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chronic myeloid leukemia cell line  (ATCC)


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    ATCC chronic myeloid leukemia cell line
    Chronic Myeloid Leukemia Cell Line, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 10821 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/chronic+myeloid+leukemia/pmc13128645-40-16-27?v=ATCC
    Average 99 stars, based on 10821 article reviews
    chronic myeloid leukemia cell line - by Bioz Stars, 2026-07
    99/100 stars

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    ATCC chronic myeloid leukemia cell line
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    ATCC chronic myeloid leukemia cell line k562
    (A) Co-culture of CAR-T, Non-CAR-T, and Strep-PE-modified NALM6 cells (1:4:1). (B) Target cells were modified with different concentrations of NHS-biotin (500, 100, 20, and 4 µM). Strep-PE label on target cell before and after co-cultured with CAR-T cells. (C) CAR-T cells were able to specifically kill Strep-PE modified NALM6 cells. (D) Unmodified and Strep-PE modified NALM6 cells were mixed at equal proportion and co-cultured with CAR-T or Non-CAR-T cells. Similar killing efficiency of unmodified and modified NALM6 cells by CAR-T cells was observed. (E-F) Shown were the gating to identify trogocytosis of Strep-PE by CAR-T cells based on background capture of Non-CAR-T counterpart (E), and summary of three independent experiments (F). (G) Improving the assay specificity by co-labeling effector cells with CD107a antibodies. (H-1) Gating strategy to identify CD10?high Strep-PEhigh killer cells (H), and inclusion of CD107a as a second marker improved the sensitivity and specificity of detecting killer cells (I). (J) Experimental schematic of co-culturing labeled target cells with different effector cells (CAR-T and NK cells). (K) Universal target labeling scheme was applicable across different cell types. (L) Labels from NALM6 cells were transferred exclusively to CAR-T cells, whereas labels from <t>K562</t> cells were transferred exclusively to NK cells, consistent with trogocytosis occurring during cognate cytotoxic interactions.
    Chronic Myeloid Leukemia Cell Line K562, 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/product/chronic+myeloid+leukemia/bio_rxiv__64898__2026__03__26__714656-193-10-16?v=ATCC
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    Procell Inc chronic myeloid leukemia cell line k562
    Generation of key components and validation of the core anti-tumor mechanism. (A) Plasmid map for overexpression of anti-TGF-βRII gene. (B) Immunoblot and densitometry of pSMAD2 signaling, downstream of TGF-β, in A549 cells, treated with recombinant TGF-β1 and A549 cells infected with plasmid-anti-TGF-βRII, or mock-infected. (C) The scheme of Ad-null (control) and Ad-anti-TGF-βRII. (D) The percentage of in vitro -cultured NK cells (CD3 − CD56 + ) on day 14 was detected by flow cytometry. The cytotoxic activity of NK cells was assessed against <t>K562</t> cells (24 h co-culture) (E) and A549 cells (F) target cells at various effector-to-target (E:T) ratios. (G) Dose-dependent oncolytic activity of Ad-null and Ad-anti-TGF-βRII in A549 cells 48 h post-infection. (H) RT-qPCR analysis confirming specific upregulation of anti-TGF-βRII mRNA in A549 cells infected with Ad-anti-TGF-βRII, but not Ad-null. (I) Western blot analysis demonstrating that Ad-anti-TGF-βRII infection, but not Ad-null, significantly reduces pSMAD2 levels in A549 cells. *p < 0.05; **p < 0.01; ***p < 0.001; ****p < 0.0001; ns means no significance by one-way ANOVA or two-way ANOVA with Tukey’s multiple comparison test. Error bars indicate SDs (n=3).
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    ATCC human chronic myeloid leukemia cells k 562
    Generation of key components and validation of the core anti-tumor mechanism. (A) Plasmid map for overexpression of anti-TGF-βRII gene. (B) Immunoblot and densitometry of pSMAD2 signaling, downstream of TGF-β, in A549 cells, treated with recombinant TGF-β1 and A549 cells infected with plasmid-anti-TGF-βRII, or mock-infected. (C) The scheme of Ad-null (control) and Ad-anti-TGF-βRII. (D) The percentage of in vitro -cultured NK cells (CD3 − CD56 + ) on day 14 was detected by flow cytometry. The cytotoxic activity of NK cells was assessed against <t>K562</t> cells (24 h co-culture) (E) and A549 cells (F) target cells at various effector-to-target (E:T) ratios. (G) Dose-dependent oncolytic activity of Ad-null and Ad-anti-TGF-βRII in A549 cells 48 h post-infection. (H) RT-qPCR analysis confirming specific upregulation of anti-TGF-βRII mRNA in A549 cells infected with Ad-anti-TGF-βRII, but not Ad-null. (I) Western blot analysis demonstrating that Ad-anti-TGF-βRII infection, but not Ad-null, significantly reduces pSMAD2 levels in A549 cells. *p < 0.05; **p < 0.01; ***p < 0.001; ****p < 0.0001; ns means no significance by one-way ANOVA or two-way ANOVA with Tukey’s multiple comparison test. Error bars indicate SDs (n=3).
