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    DSMZ cll cell lines mec 1 wt
    Validation of the cell cycle and proliferation effects of casein kinase 1δ/ε (CK1δ/ε) inhibition in vivo and in vitro. (A) Percentages of EdU‐Alexa Fluor 647+ leukemic B cells within the spleen (SPL) of treated and control TCL1 adoptive transfer (AT) recipient mice ( N (AT CTRL) = 3; N (AT + PF‐670462) = 4), tested by the t ‐test. (B) Relative cell counts (% of CTRL) originating from in vitro <t>treated</t> <t>MEC‐1</t> wild‐type (WT) cells after a 72 h treatment with PF‐670462 or MU1742 (performed on the following biological replicates: N (CTRL) = 6; N (3µM PF‐670462) = 3; N (10µM PF‐670462) = 6; N (3µM MU1742) = 3; and N (10µM MU1742) = 3), tested by the Kruskal–Wallis test with post hoc pairwise Wilcoxon rank sum tests with Benjamini–Hochberg correction. (C) Relative cell counts (% of CTRL) originating from in vitro treated HG‐3 WT cells after 72 h treatment with PF‐670462 or MU1742 (performed on the following biological replicates: N (CTRL) = 4; N (3µM PF‐670462) = 4; N (10µM PF‐670462) = 4; N (3µM MU1742) = 4; and N (10µM MU1742) = 4), tested by the Kruskal–Wallis test with post hoc pairwise Wilcoxon rank sum tests with Benjamini–Hochberg correction. (D) Cell cycle assay setup with initial CK1 inhibitor treatment and mitotic arrest with nocodazole and the representative example of cell cycle alterations between analyzed conditions in MEC‐1 and HG‐3 cell lines. (E) Cell cycle phase distribution in MEC‐1 WT cells upon 9 h pre‐treatment with 3 µM PF‐670462 and 10 µM PF‐670462 and subsequent mitotic arrest with nocodazole (performed on the following biological replicates: N (CTRL) = 11; N (NOCODAZOLE) = 11; N (3µM PF‐670462) = 7; and N (10µM PF‐670462) = 11); for all cases together, the generalized linear mixed‐effects model, followed by estimated marginal means calculation (P‐value < 0.05), was used separately for comparison of CTRL versus NOCODAZOLE and NOCODAZOLE versus PF‐670462 and corrected due to usage of 2 models. (F, G) Cell cycle phase distribution in MEC‐1 WT cells upon 9 h pre‐treatment with 3 and 10 µM concentrations of MU1742 and AH078 (respectively) and subsequent mitotic arrest with nocodazole (performed on the following biological replicates: N (CTRL) = 11; N (NOCODAZOLE) = 11; N (3µM) = 3; and N (10µM) = 3); for all cases together, the generalized linear mixed‐effects model followed by estimated marginal means calculation (P‐value < 0.05), was used separately for comparison of CTRL versus NOCODAZOLE and NOCODAZOLE versus MU1742/AH078 and corrected due to usage of 2 models. (H–J) Cell cycle phase distribution in HG‐3 WT cells upon 9 h pre‐treatment with 3 and 10 µM concentrations of PF‐670462, MU1742, and AH078 (respectively) and subsequent mitotic arrest with nocodazole (performed on the following biological replicates: N (CTRL) = 4; N (NOCODAZOLE) = 4; N (3µM) = 4; and N (10µM) = 4); for all cases together, the generalized linear mixed‐effects model, followed by estimated marginal means calculation (P‐value < 0.05), was used separately for comparison of CTRL versus NOCODAZOLE and NOCODAZOLE versus PF‐670462/MU1742/AH078 and corrected due to usage of 2 models. DMSO, dimethyl sulfoxide; PI, propidium iodide.
    Cll Cell Lines Mec 1 Wt, supplied by DSMZ, used in various techniques. Bioz Stars score: 95/100, based on 210 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Average 95 stars, based on 210 article reviews
    cll cell lines mec 1 wt - by Bioz Stars, 2026-09
    95/100 stars

    Images

    1) Product Images from "Casein kinase 1δ/ε inhibition suppresses CLL proliferation through cell‐intrinsic and microenvironmental mechanisms"

    Article Title: Casein kinase 1δ/ε inhibition suppresses CLL proliferation through cell‐intrinsic and microenvironmental mechanisms

