number of ROI. Box-and-whisker plots show all individual points on the box.** p < 0.01, *** p < 0.001. Scale bar represents 200 µm.

    Techniques Used: Whisker Assay

    human nk cell line  (ATCC)


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    ATCC human nk cell line
    Human Nk Cell Line, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    human cd16  (ATCC)


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    ATCC human cd16
    Ab27 induced ADCC against TM4SF5-expressing cancer cells. (A) ADCC assay using SNU449Cp and SNU449Tp (target cells, T) and <t>CD16-expressing</t> NK-92 cells (effector cells, E). The ratio of E:T was 20:1. (B) ADCC assay against cancer cells expressing endogenous TM4SF5 (target cells) as in (A). (C) ADCC assay against HT-29 cells using Ab27 in a dose-dependent manner. Values represent mean ± standard deviation (SD). * P < 0.05.
    Human Cd16, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    1) Product Images from "Anti-cancer Activity of Novel TM4SF5-Targeting Antibodies through TM4SF5 Neutralization and Immune Cell-Mediated Cytotoxicity"

    Article Title: Anti-cancer Activity of Novel TM4SF5-Targeting Antibodies through TM4SF5 Neutralization and Immune Cell-Mediated Cytotoxicity

    Journal: Theranostics

    doi: 10.7150/thno.15629

    Ab27 induced ADCC against TM4SF5-expressing cancer cells. (A) ADCC assay using SNU449Cp and SNU449Tp (target cells, T) and CD16-expressing NK-92 cells (effector cells, E). The ratio of E:T was 20:1. (B) ADCC assay against cancer cells expressing endogenous TM4SF5 (target cells) as in (A). (C) ADCC assay against HT-29 cells using Ab27 in a dose-dependent manner. Values represent mean ± standard deviation (SD). * P < 0.05.
    Figure Legend Snippet: Ab27 induced ADCC against TM4SF5-expressing cancer cells. (A) ADCC assay using SNU449Cp and SNU449Tp (target cells, T) and CD16-expressing NK-92 cells (effector cells, E). The ratio of E:T was 20:1. (B) ADCC assay against cancer cells expressing endogenous TM4SF5 (target cells) as in (A). (C) ADCC assay against HT-29 cells using Ab27 in a dose-dependent manner. Values represent mean ± standard deviation (SD). * P < 0.05.

    Techniques Used: Expressing, ADCC Assay, Standard Deviation

    cd16 nk 92 cells  (ATCC)


