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chronic myeloid leukemia cell line k562  (ATCC)


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    ATCC chronic myeloid leukemia cell line k562
    Chronic Myeloid Leukemia Cell Line K562, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 11049 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/k562+cell+lines/K-562/pm42888846-174-10-36
    Average 99 stars, based on 11049 article reviews
    chronic myeloid leukemia cell line k562 - by Bioz Stars, 2026-11
    99/100 stars

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    Cell Culture:

    Article Title: Compositions and methods for T-cell and cytokine activation
    Article Snippet: .. 293T, MV-4-11, OCI-AML-3, and K562 cell lines were purchased from the American Type Culture Collection (ATCC, Manassas, VA) and cultured in Dulbecco's Modified Eagle Medium (DMEM, ThermoFisher Scientific, Waltham, MA; 293T, MV-4-11), Roswell Park Memorial Institute (RPMI, ThermoScientific; OCI-AML-3), or Iscove's Modified Dulbecco's Medium (IMDM, ThermoFisher; K562) supplemented with 10% Fetal Bovine Serum (FBS, ThermoScientific). .. All cells were maintained in a humidified atmosphere containing 5% CO2 at 37° C. K562 cells expressing CD123 (K562.CD123), CLEC12A (K562.CLEC12A), or CD123 and CLEC12A (K562.CD123.CLEC12A) were generated by first subcloning the full length human CD123 (NCBI Accession: NP_002174.1) or CLEC12A coding sequence (NCBI Accession: NP_612210.4) into a pCDH lentiviral backbone (System Biosciences, Inc., Mountain View, CA).

    Modification:

    Article Title: Compositions and methods for T-cell and cytokine activation
    Article Snippet: .. 293T, MV-4-11, OCI-AML-3, and K562 cell lines were purchased from the American Type Culture Collection (ATCC, Manassas, VA) and cultured in Dulbecco's Modified Eagle Medium (DMEM, ThermoFisher Scientific, Waltham, MA; 293T, MV-4-11), Roswell Park Memorial Institute (RPMI, ThermoScientific; OCI-AML-3), or Iscove's Modified Dulbecco's Medium (IMDM, ThermoFisher; K562) supplemented with 10% Fetal Bovine Serum (FBS, ThermoScientific). .. All cells were maintained in a humidified atmosphere containing 5% CO2 at 37° C. K562 cells expressing CD123 (K562.CD123), CLEC12A (K562.CLEC12A), or CD123 and CLEC12A (K562.CD123.CLEC12A) were generated by first subcloning the full length human CD123 (NCBI Accession: NP_002174.1) or CLEC12A coding sequence (NCBI Accession: NP_612210.4) into a pCDH lentiviral backbone (System Biosciences, Inc., Mountain View, CA).

    other:

    Article Title: Anticancer activity of amide and ester derivatives of the ent-labdane 2α-hydroxyeperuic acid obtained via sonochemical synthesis
    Article Snippet: Medicinal plants are an invaluable source of specialized metabolites with unique and complex chemical structures.. This chemical diversity offers a rich resource for discovering new compounds with therapeutic potential.. One notable example is Ageratina petiolaris, which produces a mixture of esters of 2α-hydroxyeperuic acid (1) in high quantity.

    Article Title: Programmable genome editing in human cells using RNA-guided bridge recombinases.
    Article Snippet: First release: 5 February 2026 science.org (Page numbers not final at time of first release) 1 CRISPR-Cas genome editing technologies enable targeted gene disruption or correction of mutations at endogenous genomic loci using programmable guide RNAs (1).. First-generation technologies, based on CRISPR-associated nucleases Cas9 and Cas12a, can efficiently induce gene knockouts (2–7).. However, these approaches rely on the generation of DNA double-strand breaks (DSBs), which typically result in heterogeneous editing outcomes due to imprecise end-repair mechanisms and are associated with cellular genotoxicity (8– 10).