    Journal: HemaSphere

    doi: 10.1002/hem3.70343

    Validation of the cell cycle and proliferation effects of casein kinase 1δ/ε (CK1δ/ε) inhibition in vivo and in vitro. (A) Percentages of EdU‐Alexa Fluor 647+ leukemic B cells within the spleen (SPL) of treated and control TCL1 adoptive transfer (AT) recipient mice ( N (AT CTRL) = 3; N (AT + PF‐670462) = 4), tested by the t ‐test. (B) Relative cell counts (% of CTRL) originating from in vitro treated MEC‐1 wild‐type (WT) cells after a 72 h treatment with PF‐670462 or MU1742 (performed on the following biological replicates: N (CTRL) = 6; N (3µM PF‐670462) = 3; N (10µM PF‐670462) = 6; N (3µM MU1742) = 3; and N (10µM MU1742) = 3), tested by the Kruskal–Wallis test with post hoc pairwise Wilcoxon rank sum tests with Benjamini–Hochberg correction. (C) Relative cell counts (% of CTRL) originating from in vitro treated HG‐3 WT cells after 72 h treatment with PF‐670462 or MU1742 (performed on the following biological replicates: N (CTRL) = 4; N (3µM PF‐670462) = 4; N (10µM PF‐670462) = 4; N (3µM MU1742) = 4; and N (10µM MU1742) = 4), tested by the Kruskal–Wallis test with post hoc pairwise Wilcoxon rank sum tests with Benjamini–Hochberg correction. (D) Cell cycle assay setup with initial CK1 inhibitor treatment and mitotic arrest with nocodazole and the representative example of cell cycle alterations between analyzed conditions in MEC‐1 and HG‐3 cell lines. (E) Cell cycle phase distribution in MEC‐1 WT cells upon 9 h pre‐treatment with 3 µM PF‐670462 and 10 µM PF‐670462 and subsequent mitotic arrest with nocodazole (performed on the following biological replicates: N (CTRL) = 11; N (NOCODAZOLE) = 11; N (3µM PF‐670462) = 7; and N (10µM PF‐670462) = 11); for all cases together, the generalized linear mixed‐effects model, followed by estimated marginal means calculation (P‐value < 0.05), was used separately for comparison of CTRL versus NOCODAZOLE and NOCODAZOLE versus PF‐670462 and corrected due to usage of 2 models. (F, G) Cell cycle phase distribution in MEC‐1 WT cells upon 9 h pre‐treatment with 3 and 10 µM concentrations of MU1742 and AH078 (respectively) and subsequent mitotic arrest with nocodazole (performed on the following biological replicates: N (CTRL) = 11; N (NOCODAZOLE) = 11; N (3µM) = 3; and N (10µM) = 3); for all cases together, the generalized linear mixed‐effects model followed by estimated marginal means calculation (P‐value < 0.05), was used separately for comparison of CTRL versus NOCODAZOLE and NOCODAZOLE versus MU1742/AH078 and corrected due to usage of 2 models. (H–J) Cell cycle phase distribution in HG‐3 WT cells upon 9 h pre‐treatment with 3 and 10 µM concentrations of PF‐670462, MU1742, and AH078 (respectively) and subsequent mitotic arrest with nocodazole (performed on the following biological replicates: N (CTRL) = 4; N (NOCODAZOLE) = 4; N (3µM) = 4; and N (10µM) = 4); for all cases together, the generalized linear mixed‐effects model, followed by estimated marginal means calculation (P‐value < 0.05), was used separately for comparison of CTRL versus NOCODAZOLE and NOCODAZOLE versus PF‐670462/MU1742/AH078 and corrected due to usage of 2 models. DMSO, dimethyl sulfoxide; PI, propidium iodide.
    Figure Legend Snippet: Validation of the cell cycle and proliferation effects of casein kinase 1δ/ε (CK1δ/ε) inhibition in vivo and in vitro. (A) Percentages of EdU‐Alexa Fluor 647+ leukemic B cells within the spleen (SPL) of treated and control TCL1 adoptive transfer (AT) recipient mice ( N (AT CTRL) = 3; N (AT + PF‐670462) = 4), tested by the t ‐test. (B) Relative cell counts (% of CTRL) originating from in vitro treated MEC‐1 wild‐type (WT) cells after a 72 h treatment with PF‐670462 or MU1742 (performed on the following biological replicates: N (CTRL) = 6; N (3µM PF‐670462) = 3; N (10µM PF‐670462) = 6; N (3µM MU1742) = 3; and N (10µM MU1742) = 3), tested by the Kruskal–Wallis test with post hoc pairwise Wilcoxon rank sum tests with Benjamini–Hochberg correction. (C) Relative cell counts (% of CTRL) originating from in vitro treated HG‐3 WT cells after 72 h treatment with PF‐670462 or MU1742 (performed on the following biological replicates: N (CTRL) = 4; N (3µM PF‐670462) = 4; N (10µM PF‐670462) = 4; N (3µM MU1742) = 4; and N (10µM MU1742) = 4), tested by the Kruskal–Wallis test with post hoc pairwise Wilcoxon rank sum tests with Benjamini–Hochberg correction. (D) Cell cycle assay setup with initial CK1 inhibitor treatment and mitotic arrest with nocodazole and the representative example of cell cycle alterations between analyzed conditions in MEC‐1 and HG‐3 cell lines. (E) Cell cycle phase distribution in MEC‐1 WT cells upon 9 h pre‐treatment with 3 µM PF‐670462 and 10 µM PF‐670462 and subsequent mitotic arrest with nocodazole (performed on the following biological replicates: N (CTRL) = 11; N (NOCODAZOLE) = 11; N (3µM PF‐670462) = 7; and N (10µM PF‐670462) = 11); for all cases together, the generalized linear mixed‐effects model, followed by estimated marginal means calculation (P‐value < 0.05), was used separately for comparison of CTRL versus NOCODAZOLE and NOCODAZOLE versus PF‐670462 and corrected due to usage of 2 models. (F, G) Cell cycle phase distribution in MEC‐1 WT cells upon 9 h pre‐treatment with 3 and 10 µM concentrations of MU1742 and AH078 (respectively) and subsequent mitotic arrest with nocodazole (performed on the following biological replicates: N (CTRL) = 11; N (NOCODAZOLE) = 11; N (3µM) = 3; and N (10µM) = 3); for all cases together, the generalized linear mixed‐effects model followed by estimated marginal means calculation (P‐value < 0.05), was used separately for comparison of CTRL versus NOCODAZOLE and NOCODAZOLE versus MU1742/AH078 and corrected due to usage of 2 models. (H–J) Cell cycle phase distribution in HG‐3 WT cells upon 9 h pre‐treatment with 3 and 10 µM concentrations of PF‐670462, MU1742, and AH078 (respectively) and subsequent mitotic arrest with nocodazole (performed on the following biological replicates: N (CTRL) = 4; N (NOCODAZOLE) = 4; N (3µM) = 4; and N (10µM) = 4); for all cases together, the generalized linear mixed‐effects model, followed by estimated marginal means calculation (P‐value < 0.05), was used separately for comparison of CTRL versus NOCODAZOLE and NOCODAZOLE versus PF‐670462/MU1742/AH078 and corrected due to usage of 2 models. DMSO, dimethyl sulfoxide; PI, propidium iodide.