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    ATCC cd16 nk 92 cells
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    ATCC nk92 egfp cd16 pta 8836 cell lines
    Neuroblastoma-derived sEVs modulate NK cell maturation in vivo and NK cell-mediated ADCC in vitro. (A) Schematic of NK cell subpopulations. Created with BioRender.com. (B) Representative flow cytometry plots of splenic NK cell subpopulations isolated from 9464D-GD2 tumor-bearing mice receiving the indicated treatments as described in . (C) Quantification of the percentage of immature splenic NK cell (CD27 +CD11b-; left panel) and mature NK cell (CD27- CD11b+; right panel) subpopulations in 9464D-GD2 tumor-bearing mice treated as described in . Mean±SEM, n=7 per group. Student’s t-test. *p<0.05; **p<0.01; ***p<0.001. (D–G) Human (IMR32) or murine (9464D-GD2) neuroblastoma cells treated as indicated in the presence or absence of <t>NK92-CD16-EGFP</t> cells (NK) and monitored for viability utilizing cell impermeant nucleic acid stain YOYO-3 with the IncuCyte S3 Live-Cell Analysis System. The cell-by-cell analysis module was used to quantify viable tumor cells (YOYO3- EGFP-). (D) Kinetic analysis of the IMR32 in vitro NK-cell-mediated ADCC assay. Mean±SEM, n=6. Viable cells calculated as percentage of viable cells in each treatment condition divided by viable cells in untreated control group. (E) Percentage of viable IMR32 cells at 24 hours, n=6. Mean±SD. One-way ANOVA with Tukey’s/Sidak’s post hoc tests. **p<0.01; ***p<0.001. (F) Kinetic analysis of the 9464D-GD2 in vitro NK-cell-mediated ADCC assay. Mean±SEM, n=4. Viable cells calculated as percentage of viable cells in each treatment condition divided by viable cells in untreated control group. (G) Percentage of viable 9464D-GD2 cells at 24 hours, n=4. Mean±SD. One-way ANOVA with Tukey’s/Sidak’s post hoc tests. *p<0.05; **p<0.01; ***p<0.001. ADCC, antibody-dependent cell-mediated cytotoxicity; ANOVA, analysis of variance; DN, double negative; DP, double positive; sEV, small extracellular vesicle.
    Nk92 Egfp Cd16 Pta 8836 Cell Lines, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    ATCC cd16 nk 92
    Neuroblastoma-derived sEVs modulate NK cell maturation in vivo and NK cell-mediated ADCC in vitro. (A) Schematic of NK cell subpopulations. Created with BioRender.com. (B) Representative flow cytometry plots of splenic NK cell subpopulations isolated from 9464D-GD2 tumor-bearing mice receiving the indicated treatments as described in . (C) Quantification of the percentage of immature splenic NK cell (CD27 +CD11b-; left panel) and mature NK cell (CD27- CD11b+; right panel) subpopulations in 9464D-GD2 tumor-bearing mice treated as described in . Mean±SEM, n=7 per group. Student’s t-test. *p<0.05; **p<0.01; ***p<0.001. (D–G) Human (IMR32) or murine (9464D-GD2) neuroblastoma cells treated as indicated in the presence or absence of <t>NK92-CD16-EGFP</t> cells (NK) and monitored for viability utilizing cell impermeant nucleic acid stain YOYO-3 with the IncuCyte S3 Live-Cell Analysis System. The cell-by-cell analysis module was used to quantify viable tumor cells (YOYO3- EGFP-). (D) Kinetic analysis of the IMR32 in vitro NK-cell-mediated ADCC assay. Mean±SEM, n=6. Viable cells calculated as percentage of viable cells in each treatment condition divided by viable cells in untreated control group. (E) Percentage of viable IMR32 cells at 24 hours, n=6. Mean±SD. One-way ANOVA with Tukey’s/Sidak’s post hoc tests. **p<0.01; ***p<0.001. (F) Kinetic analysis of the 9464D-GD2 in vitro NK-cell-mediated ADCC assay. Mean±SEM, n=4. Viable cells calculated as percentage of viable cells in each treatment condition divided by viable cells in untreated control group. (G) Percentage of viable 9464D-GD2 cells at 24 hours, n=4. Mean±SD. One-way ANOVA with Tukey’s/Sidak’s post hoc tests. *p<0.05; **p<0.01; ***p<0.001. ADCC, antibody-dependent cell-mediated cytotoxicity; ANOVA, analysis of variance; DN, double negative; DP, double positive; sEV, small extracellular vesicle.
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    ATCC human nk cell line
    Neuroblastoma-derived sEVs modulate NK cell maturation in vivo and NK cell-mediated ADCC in vitro. (A) Schematic of NK cell subpopulations. Created with BioRender.com. (B) Representative flow cytometry plots of splenic NK cell subpopulations isolated from 9464D-GD2 tumor-bearing mice receiving the indicated treatments as described in . (C) Quantification of the percentage of immature splenic NK cell (CD27 +CD11b-; left panel) and mature NK cell (CD27- CD11b+; right panel) subpopulations in 9464D-GD2 tumor-bearing mice treated as described in . Mean±SEM, n=7 per group. Student’s t-test. *p<0.05; **p<0.01; ***p<0.001. (D–G) Human (IMR32) or murine (9464D-GD2) neuroblastoma cells treated as indicated in the presence or absence of <t>NK92-CD16-EGFP</t> cells (NK) and monitored for viability utilizing cell impermeant nucleic acid stain YOYO-3 with the IncuCyte S3 Live-Cell Analysis System. The cell-by-cell analysis module was used to quantify viable tumor cells (YOYO3- EGFP-). (D) Kinetic analysis of the IMR32 in vitro NK-cell-mediated ADCC assay. Mean±SEM, n=6. Viable cells calculated as percentage of viable cells in each treatment condition divided by viable cells in untreated control group. (E) Percentage of viable IMR32 cells at 24 hours, n=6. Mean±SD. One-way ANOVA with Tukey’s/Sidak’s post hoc tests. **p<0.01; ***p<0.001. (F) Kinetic analysis of the 9464D-GD2 in vitro NK-cell-mediated ADCC assay. Mean±SEM, n=4. Viable cells calculated as percentage of viable cells in each treatment condition divided by viable cells in untreated control group. (G) Percentage of viable 9464D-GD2 cells at 24 hours, n=4. Mean±SD. One-way ANOVA with Tukey’s/Sidak’s post hoc tests. *p<0.05; **p<0.01; ***p<0.001. ADCC, antibody-dependent cell-mediated cytotoxicity; ANOVA, analysis of variance; DN, double negative; DP, double positive; sEV, small extracellular vesicle.
    Human Nk Cell Line, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    ATCC human nk 92 cell line