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    Cytotoxic capacity of HCC-derived MAIT cells. (A, B) Representative flow cytometry plots illustrating the cytotoxic potential of MAIT and NK cells ex vivo and following 96 hours of IL-15 stimulation. (C, D) Differences in cytotoxicity of blood-derived MAIT and NK cells from healthy participants (HD) and HCC patients (HCC), analyzed ex vivo and after IL-15 stimulation at an effector-to-target ratio of 20:1, n =7-8/group. (E, F) Differences in cytotoxicity of peritumour and tumour-derived MAIT and NK cells from HCC patients. The cytotoxicity assay was conducted either ex vivo or over a 96-hour period with IL-15 at a ratio of 1:20, n =5-7/group. (G, H) Induction of NKG2D and Granzyme B on peripheral blood, peritumour and tumour-derived MAIT cells after 96 hours of IL-15 stimulation. (I) Inhibition of the cytotoxic capacity of peripheral MAIT and NK cells from HCC patients following 96-hour IL-15 stimulation, using a neutralizing antibody against NKG2D or the Granzyme B inhibitor concanamycin A (CMA), at an ratio of 1:20, n = 5-6/group. (J, K) Inhibition of MAIT and NK cell cytotoxicity from HCC peritumoral and tumour samples using CMA after 96-hour IL-15 stimulation at an ratio of 1:20 (n = 5–6 per group). HD: n = 6–9; HCC: n = 5–6. Non-significant (n.s.): p > 0.05; *p < 0.05; **p < 0.01; ***p < 0.001, as calculated using ordinary one-way ANOVA, Kruskal–Wallis test (C–F, I), a two-tailed paired t-test or a two-tailed Wilcoxon matched-pairs signed-rank test (G, H).
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    Cytotoxic capacity of HCC-derived MAIT cells. (A, B) Representative flow cytometry plots illustrating the cytotoxic potential of MAIT and NK cells ex vivo and following 96 hours of IL-15 stimulation. (C, D) Differences in cytotoxicity of blood-derived MAIT and NK cells from healthy participants (HD) and HCC patients (HCC), analyzed ex vivo and after IL-15 stimulation at an effector-to-target ratio of 20:1, n =7-8/group. (E, F) Differences in cytotoxicity of peritumour and tumour-derived MAIT and NK cells from HCC patients. The cytotoxicity assay was conducted either ex vivo or over a 96-hour period with IL-15 at a ratio of 1:20, n =5-7/group. (G, H) Induction of NKG2D and Granzyme B on peripheral blood, peritumour and tumour-derived MAIT cells after 96 hours of IL-15 stimulation. (I) Inhibition of the cytotoxic capacity of peripheral MAIT and NK cells from HCC patients following 96-hour IL-15 stimulation, using a neutralizing antibody against NKG2D or the Granzyme B inhibitor concanamycin A (CMA), at an ratio of 1:20, n = 5-6/group. (J, K) Inhibition of MAIT and NK cell cytotoxicity from HCC peritumoral and tumour samples using CMA after 96-hour IL-15 stimulation at an ratio of 1:20 (n = 5–6 per group). HD: n = 6–9; HCC: n = 5–6. Non-significant (n.s.): p > 0.05; *p < 0.05; **p < 0.01; ***p < 0.001, as calculated using ordinary one-way ANOVA, Kruskal–Wallis test (C–F, I), a two-tailed paired t-test or a two-tailed Wilcoxon matched-pairs signed-rank test (G, H).
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    Cytotoxic capacity of HCC-derived MAIT cells. (A, B) Representative flow cytometry plots illustrating the cytotoxic potential of MAIT and NK cells ex vivo and following 96 hours of IL-15 stimulation. (C, D) Differences in cytotoxicity of blood-derived MAIT and NK cells from healthy participants (HD) and HCC patients (HCC), analyzed ex vivo and after IL-15 stimulation at an effector-to-target ratio of 20:1, n =7-8/group. (E, F) Differences in cytotoxicity of peritumour and tumour-derived MAIT and NK cells from HCC patients. The cytotoxicity assay was conducted either ex vivo or over a 96-hour period with IL-15 at a ratio of 1:20, n =5-7/group. (G, H) Induction of NKG2D and Granzyme B on peripheral blood, peritumour and tumour-derived MAIT cells after 96 hours of IL-15 stimulation. (I) Inhibition of the cytotoxic capacity of peripheral MAIT and NK cells from HCC patients following 96-hour IL-15 stimulation, using a neutralizing antibody against NKG2D or the Granzyme B inhibitor concanamycin A (CMA), at an ratio of 1:20, n = 5-6/group. (J, K) Inhibition of MAIT and NK cell cytotoxicity from HCC peritumoral and tumour samples using CMA after 96-hour IL-15 stimulation at an ratio of 1:20 (n = 5–6 per group). HD: n = 6–9; HCC: n = 5–6. Non-significant (n.s.): p > 0.05; *p < 0.05; **p < 0.01; ***p < 0.001, as calculated using ordinary one-way ANOVA, Kruskal–Wallis test (C–F, I), a two-tailed paired t-test or a two-tailed Wilcoxon matched-pairs signed-rank test (G, H).
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    Image Search Results