    Techniques Used: Biomarker Discovery, Inhibition, In Vivo, In Vitro, Control, Adoptive Transfer Assay, Cell Cycle Assay, Comparison

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    Cell Culture:

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    Suspension:

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    Incubation:

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    Article Title: Ezrin is highly expressed and a druggable target in chronic lymphocytic leukemia.
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    Article Title: Combination of anti CD19 antibody with a BCL-2 inhibitor and uses thereof
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    Fluorescence:

    Article Title: Auranofin Induces Lethal Oxidative and Endoplasmic Reticulum Stress and Exerts Potent Preclinical Activity against Chronic Lymphocytic Leukemia
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    Article Title: Improving CLL Vγ9Vδ2-T-cell fitness for cellular therapy by ex vivo activation and ibrutinib.
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    Article Title: Ezrin is highly expressed and a druggable target in chronic lymphocytic leukemia.
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    Article Title: EZN-2208 treatment suppresses chronic lymphocytic leukaemia by interfering with environmental protection and increases response to fludarabine
    Article Snippet: MEC-1 and HS5 cells (DSMZ and ATCC) were maintained in RPMI-1640 and DMEM supplemented with 10% FBS and 1% Pen-Strep antibiotics (Lonza) at 37°C in a humidified atmosphere containing 5 and 10% CO 2 .