    Neuroblastoma-derived sEVs modulate NK cell maturation in vivo and NK cell-mediated ADCC in vitro. (A) Schematic of NK cell subpopulations. Created with BioRender.com. (B) Representative flow cytometry plots of splenic NK cell subpopulations isolated from 9464D-GD2 tumor-bearing mice receiving the indicated treatments as described in . (C) Quantification of the percentage of immature splenic NK cell (CD27 +CD11b-; left panel) and mature NK cell (CD27- CD11b+; right panel) subpopulations in 9464D-GD2 tumor-bearing mice treated as described in . Mean±SEM, n=7 per group. Student’s t-test. *p<0.05; **p<0.01; ***p<0.001. (D–G) Human (IMR32) or murine (9464D-GD2) neuroblastoma cells treated as indicated in the presence or absence of <t>NK92-CD16-EGFP</t> cells (NK) and monitored for viability utilizing cell impermeant nucleic acid stain YOYO-3 with the IncuCyte S3 Live-Cell Analysis System. The cell-by-cell analysis module was used to quantify viable tumor cells (YOYO3- EGFP-). (D) Kinetic analysis of the IMR32 in vitro NK-cell-mediated ADCC assay. Mean±SEM, n=6. Viable cells calculated as percentage of viable cells in each treatment condition divided by viable cells in untreated control group. (E) Percentage of viable IMR32 cells at 24 hours, n=6. Mean±SD. One-way ANOVA with Tukey’s/Sidak’s post hoc tests. **p<0.01; ***p<0.001. (F) Kinetic analysis of the 9464D-GD2 in vitro NK-cell-mediated ADCC assay. Mean±SEM, n=4. Viable cells calculated as percentage of viable cells in each treatment condition divided by viable cells in untreated control group. (G) Percentage of viable 9464D-GD2 cells at 24 hours, n=4. Mean±SD. One-way ANOVA with Tukey’s/Sidak’s post hoc tests. *p<0.05; **p<0.01; ***p<0.001. ADCC, antibody-dependent cell-mediated cytotoxicity; ANOVA, analysis of variance; DN, double negative; DP, double positive; sEV, small extracellular vesicle.
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    ATCC natural killer nk 92 lineages
    Neuroblastoma-derived sEVs modulate NK cell maturation in vivo and NK cell-mediated ADCC in vitro. (A) Schematic of NK cell subpopulations. Created with BioRender.com. (B) Representative flow cytometry plots of splenic NK cell subpopulations isolated from 9464D-GD2 tumor-bearing mice receiving the indicated treatments as described in . (C) Quantification of the percentage of immature splenic NK cell (CD27 +CD11b-; left panel) and mature NK cell (CD27- CD11b+; right panel) subpopulations in 9464D-GD2 tumor-bearing mice treated as described in . Mean±SEM, n=7 per group. Student’s t-test. *p<0.05; **p<0.01; ***p<0.001. (D–G) Human (IMR32) or murine (9464D-GD2) neuroblastoma cells treated as indicated in the presence or absence of <t>NK92-CD16-EGFP</t> cells (NK) and monitored for viability utilizing cell impermeant nucleic acid stain YOYO-3 with the IncuCyte S3 Live-Cell Analysis System. The cell-by-cell analysis module was used to quantify viable tumor cells (YOYO3- EGFP-). (D) Kinetic analysis of the IMR32 in vitro NK-cell-mediated ADCC assay. Mean±SEM, n=6. Viable cells calculated as percentage of viable cells in each treatment condition divided by viable cells in untreated control group. (E) Percentage of viable IMR32 cells at 24 hours, n=6. Mean±SD. One-way ANOVA with Tukey’s/Sidak’s post hoc tests. **p<0.01; ***p<0.001. (F) Kinetic analysis of the 9464D-GD2 in vitro NK-cell-mediated ADCC assay. Mean±SEM, n=4. Viable cells calculated as percentage of viable cells in each treatment condition divided by viable cells in untreated control group. (G) Percentage of viable 9464D-GD2 cells at 24 hours, n=4. Mean±SD. One-way ANOVA with Tukey’s/Sidak’s post hoc tests. *p<0.05; **p<0.01; ***p<0.001. ADCC, antibody-dependent cell-mediated cytotoxicity; ANOVA, analysis of variance; DN, double negative; DP, double positive; sEV, small extracellular vesicle.
    Natural Killer Nk 92 Lineages, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    ATCC natural killer cell line nk
    VPA enhances the sensitivity of pancreatic cancer cells to NK cell-mediated lysis via a NKG2D-dependent mechanism. (A) VPA sensitized pancreatic cancer cells to NK cell-mediated lysis; * P < 0.05; ** P < 0.01. (B) Blockade of NKG2D attenuated the ability of VPA to sensitize pancreatic cancer cells to NK cell-mediated lysis; * P < 0.05 for VPA + IgG vs. VPA + NKG2D; ** P < 0.01 for VPA + IgG vs. VPA + NKG2D. Data are mean ± SD of a single experiment performed in triplicate, all results were reproducible in three independent experiments. E:T, effector/ target ratio.
    Natural Killer Cell Line Nk, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    ATCC human nk cell line nk
    Intratumoral infiltration of <t>NK</t> <t>cells,</t> induced by miR-124 EVs in a tri-culture system. (A) U373MG and microglia were embedded in a collagen gel at a ratio of 2:1, 2 days before seeding of NK cells. Representative images of NK cells on ( B ) day 2 and ( C ) day 4 in the microfluidic device treated with miR-NC EVs or miR-124 EVs. Live NK cells were immunostained with PE-conjugated CD 45 (red). (D) Maximum infiltration distance, ( E ) average infiltration distance, and ( F ) infiltration area of NK cells were investigated. N indicates the total number of ROI. Box-and-whisker plots show all individual points on the box.** p < 0.01, *** p < 0.001. Scale bar represents 200 µm.
    Human Nk Cell Line Nk, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    ATCC human cd16
    Ab27 induced ADCC against TM4SF5-expressing cancer cells. (A) ADCC assay using SNU449Cp and SNU449Tp (target cells, T) and <t>CD16-expressing</t> NK-92 cells (effector cells, E). The ratio of E:T was 20:1. (B) ADCC assay against cancer cells expressing endogenous TM4SF5 (target cells) as in (A). (C) ADCC assay against HT-29 cells using Ab27 in a dose-dependent manner. Values represent mean ± standard deviation (SD). * P < 0.05.
    Human Cd16, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    ATCC cd16 nk 92 cells
    Ab27 induced ADCC against TM4SF5-expressing cancer cells. (A) ADCC assay using SNU449Cp and SNU449Tp (target cells, T) and <t>CD16-expressing</t> NK-92 cells (effector cells, E). The ratio of E:T was 20:1. (B) ADCC assay against cancer cells expressing endogenous TM4SF5 (target cells) as in (A). (C) ADCC assay against HT-29 cells using Ab27 in a dose-dependent manner. Values represent mean ± standard deviation (SD). * P < 0.05.
    Cd16 Nk 92 Cells, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Image Search Results