    Human Chronic Myeloid Leukemia Cells K 562, 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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    DSMZ chronic myeloid leukemia cell line k562
    Generation of key components and validation of the core anti-tumor mechanism. (A) Plasmid map for overexpression of anti-TGF-βRII gene. (B) Immunoblot and densitometry of pSMAD2 signaling, downstream of TGF-β, in A549 cells, treated with recombinant TGF-β1 and A549 cells infected with plasmid-anti-TGF-βRII, or mock-infected. (C) The scheme of Ad-null (control) and Ad-anti-TGF-βRII. (D) The percentage of in vitro -cultured NK cells (CD3 − CD56 + ) on day 14 was detected by flow cytometry. The cytotoxic activity of NK cells was assessed against <t>K562</t> cells (24 h co-culture) (E) and A549 cells (F) target cells at various effector-to-target (E:T) ratios. (G) Dose-dependent oncolytic activity of Ad-null and Ad-anti-TGF-βRII in A549 cells 48 h post-infection. (H) RT-qPCR analysis confirming specific upregulation of anti-TGF-βRII mRNA in A549 cells infected with Ad-anti-TGF-βRII, but not Ad-null. (I) Western blot analysis demonstrating that Ad-anti-TGF-βRII infection, but not Ad-null, significantly reduces pSMAD2 levels in A549 cells. *p < 0.05; **p < 0.01; ***p < 0.001; ****p < 0.0001; ns means no significance by one-way ANOVA or two-way ANOVA with Tukey’s multiple comparison test. Error bars indicate SDs (n=3).
    Chronic Myeloid Leukemia Cell Line K562, supplied by DSMZ, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Musashi Engineering Inc chronic myeloid leukemia
    Generation of key components and validation of the core anti-tumor mechanism. (A) Plasmid map for overexpression of anti-TGF-βRII gene. (B) Immunoblot and densitometry of pSMAD2 signaling, downstream of TGF-β, in A549 cells, treated with recombinant TGF-β1 and A549 cells infected with plasmid-anti-TGF-βRII, or mock-infected. (C) The scheme of Ad-null (control) and Ad-anti-TGF-βRII. (D) The percentage of in vitro -cultured NK cells (CD3 − CD56 + ) on day 14 was detected by flow cytometry. The cytotoxic activity of NK cells was assessed against <t>K562</t> cells (24 h co-culture) (E) and A549 cells (F) target cells at various effector-to-target (E:T) ratios. (G) Dose-dependent oncolytic activity of Ad-null and Ad-anti-TGF-βRII in A549 cells 48 h post-infection. (H) RT-qPCR analysis confirming specific upregulation of anti-TGF-βRII mRNA in A549 cells infected with Ad-anti-TGF-βRII, but not Ad-null. (I) Western blot analysis demonstrating that Ad-anti-TGF-βRII infection, but not Ad-null, significantly reduces pSMAD2 levels in A549 cells. *p < 0.05; **p < 0.01; ***p < 0.001; ****p < 0.0001; ns means no significance by one-way ANOVA or two-way ANOVA with Tukey’s multiple comparison test. Error bars indicate SDs (n=3).
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    https://www.bioz.com/product/chronic+myeloid+leukemia/pm41353321-23-1-4?v=Musashi+Engineering+Inc
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    (A) Co-culture of CAR-T, Non-CAR-T, and Strep-PE-modified NALM6 cells (1:4:1). (B) Target cells were modified with different concentrations of NHS-biotin (500, 100, 20, and 4 µM). Strep-PE label on target cell before and after co-cultured with CAR-T cells. (C) CAR-T cells were able to specifically kill Strep-PE modified NALM6 cells. (D) Unmodified and Strep-PE modified NALM6 cells were mixed at equal proportion and co-cultured with CAR-T or Non-CAR-T cells. Similar killing efficiency of unmodified and modified NALM6 cells by CAR-T cells was observed. (E-F) Shown were the gating to identify trogocytosis of Strep-PE by CAR-T cells based on background capture of Non-CAR-T counterpart (E), and summary of three independent experiments (F). (G) Improving the assay specificity by co-labeling effector cells with CD107a antibodies. (H-1) Gating strategy to identify CD10?high Strep-PEhigh killer cells (H), and inclusion of CD107a as a second marker improved the sensitivity and specificity of detecting killer cells (I). (J) Experimental schematic of co-culturing labeled target cells with different effector cells (CAR-T and NK cells). (K) Universal target labeling scheme was applicable across different cell types. (L) Labels from NALM6 cells were transferred exclusively to CAR-T cells, whereas labels from K562 cells were transferred exclusively to NK cells, consistent with trogocytosis occurring during cognate cytotoxic interactions.