    Article Title: Combination of anti CD19 antibody with a BCL-2 inhibitor and uses thereof
    Article Snippet: MEC-1 cells (DSMZ# ACC497) are a chronic B-cell leukemia cell line.

    Staining:

    Article Title: Auranofin Induces Lethal Oxidative and Endoplasmic Reticulum Stress and Exerts Potent Preclinical Activity against Chronic Lymphocytic Leukemia
    Article Snippet: Cell lines and primary CLL cells Human chronic B-cell leukemia, MEC-1 cells were obtained from the DSMZ).

    Article Title: Multivalent FV antibodies
    Article Snippet: Assessment of Cell-Binding and Cytotoxic Activity Mediated by Trispecific Antibody Molecules Study Procedures: Cells and Cell Culture CD19+/CD30+ MEC-1 (DSMZ, cat.: ACC 497), CD19+/CD30− Raji (DSMZ, cat.: ACC 319), and CD19−/CD30+ KARPAS-299 (DSMZ, cat.: ACC 31) cells were cultured under standard conditions in RPMI 1640 (cat.: 21875-034) or IMDM (cat.: 12440-053) medium supplemented with 10% heat-inactivated fetal calf serum (FCS) (cat.: 10270-106), 100 U/mL penicillin G, 100 μg/mL streptomycin (cat: 1540-122), and 2 mM L-glutamine (cat: 25030-024; all Invitrogen, Karlsruhe, Germany) herein referred to as complete RPMI medium, as recommended by the supplier of the cell lines.

    Article Title: Improving CLL Vγ9Vδ2-T-cell fitness for cellular therapy by ex vivo activation and ibrutinib.
    Article Snippet: HC-Vγ9Vδ2-T cells or Mec-1 (DSMZ) cells were lysed with NP-40 lysis buffer.

    Article Title: A mathematical model of subpopulation kinetics for the deconvolution of leukaemia heterogeneity
    Article Snippet: MEC-1 (DSMZ, Germany) cells were cultured in IMDM + 20% FBS + 1% P/S for 1 week, and in IMDM + 10% FBS + 1% P/S thereafter.

    Article Title: Ezrin is highly expressed and a druggable target in chronic lymphocytic leukemia.
    Article Snippet: Aims: Despite the development of therapeutic strategies for chronic lymphocytic leukemia (CLL), most patients remain incurable, relapse, or refractory to current treatments, indicating the need to expand the antineoplastic repertoire for this disease.. Ezrin (EZR) is a known oncogene in solid tumors and plays a key role in cell survival and BCR-mediated signaling activation in B-cell lymphomas.. However, its role in hematological neoplasms remains poorly explored.

    Article Title: EZN-2208 treatment suppresses chronic lymphocytic leukaemia by interfering with environmental protection and increases response to fludarabine
    Article Snippet: MEC-1 and HS5 cells (DSMZ and ATCC) were maintained in RPMI-1640 and DMEM supplemented with 10% FBS and 1% Pen-Strep antibiotics (Lonza) at 37°C in a humidified atmosphere containing 5 and 10% CO 2 .

    Article Title: Combination of anti CD19 antibody with a BCL-2 inhibitor and uses thereof
    Article Snippet: MEC-1 cells (DSMZ# ACC497) are a chronic B-cell leukemia cell line.

    Concentration Assay:

    Article Title: Auranofin Induces Lethal Oxidative and Endoplasmic Reticulum Stress and Exerts Potent Preclinical Activity against Chronic Lymphocytic Leukemia
    Article Snippet: Cell lines and primary CLL cells Human chronic B-cell leukemia, MEC-1 cells were obtained from the DSMZ).

    Article Title: Multivalent FV antibodies
    Article Snippet: Assessment of Cell-Binding and Cytotoxic Activity Mediated by Trispecific Antibody Molecules Study Procedures: Cells and Cell Culture CD19+/CD30+ MEC-1 (DSMZ, cat.: ACC 497), CD19+/CD30− Raji (DSMZ, cat.: ACC 319), and CD19−/CD30+ KARPAS-299 (DSMZ, cat.: ACC 31) cells were cultured under standard conditions in RPMI 1640 (cat.: 21875-034) or IMDM (cat.: 12440-053) medium supplemented with 10% heat-inactivated fetal calf serum (FCS) (cat.: 10270-106), 100 U/mL penicillin G, 100 μg/mL streptomycin (cat: 1540-122), and 2 mM L-glutamine (cat: 25030-024; all Invitrogen, Karlsruhe, Germany) herein referred to as complete RPMI medium, as recommended by the supplier of the cell lines.