    Neuroblastoma-derived sEVs modulate NK cell maturation in vivo and NK cell-mediated ADCC in vitro. (A) Schematic of NK cell subpopulations. Created with BioRender.com. (B) Representative flow cytometry plots of splenic NK cell subpopulations isolated from 9464D-GD2 tumor-bearing mice receiving the indicated treatments as described in . (C) Quantification of the percentage of immature splenic NK cell (CD27 +CD11b-; left panel) and mature NK cell (CD27- CD11b+; right panel) subpopulations in 9464D-GD2 tumor-bearing mice treated as described in . Mean±SEM, n=7 per group. Student’s t-test. *p<0.05; **p<0.01; ***p<0.001. (D–G) Human (IMR32) or murine (9464D-GD2) neuroblastoma cells treated as indicated in the presence or absence of NK92-CD16-EGFP cells (NK) and monitored for viability utilizing cell impermeant nucleic acid stain YOYO-3 with the IncuCyte S3 Live-Cell Analysis System. The cell-by-cell analysis module was used to quantify viable tumor cells (YOYO3- EGFP-). (D) Kinetic analysis of the IMR32 in vitro NK-cell-mediated ADCC assay. Mean±SEM, n=6. Viable cells calculated as percentage of viable cells in each treatment condition divided by viable cells in untreated control group. (E) Percentage of viable IMR32 cells at 24 hours, n=6. Mean±SD. One-way ANOVA with Tukey’s/Sidak’s post hoc tests. **p<0.01; ***p<0.001. (F) Kinetic analysis of the 9464D-GD2 in vitro NK-cell-mediated ADCC assay. Mean±SEM, n=4. Viable cells calculated as percentage of viable cells in each treatment condition divided by viable cells in untreated control group. (G) Percentage of viable 9464D-GD2 cells at 24 hours, n=4. Mean±SD. One-way ANOVA with Tukey’s/Sidak’s post hoc tests. *p<0.05; **p<0.01; ***p<0.001. ADCC, antibody-dependent cell-mediated cytotoxicity; ANOVA, analysis of variance; DN, double negative; DP, double positive; sEV, small extracellular vesicle.