    Cytotoxic capacity of HCC-derived MAIT cells. (A, B) Representative flow cytometry plots illustrating the cytotoxic potential of MAIT and NK cells ex vivo and following 96 hours of IL-15 stimulation. (C, D) Differences in cytotoxicity of blood-derived MAIT and NK cells from healthy participants (HD) and HCC patients (HCC), analyzed ex vivo and after IL-15 stimulation at an effector-to-target ratio of 20:1, n =7-8/group. (E, F) Differences in cytotoxicity of peritumour and tumour-derived MAIT and NK cells from HCC patients. The cytotoxicity assay was conducted either ex vivo or over a 96-hour period with IL-15 at a ratio of 1:20, n =5-7/group. (G, H) Induction of NKG2D and Granzyme B on peripheral blood, peritumour and tumour-derived MAIT cells after 96 hours of IL-15 stimulation. (I) Inhibition of the cytotoxic capacity of peripheral MAIT and NK cells from HCC patients following 96-hour IL-15 stimulation, using a neutralizing antibody against NKG2D or the Granzyme B inhibitor concanamycin A (CMA), at an ratio of 1:20, n = 5-6/group. (J, K) Inhibition of MAIT and NK cell cytotoxicity from HCC peritumoral and tumour samples using CMA after 96-hour IL-15 stimulation at an ratio of 1:20 (n = 5–6 per group). HD: n = 6–9; HCC: n = 5–6. Non-significant (n.s.): p > 0.05; *p < 0.05; **p < 0.01; ***p < 0.001, as calculated using ordinary one-way ANOVA, Kruskal–Wallis test (C–F, I), a two-tailed paired t-test or a two-tailed Wilcoxon matched-pairs signed-rank test (G, H).

    Journal: Frontiers in Immunology

    Article Title: Comparative profiling of MAIT cells across gastrointestinal cancers identifies conserved NK receptor dysregulation and HCC-specific defects in cytotoxicity and XBP1s signaling

    doi: 10.3389/fimmu.2026.1924000

    Figure Lengend Snippet: Cytotoxic capacity of HCC-derived MAIT cells. (A, B) Representative flow cytometry plots illustrating the cytotoxic potential of MAIT and NK cells ex vivo and following 96 hours of IL-15 stimulation. (C, D) Differences in cytotoxicity of blood-derived MAIT and NK cells from healthy participants (HD) and HCC patients (HCC), analyzed ex vivo and after IL-15 stimulation at an effector-to-target ratio of 20:1, n =7-8/group. (E, F) Differences in cytotoxicity of peritumour and tumour-derived MAIT and NK cells from HCC patients. The cytotoxicity assay was conducted either ex vivo or over a 96-hour period with IL-15 at a ratio of 1:20, n =5-7/group. (G, H) Induction of NKG2D and Granzyme B on peripheral blood, peritumour and tumour-derived MAIT cells after 96 hours of IL-15 stimulation. (I) Inhibition of the cytotoxic capacity of peripheral MAIT and NK cells from HCC patients following 96-hour IL-15 stimulation, using a neutralizing antibody against NKG2D or the Granzyme B inhibitor concanamycin A (CMA), at an ratio of 1:20, n = 5-6/group. (J, K) Inhibition of MAIT and NK cell cytotoxicity from HCC peritumoral and tumour samples using CMA after 96-hour IL-15 stimulation at an ratio of 1:20 (n = 5–6 per group). HD: n = 6–9; HCC: n = 5–6. Non-significant (n.s.): p > 0.05; *p < 0.05; **p < 0.01; ***p < 0.001, as calculated using ordinary one-way ANOVA, Kruskal–Wallis test (C–F, I), a two-tailed paired t-test or a two-tailed Wilcoxon matched-pairs signed-rank test (G, H).

    Article Snippet: The K562 cell line (chronic myelogenous leukaemia; ATCC CCL-243; RRID: CVCL_K562) was cultured in RPMI 1640 medium containing 0.3 mg/ml glutamine 100 U/ml penicillin, 0.1 mg/ml streptomycin and 10% FBS.