    Article Title: Improving CLL Vγ9Vδ2-T-cell fitness for cellular therapy by ex vivo activation and ibrutinib.
    Article Snippet: HC-Vγ9Vδ2-T cells or Mec-1 (DSMZ) cells were lysed with NP-40 lysis buffer.

    Article Title: A mathematical model of subpopulation kinetics for the deconvolution of leukaemia heterogeneity
    Article Snippet: MEC-1 (DSMZ, Germany) cells were cultured in IMDM + 20% FBS + 1% P/S for 1 week, and in IMDM + 10% FBS + 1% P/S thereafter.

    Article Title: Ezrin is highly expressed and a druggable target in chronic lymphocytic leukemia.
    Article Snippet: Aims: Despite the development of therapeutic strategies for chronic lymphocytic leukemia (CLL), most patients remain incurable, relapse, or refractory to current treatments, indicating the need to expand the antineoplastic repertoire for this disease.. Ezrin (EZR) is a known oncogene in solid tumors and plays a key role in cell survival and BCR-mediated signaling activation in B-cell lymphomas.. However, its role in hematological neoplasms remains poorly explored.

    Article Title: EZN-2208 treatment suppresses chronic lymphocytic leukaemia by interfering with environmental protection and increases response to fludarabine
    Article Snippet: MEC-1 and HS5 cells (DSMZ and ATCC) were maintained in RPMI-1640 and DMEM supplemented with 10% FBS and 1% Pen-Strep antibiotics (Lonza) at 37°C in a humidified atmosphere containing 5 and 10% CO 2 .

    Article Title: Combination of anti CD19 antibody with a BCL-2 inhibitor and uses thereof
    Article Snippet: MEC-1 cells (DSMZ# ACC497) are a chronic B-cell leukemia cell line.

    Co-Culture Assay:

    Article Title: Auranofin Induces Lethal Oxidative and Endoplasmic Reticulum Stress and Exerts Potent Preclinical Activity against Chronic Lymphocytic Leukemia
    Article Snippet: Cell lines and primary CLL cells Human chronic B-cell leukemia, MEC-1 cells were obtained from the DSMZ).

    Article Title: Multivalent FV antibodies
    Article Snippet: Assessment of Cell-Binding and Cytotoxic Activity Mediated by Trispecific Antibody Molecules Study Procedures: Cells and Cell Culture CD19+/CD30+ MEC-1 (DSMZ, cat.: ACC 497), CD19+/CD30− Raji (DSMZ, cat.: ACC 319), and CD19−/CD30+ KARPAS-299 (DSMZ, cat.: ACC 31) cells were cultured under standard conditions in RPMI 1640 (cat.: 21875-034) or IMDM (cat.: 12440-053) medium supplemented with 10% heat-inactivated fetal calf serum (FCS) (cat.: 10270-106), 100 U/mL penicillin G, 100 μg/mL streptomycin (cat: 1540-122), and 2 mM L-glutamine (cat: 25030-024; all Invitrogen, Karlsruhe, Germany) herein referred to as complete RPMI medium, as recommended by the supplier of the cell lines.

    Article Title: Improving CLL Vγ9Vδ2-T-cell fitness for cellular therapy by ex vivo activation and ibrutinib.
    Article Snippet: HC-Vγ9Vδ2-T cells or Mec-1 (DSMZ) cells were lysed with NP-40 lysis buffer.

    Article Title: A mathematical model of subpopulation kinetics for the deconvolution of leukaemia heterogeneity
    Article Snippet: MEC-1 (DSMZ, Germany) cells were cultured in IMDM + 20% FBS + 1% P/S for 1 week, and in IMDM + 10% FBS + 1% P/S thereafter.

    Article Title: Ezrin is highly expressed and a druggable target in chronic lymphocytic leukemia.
    Article Snippet: Aims: Despite the development of therapeutic strategies for chronic lymphocytic leukemia (CLL), most patients remain incurable, relapse, or refractory to current treatments, indicating the need to expand the antineoplastic repertoire for this disease.. Ezrin (EZR) is a known oncogene in solid tumors and plays a key role in cell survival and BCR-mediated signaling activation in B-cell lymphomas.. However, its role in hematological neoplasms remains poorly explored.