    Journal: Journal for Immunotherapy of Cancer

    Article Title: Small extracellular vesicles induce resistance to anti-GD2 immunotherapy unveiling tipifarnib as an adjunct to neuroblastoma immunotherapy

    doi: 10.1136/jitc-2021-004399

    Figure Lengend Snippet: Neuroblastoma-derived sEVs modulate NK cell maturation in vivo and NK cell-mediated ADCC in vitro. (A) Schematic of NK cell subpopulations. Created with BioRender.com. (B) Representative flow cytometry plots of splenic NK cell subpopulations isolated from 9464D-GD2 tumor-bearing mice receiving the indicated treatments as described in . (C) Quantification of the percentage of immature splenic NK cell (CD27 +CD11b-; left panel) and mature NK cell (CD27- CD11b+; right panel) subpopulations in 9464D-GD2 tumor-bearing mice treated as described in . Mean±SEM, n=7 per group. Student’s t-test. *p<0.05; **p<0.01; ***p<0.001. (D–G) Human (IMR32) or murine (9464D-GD2) neuroblastoma cells treated as indicated in the presence or absence of NK92-CD16-EGFP cells (NK) and monitored for viability utilizing cell impermeant nucleic acid stain YOYO-3 with the IncuCyte S3 Live-Cell Analysis System. The cell-by-cell analysis module was used to quantify viable tumor cells (YOYO3- EGFP-). (D) Kinetic analysis of the IMR32 in vitro NK-cell-mediated ADCC assay. Mean±SEM, n=6. Viable cells calculated as percentage of viable cells in each treatment condition divided by viable cells in untreated control group. (E) Percentage of viable IMR32 cells at 24 hours, n=6. Mean±SD. One-way ANOVA with Tukey’s/Sidak’s post hoc tests. **p<0.01; ***p<0.001. (F) Kinetic analysis of the 9464D-GD2 in vitro NK-cell-mediated ADCC assay. Mean±SEM, n=4. Viable cells calculated as percentage of viable cells in each treatment condition divided by viable cells in untreated control group. (G) Percentage of viable 9464D-GD2 cells at 24 hours, n=4. Mean±SD. One-way ANOVA with Tukey’s/Sidak’s post hoc tests. *p<0.05; **p<0.01; ***p<0.001. ADCC, antibody-dependent cell-mediated cytotoxicity; ANOVA, analysis of variance; DN, double negative; DP, double positive; sEV, small extracellular vesicle.