    Journal: bioRxiv

    Article Title: DynaKiller-Scan: Multimodal characterization of single-cell killing dynamics via combinatorial encoding of target lysis

    doi: 10.64898/2026.03.26.714656

    Figure Lengend Snippet: (A) Co-culture of CAR-T, Non-CAR-T, and Strep-PE-modified NALM6 cells (1:4:1). (B) Target cells were modified with different concentrations of NHS-biotin (500, 100, 20, and 4 µM). Strep-PE label on target cell before and after co-cultured with CAR-T cells. (C) CAR-T cells were able to specifically kill Strep-PE modified NALM6 cells. (D) Unmodified and Strep-PE modified NALM6 cells were mixed at equal proportion and co-cultured with CAR-T or Non-CAR-T cells. Similar killing efficiency of unmodified and modified NALM6 cells by CAR-T cells was observed. (E-F) Shown were the gating to identify trogocytosis of Strep-PE by CAR-T cells based on background capture of Non-CAR-T counterpart (E), and summary of three independent experiments (F). (G) Improving the assay specificity by co-labeling effector cells with CD107a antibodies. (H-1) Gating strategy to identify CD10?high Strep-PEhigh killer cells (H), and inclusion of CD107a as a second marker improved the sensitivity and specificity of detecting killer cells (I). (J) Experimental schematic of co-culturing labeled target cells with different effector cells (CAR-T and NK cells). (K) Universal target labeling scheme was applicable across different cell types. (L) Labels from NALM6 cells were transferred exclusively to CAR-T cells, whereas labels from K562 cells were transferred exclusively to NK cells, consistent with trogocytosis occurring during cognate cytotoxic interactions.

    Article Snippet: Human B-cell precursor leukemia cell line NALM6 (ATCC, CRL-3273) and chronic myeloid leukemia cell line K562 (ATCC, CCL-243) were maintained in RPMI 1640 medium with 10% FBS.

    Techniques: Co-Culture Assay, Modification, Cell Culture, Labeling, Marker

    Generation of key components and validation of the core anti-tumor mechanism. (A) Plasmid map for overexpression of anti-TGF-βRII gene. (B) Immunoblot and densitometry of pSMAD2 signaling, downstream of TGF-β, in A549 cells, treated with recombinant TGF-β1 and A549 cells infected with plasmid-anti-TGF-βRII, or mock-infected. (C) The scheme of Ad-null (control) and Ad-anti-TGF-βRII. (D) The percentage of in vitro -cultured NK cells (CD3 − CD56 + ) on day 14 was detected by flow cytometry. The cytotoxic activity of NK cells was assessed against K562 cells (24 h co-culture) (E) and A549 cells (F) target cells at various effector-to-target (E:T) ratios. (G) Dose-dependent oncolytic activity of Ad-null and Ad-anti-TGF-βRII in A549 cells 48 h post-infection. (H) RT-qPCR analysis confirming specific upregulation of anti-TGF-βRII mRNA in A549 cells infected with Ad-anti-TGF-βRII, but not Ad-null. (I) Western blot analysis demonstrating that Ad-anti-TGF-βRII infection, but not Ad-null, significantly reduces pSMAD2 levels in A549 cells. *p < 0.05; **p < 0.01; ***p < 0.001; ****p < 0.0001; ns means no significance by one-way ANOVA or two-way ANOVA with Tukey’s multiple comparison test. Error bars indicate SDs (n=3).

    Journal: Frontiers in Immunology

    Article Title: Oncolytic adenovirus encoding a TGF-β inhibitor synergizes with PD-1 blockade to potentiate NK cell cytotoxicity against NSCLC

    doi: 10.3389/fimmu.2026.1759236

    Figure Lengend Snippet: Generation of key components and validation of the core anti-tumor mechanism. (A) Plasmid map for overexpression of anti-TGF-βRII gene. (B) Immunoblot and densitometry of pSMAD2 signaling, downstream of TGF-β, in A549 cells, treated with recombinant TGF-β1 and A549 cells infected with plasmid-anti-TGF-βRII, or mock-infected. (C) The scheme of Ad-null (control) and Ad-anti-TGF-βRII. (D) The percentage of in vitro -cultured NK cells (CD3 − CD56 + ) on day 14 was detected by flow cytometry. The cytotoxic activity of NK cells was assessed against K562 cells (24 h co-culture) (E) and A549 cells (F) target cells at various effector-to-target (E:T) ratios. (G) Dose-dependent oncolytic activity of Ad-null and Ad-anti-TGF-βRII in A549 cells 48 h post-infection. (H) RT-qPCR analysis confirming specific upregulation of anti-TGF-βRII mRNA in A549 cells infected with Ad-anti-TGF-βRII, but not Ad-null. (I) Western blot analysis demonstrating that Ad-anti-TGF-βRII infection, but not Ad-null, significantly reduces pSMAD2 levels in A549 cells. *p < 0.05; **p < 0.01; ***p < 0.001; ****p < 0.0001; ns means no significance by one-way ANOVA or two-way ANOVA with Tukey’s multiple comparison test. Error bars indicate SDs (n=3).

    Article Snippet: The human embryonic kidney cell line HEK293, the A549 lung adenocarcinoma cell line, and the human chronic myeloid leukemia cell line K562 were obtained from Procell Biotechnology Co., Ltd. (Wuhan, China).

    Techniques: Biomarker Discovery, Plasmid Preparation, Over Expression, Western Blot, Recombinant, Infection, Control, In Vitro, Cell Culture, Flow Cytometry, Activity Assay, Co-Culture Assay, Quantitative RT-PCR, Comparison