    Article Title: EZN-2208 treatment suppresses chronic lymphocytic leukaemia by interfering with environmental protection and increases response to fludarabine
    Article Snippet: MEC-1 and HS5 cells (DSMZ and ATCC) were maintained in RPMI-1640 and DMEM supplemented with 10% FBS and 1% Pen-Strep antibiotics (Lonza) at 37°C in a humidified atmosphere containing 5 and 10% CO 2 .

    Article Title: Combination of anti CD19 antibody with a BCL-2 inhibitor and uses thereof
    Article Snippet: MEC-1 cells (DSMZ# ACC497) are a chronic B-cell leukemia cell line.



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    DSMZ cll cell line mec1
    The disease model (A) Recirculation of <t>MEC1</t> <t>CLL</t> cells in the “niche” conformation with the microenvironment. Immunofluorescence images showing CD45 + (green) MEC1 cells in the LN and BM microenvironments. Z Stacks were acquired using a 20× (a, d), a 30× (c), a 60× (e, f), and a 60× with 1.5 zoom (b) objective lens. Scale bars, 50 μm. (B) Flow cytometry analysis of CLL-specific markers on circulating cells in the LN model. (C) Flow cytometry analysis of CLL-specific markers on circulating cells in the BM model. For all the markers, data are represented by fold change relative to the 2D condition. All data are represented by mean ± SEM. For each model (LN and BM) two independent experiments (EXP.1 in black, EXP.2 in pink), with four replicates each were performed.
    Cll Cell Line Mec1, supplied by DSMZ, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Average 95 stars, based on 1 article reviews
    cll cell line mec1 - by Bioz Stars, 2026-09
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    mec-1 cells dsmz# acc497  (DSMZ)
    90
    DSMZ mec-1 cells dsmz# acc497
    The disease model (A) Recirculation of <t>MEC1</t> <t>CLL</t> cells in the “niche” conformation with the microenvironment. Immunofluorescence images showing CD45 + (green) MEC1 cells in the LN and BM microenvironments. Z Stacks were acquired using a 20× (a, d), a 30× (c), a 60× (e, f), and a 60× with 1.5 zoom (b) objective lens. Scale bars, 50 μm. (B) Flow cytometry analysis of CLL-specific markers on circulating cells in the LN model. (C) Flow cytometry analysis of CLL-specific markers on circulating cells in the BM model. For all the markers, data are represented by fold change relative to the 2D condition. All data are represented by mean ± SEM. For each model (LN and BM) two independent experiments (EXP.1 in black, EXP.2 in pink), with four replicates each were performed.
    Mec 1 Cells Dsmz# Acc497, supplied by DSMZ, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/mec-1+cells/mec+1+cell+line/us12358983-232-0-2
    Average 90 stars, based on 1 article reviews
    mec-1 cells dsmz# acc497 - by Bioz Stars, 2026-09
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    mec-1 cells  (DSMZ)
    90
    DSMZ mec-1 cells
    The disease model (A) Recirculation of <t>MEC1</t> <t>CLL</t> cells in the “niche” conformation with the microenvironment. Immunofluorescence images showing CD45 + (green) MEC1 cells in the LN and BM microenvironments. Z Stacks were acquired using a 20× (a, d), a 30× (c), a 60× (e, f), and a 60× with 1.5 zoom (b) objective lens. Scale bars, 50 μm. (B) Flow cytometry analysis of CLL-specific markers on circulating cells in the LN model. (C) Flow cytometry analysis of CLL-specific markers on circulating cells in the BM model. For all the markers, data are represented by fold change relative to the 2D condition. All data are represented by mean ± SEM. For each model (LN and BM) two independent experiments (EXP.1 in black, EXP.2 in pink), with four replicates each were performed.
    Mec 1 Cells, supplied by DSMZ, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/mec-1+cells/mec+1+cell+line/us12358983-99-0-2
    Average 90 stars, based on 1 article reviews
    mec-1 cells - by Bioz Stars, 2026-09
    90/100 stars
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    Image Search Results