    Article Snippet: Human IMR32 neuroblastoma (CCL-127), HEK 293T/17 (CRL-11268), and NK92-EGFP-CD16 (PTA-8836) cell lines were purchased from ATCC.

    Techniques: Derivative Assay, In Vivo, In Vitro, Flow Cytometry, Isolation, Staining, ADCC Assay

    VPA enhances the sensitivity of pancreatic cancer cells to NK cell-mediated lysis via a NKG2D-dependent mechanism. (A) VPA sensitized pancreatic cancer cells to NK cell-mediated lysis; * P < 0.05; ** P < 0.01. (B) Blockade of NKG2D attenuated the ability of VPA to sensitize pancreatic cancer cells to NK cell-mediated lysis; * P < 0.05 for VPA + IgG vs. VPA + NKG2D; ** P < 0.01 for VPA + IgG vs. VPA + NKG2D. Data are mean ± SD of a single experiment performed in triplicate, all results were reproducible in three independent experiments. E:T, effector/ target ratio.

    Journal: BMC Cancer

    Article Title: Valproic acid sensitizes pancreatic cancer cells to natural killer cell-mediated lysis by upregulating MICA and MICB via the PI3K/Akt signaling pathway

    doi: 10.1186/1471-2407-14-370

    Figure Lengend Snippet: VPA enhances the sensitivity of pancreatic cancer cells to NK cell-mediated lysis via a NKG2D-dependent mechanism. (A) VPA sensitized pancreatic cancer cells to NK cell-mediated lysis; * P < 0.05; ** P < 0.01. (B) Blockade of NKG2D attenuated the ability of VPA to sensitize pancreatic cancer cells to NK cell-mediated lysis; * P < 0.05 for VPA + IgG vs. VPA + NKG2D; ** P < 0.01 for VPA + IgG vs. VPA + NKG2D. Data are mean ± SD of a single experiment performed in triplicate, all results were reproducible in three independent experiments. E:T, effector/ target ratio.

    Article Snippet: The human pancreatic adenocarcinoma cell lines PANC-1, MIA PaCa-2, and BxPC-3, and the human natural killer cell line NK-92 were obtained from the American Type Culture Collection (ATCC; Manassas, VA, USA).

    Techniques: Lysis

    PI3K/Akt signaling is required for VPA-induced upregulation of MICA and MICB in pancreatic cancer cells. (A, B) Quantitative real-time RT-PCR analysis. The VPA-induced upregulation of MICA and MICB mRNA expression were inhibited by the HER2/HER3 inhibitor lapatinib and the PI3K inhibitor LY294002, but not by the ATM/ATR inhibitor caffeine. Data are mean ± SD of a single experiment performed in triplicate, all results were reproducible in three independent experiments. * P < 0.05; ** P < 0.01; ns P > 0.05. (C) Flow cytometry analysis. The VPA-induced upregulation of MICA and MICB protein expression on the cell surface were inhibited by the PI3K inhibitor LY294002. MFI, mean fluorescence intensity; * P < 0.05. (D) Western blotting analysis. Transfection of the PI3KCA siRNA inhibited PI3KCA protein expression at 48 h post-transfection. NC, negative control; siR1-3, PI3KCA_siR sequence 1-3; ** P < 0.01. (E) Quantitative real-time RT-PCR analysis. VPA-induced upregulation of MICA and MICB mRNA expression were attenuated in PI3KCA-knockdown cells; Data are mean ± SD of a single experiment performed in triplicate, all results were reproducible in three independent experiments. ** P < 0.01. (F) Flow cytometric analysis. VPA-induced upregulation of MICA and MICB protein expression on the cell surface were attenuated in PI3KCA-knockdown cells. MFI, mean fluorescence intensity; * P < 0.05; ** P < 0.01. (G) LDH release assay. The VPA-induced susceptibility of cancer cells to NK cell-mediated cell lysis was reduced in PI3KCA-knockdown cells. Data are mean ± SD of a single experiment performed in triplicate, all results were reproducible in three independent experiments. ** P < 0.01 and * P < 0.05 for NC vs. siR2; ▲▲ P < 0.01 and ▲ P < 0.05 for NC vs. siR3. siR2, PI3KCA siR sequence 2; siR3, PI3KCA siR sequence 3.