    Techniques: Derivative Assay, Flow Cytometry, Ex Vivo, Cytotoxicity Assay, Inhibition, Two Tailed Test

    XBP1s activation in peripheral and tissue-derived MAIT cells. (A) Representative flow cytometry contour plots illustrating XBP1s expression in MAIT cells isolated from peripheral blood, peritumoral tissue, and tumour tissue of patients with HCC. (B) Frequencies of XBP1s + MAIT cells in peripheral blood from age-matched healthy donors (HD, n = 8) and in peripheral blood- and tissue-derived (peritumoral and tumour) MAIT cells from patients with HCC, n=6-10/tissue. (C) Frequencies of peripheral XBP1s + MAIT cells - isolated from healthy donors (HD, n = 8) and patients with HCC (n = 6–8), or from (D) peritumour and tumour HCC tissue - analyzed ex vivo or following functional stimulation to modulate cytotoxic capacity using the ER stress inducers thapsigargin (TG) and tunicamycin (TM), or IL-15 for 24 or 96 hours; n = 8–12/group. (E) Frequencies of peripheral MAIT cells expressing NKG2D or Granzyme B - isolated from healthy donors (HD, n = 8) and patients with HCC (n = 6–8), or from (F) peritumour and tumour HCC tissue - analyzed ex vivo or following functional stimulation to modulate cytotoxic capacity using the ER stress inducers TG and TM or IL-15 for 24 or 96 hours; n = 8–12/group. (G) Correlation analysis between XBP1s and Granzyme B in peripheral MAIT cells from age-matched healthy donors and HCC patients (left panel), and in peritumoral and tumour MAIT cells from HCC tissue (right panel) after IL-15 stimulation for 96 hours. (H) Cytotoxic capacity of peripheral MAIT cells isolated from healthy donors ex vivo or following 96-hour stimulation with IL-15 or the ER stress inducers TG and TM (n = 3–7 per group). Non-significant (n.s.): p > 0.05; *p < 0.05; **p < 0.01; ***p < 0.001, as calculated by a two-tailed paired t-test, two-tailed Wilcoxon matched-pairs signed-rank test (C–F), ordinary one-way ANOVA or Kruskal–Wallis test (B, H) and simple linear regression.

    Journal: Frontiers in Immunology

    Article Title: Comparative profiling of MAIT cells across gastrointestinal cancers identifies conserved NK receptor dysregulation and HCC-specific defects in cytotoxicity and XBP1s signaling

    doi: 10.3389/fimmu.2026.1924000

    Figure Lengend Snippet: XBP1s activation in peripheral and tissue-derived MAIT cells. (A) Representative flow cytometry contour plots illustrating XBP1s expression in MAIT cells isolated from peripheral blood, peritumoral tissue, and tumour tissue of patients with HCC. (B) Frequencies of XBP1s + MAIT cells in peripheral blood from age-matched healthy donors (HD, n = 8) and in peripheral blood- and tissue-derived (peritumoral and tumour) MAIT cells from patients with HCC, n=6-10/tissue. (C) Frequencies of peripheral XBP1s + MAIT cells - isolated from healthy donors (HD, n = 8) and patients with HCC (n = 6–8), or from (D) peritumour and tumour HCC tissue - analyzed ex vivo or following functional stimulation to modulate cytotoxic capacity using the ER stress inducers thapsigargin (TG) and tunicamycin (TM), or IL-15 for 24 or 96 hours; n = 8–12/group. (E) Frequencies of peripheral MAIT cells expressing NKG2D or Granzyme B - isolated from healthy donors (HD, n = 8) and patients with HCC (n = 6–8), or from (F) peritumour and tumour HCC tissue - analyzed ex vivo or following functional stimulation to modulate cytotoxic capacity using the ER stress inducers TG and TM or IL-15 for 24 or 96 hours; n = 8–12/group. (G) Correlation analysis between XBP1s and Granzyme B in peripheral MAIT cells from age-matched healthy donors and HCC patients (left panel), and in peritumoral and tumour MAIT cells from HCC tissue (right panel) after IL-15 stimulation for 96 hours. (H) Cytotoxic capacity of peripheral MAIT cells isolated from healthy donors ex vivo or following 96-hour stimulation with IL-15 or the ER stress inducers TG and TM (n = 3–7 per group). Non-significant (n.s.): p > 0.05; *p < 0.05; **p < 0.01; ***p < 0.001, as calculated by a two-tailed paired t-test, two-tailed Wilcoxon matched-pairs signed-rank test (C–F), ordinary one-way ANOVA or Kruskal–Wallis test (B, H) and simple linear regression.

    Article Snippet: The K562 cell line (chronic myelogenous leukaemia; ATCC CCL-243; RRID: CVCL_K562) was cultured in RPMI 1640 medium containing 0.3 mg/ml glutamine 100 U/ml penicillin, 0.1 mg/ml streptomycin and 10% FBS.

    Techniques: Activation Assay, Tissue, Derivative Assay, Flow Cytometry, Expressing, Isolation, Ex Vivo, Functional Assay, Analysis, Two Tailed Test