    Journal: BMC Cancer

    Article Title: Valproic acid sensitizes pancreatic cancer cells to natural killer cell-mediated lysis by upregulating MICA and MICB via the PI3K/Akt signaling pathway

    doi: 10.1186/1471-2407-14-370

    Figure Lengend Snippet: PI3K/Akt signaling is required for VPA-induced upregulation of MICA and MICB in pancreatic cancer cells. (A, B) Quantitative real-time RT-PCR analysis. The VPA-induced upregulation of MICA and MICB mRNA expression were inhibited by the HER2/HER3 inhibitor lapatinib and the PI3K inhibitor LY294002, but not by the ATM/ATR inhibitor caffeine. Data are mean ± SD of a single experiment performed in triplicate, all results were reproducible in three independent experiments. * P < 0.05; ** P < 0.01; ns P > 0.05. (C) Flow cytometry analysis. The VPA-induced upregulation of MICA and MICB protein expression on the cell surface were inhibited by the PI3K inhibitor LY294002. MFI, mean fluorescence intensity; * P < 0.05. (D) Western blotting analysis. Transfection of the PI3KCA siRNA inhibited PI3KCA protein expression at 48 h post-transfection. NC, negative control; siR1-3, PI3KCA_siR sequence 1-3; ** P < 0.01. (E) Quantitative real-time RT-PCR analysis. VPA-induced upregulation of MICA and MICB mRNA expression were attenuated in PI3KCA-knockdown cells; Data are mean ± SD of a single experiment performed in triplicate, all results were reproducible in three independent experiments. ** P < 0.01. (F) Flow cytometric analysis. VPA-induced upregulation of MICA and MICB protein expression on the cell surface were attenuated in PI3KCA-knockdown cells. MFI, mean fluorescence intensity; * P < 0.05; ** P < 0.01. (G) LDH release assay. The VPA-induced susceptibility of cancer cells to NK cell-mediated cell lysis was reduced in PI3KCA-knockdown cells. Data are mean ± SD of a single experiment performed in triplicate, all results were reproducible in three independent experiments. ** P < 0.01 and * P < 0.05 for NC vs. siR2; ▲▲ P < 0.01 and ▲ P < 0.05 for NC vs. siR3. siR2, PI3KCA siR sequence 2; siR3, PI3KCA siR sequence 3.

    Article Snippet: The human pancreatic adenocarcinoma cell lines PANC-1, MIA PaCa-2, and BxPC-3, and the human natural killer cell line NK-92 were obtained from the American Type Culture Collection (ATCC; Manassas, VA, USA).

    Techniques: Quantitative RT-PCR, Expressing, Flow Cytometry, Fluorescence, Western Blot, Transfection, Negative Control, Sequencing, Lactate Dehydrogenase Assay, Lysis

    VPA sensitizes pancreatic cancer cells to NK cell-mediated lysis in vivo by upregulating the expression of MICA and MICB. (A, B) Excised xenograft tumors and growth curves for the xenografts; VPA enhanced the growth inhibitory effect of NK cells in vivo ; this effect was attenuated by the PI3K inhibitor LY294002. Data are mean ± SD of five mice per group; * P < 0.05 for NK-92 vs. NK-92 + VPA; Δ P < 0.05 for NK-92 + VPA + LY294002 vs. NK-92 + VPA. (C) Immunohistochemical staining and quantification of MICA and MICB expression in the xenograft tumors; VPA significantly upregulated the expression of MICA and MICB in the pancreatic cancer xenograft tumors in vivo , this effect was attenuated by the PI3K inhibitor LY294002.

    Journal: BMC Cancer

    Article Title: Valproic acid sensitizes pancreatic cancer cells to natural killer cell-mediated lysis by upregulating MICA and MICB via the PI3K/Akt signaling pathway

    doi: 10.1186/1471-2407-14-370

    Figure Lengend Snippet: VPA sensitizes pancreatic cancer cells to NK cell-mediated lysis in vivo by upregulating the expression of MICA and MICB. (A, B) Excised xenograft tumors and growth curves for the xenografts; VPA enhanced the growth inhibitory effect of NK cells in vivo ; this effect was attenuated by the PI3K inhibitor LY294002. Data are mean ± SD of five mice per group; * P < 0.05 for NK-92 vs. NK-92 + VPA; Δ P < 0.05 for NK-92 + VPA + LY294002 vs. NK-92 + VPA. (C) Immunohistochemical staining and quantification of MICA and MICB expression in the xenograft tumors; VPA significantly upregulated the expression of MICA and MICB in the pancreatic cancer xenograft tumors in vivo , this effect was attenuated by the PI3K inhibitor LY294002.

    Article Snippet: The human pancreatic adenocarcinoma cell lines PANC-1, MIA PaCa-2, and BxPC-3, and the human natural killer cell line NK-92 were obtained from the American Type Culture Collection (ATCC; Manassas, VA, USA).

    Techniques: Lysis, In Vivo, Expressing, Immunohistochemical staining, Staining

    Intratumoral infiltration of NK cells, induced by miR-124 EVs in a tri-culture system. (A) U373MG and microglia were embedded in a collagen gel at a ratio of 2:1, 2 days before seeding of NK cells. Representative images of NK cells on ( B ) day 2 and ( C ) day 4 in the microfluidic device treated with miR-NC EVs or miR-124 EVs. Live NK cells were immunostained with PE-conjugated CD 45 (red). (D) Maximum infiltration distance, ( E ) average infiltration distance, and ( F ) infiltration area of NK cells were investigated. N indicates the total number of ROI. Box-and-whisker plots show all individual points on the box.** p < 0.01, *** p < 0.001. Scale bar represents 200 µm.

    Journal: Theranostics

    Article Title: Inhibition of tumor progression and M2 microglial polarization by extracellular vesicle-mediated microRNA-124 in a 3D microfluidic glioblastoma microenvironment

    doi: 10.7150/thno.60851

    Figure Lengend Snippet: Intratumoral infiltration of NK cells, induced by miR-124 EVs in a tri-culture system. (A) U373MG and microglia were embedded in a collagen gel at a ratio of 2:1, 2 days before seeding of NK cells. Representative images of NK cells on ( B ) day 2 and ( C ) day 4 in the microfluidic device treated with miR-NC EVs or miR-124 EVs. Live NK cells were immunostained with PE-conjugated CD 45 (red). (D) Maximum infiltration distance, ( E ) average infiltration distance, and ( F ) infiltration area of NK cells were investigated. N indicates the total number of ROI. Box-and-whisker plots show all individual points on the box.** p < 0.01, *** p < 0.001. Scale bar represents 200 µm.

    Article Snippet: The human NK cell line NK-92 was purchased from American Type Culture Collection (ATCC, USA).

    Techniques: Whisker Assay

    Ab27 induced ADCC against TM4SF5-expressing cancer cells. (A) ADCC assay using SNU449Cp and SNU449Tp (target cells, T) and CD16-expressing NK-92 cells (effector cells, E). The ratio of E:T was 20:1. (B) ADCC assay against cancer cells expressing endogenous TM4SF5 (target cells) as in (A). (C) ADCC assay against HT-29 cells using Ab27 in a dose-dependent manner. Values represent mean ± standard deviation (SD). * P < 0.05.

    Journal: Theranostics

    Article Title: Anti-cancer Activity of Novel TM4SF5-Targeting Antibodies through TM4SF5 Neutralization and Immune Cell-Mediated Cytotoxicity

    doi: 10.7150/thno.15629

    Figure Lengend Snippet: Ab27 induced ADCC against TM4SF5-expressing cancer cells. (A) ADCC assay using SNU449Cp and SNU449Tp (target cells, T) and CD16-expressing NK-92 cells (effector cells, E). The ratio of E:T was 20:1. (B) ADCC assay against cancer cells expressing endogenous TM4SF5 (target cells) as in (A). (C) ADCC assay against HT-29 cells using Ab27 in a dose-dependent manner. Values represent mean ± standard deviation (SD). * P < 0.05.

    Article Snippet: NK-92 cells expressing human CD16 (ATCC) were used as effector cells (E).

    Techniques: Expressing, ADCC Assay, Standard Deviation