    Validation of the cell cycle and proliferation effects of casein kinase 1δ/ε (CK1δ/ε) inhibition in vivo and in vitro. (A) Percentages of EdU‐Alexa Fluor 647+ leukemic B cells within the spleen (SPL) of treated and control TCL1 adoptive transfer (AT) recipient mice ( N (AT CTRL) = 3; N (AT + PF‐670462) = 4), tested by the t ‐test. (B) Relative cell counts (% of CTRL) originating from in vitro treated MEC‐1 wild‐type (WT) cells after a 72 h treatment with PF‐670462 or MU1742 (performed on the following biological replicates: N (CTRL) = 6; N (3µM PF‐670462) = 3; N (10µM PF‐670462) = 6; N (3µM MU1742) = 3; and N (10µM MU1742) = 3), tested by the Kruskal–Wallis test with post hoc pairwise Wilcoxon rank sum tests with Benjamini–Hochberg correction. (C) Relative cell counts (% of CTRL) originating from in vitro treated HG‐3 WT cells after 72 h treatment with PF‐670462 or MU1742 (performed on the following biological replicates: N (CTRL) = 4; N (3µM PF‐670462) = 4; N (10µM PF‐670462) = 4; N (3µM MU1742) = 4; and N (10µM MU1742) = 4), tested by the Kruskal–Wallis test with post hoc pairwise Wilcoxon rank sum tests with Benjamini–Hochberg correction. (D) Cell cycle assay setup with initial CK1 inhibitor treatment and mitotic arrest with nocodazole and the representative example of cell cycle alterations between analyzed conditions in MEC‐1 and HG‐3 cell lines. (E) Cell cycle phase distribution in MEC‐1 WT cells upon 9 h pre‐treatment with 3 µM PF‐670462 and 10 µM PF‐670462 and subsequent mitotic arrest with nocodazole (performed on the following biological replicates: N (CTRL) = 11; N (NOCODAZOLE) = 11; N (3µM PF‐670462) = 7; and N (10µM PF‐670462) = 11); for all cases together, the generalized linear mixed‐effects model, followed by estimated marginal means calculation (P‐value < 0.05), was used separately for comparison of CTRL versus NOCODAZOLE and NOCODAZOLE versus PF‐670462 and corrected due to usage of 2 models. (F, G) Cell cycle phase distribution in MEC‐1 WT cells upon 9 h pre‐treatment with 3 and 10 µM concentrations of MU1742 and AH078 (respectively) and subsequent mitotic arrest with nocodazole (performed on the following biological replicates: N (CTRL) = 11; N (NOCODAZOLE) = 11; N (3µM) = 3; and N (10µM) = 3); for all cases together, the generalized linear mixed‐effects model followed by estimated marginal means calculation (P‐value < 0.05), was used separately for comparison of CTRL versus NOCODAZOLE and NOCODAZOLE versus MU1742/AH078 and corrected due to usage of 2 models. (H–J) Cell cycle phase distribution in HG‐3 WT cells upon 9 h pre‐treatment with 3 and 10 µM concentrations of PF‐670462, MU1742, and AH078 (respectively) and subsequent mitotic arrest with nocodazole (performed on the following biological replicates: N (CTRL) = 4; N (NOCODAZOLE) = 4; N (3µM) = 4; and N (10µM) = 4); for all cases together, the generalized linear mixed‐effects model, followed by estimated marginal means calculation (P‐value < 0.05), was used separately for comparison of CTRL versus NOCODAZOLE and NOCODAZOLE versus PF‐670462/MU1742/AH078 and corrected due to usage of 2 models. DMSO, dimethyl sulfoxide; PI, propidium iodide.

    Journal: HemaSphere

    Article Title: Casein kinase 1δ/ε inhibition suppresses CLL proliferation through cell‐intrinsic and microenvironmental mechanisms

    doi: 10.1002/hem3.70343

    Figure Lengend Snippet: Validation of the cell cycle and proliferation effects of casein kinase 1δ/ε (CK1δ/ε) inhibition in vivo and in vitro. (A) Percentages of EdU‐Alexa Fluor 647+ leukemic B cells within the spleen (SPL) of treated and control TCL1 adoptive transfer (AT) recipient mice ( N (AT CTRL) = 3; N (AT + PF‐670462) = 4), tested by the t ‐test. (B) Relative cell counts (% of CTRL) originating from in vitro treated MEC‐1 wild‐type (WT) cells after a 72 h treatment with PF‐670462 or MU1742 (performed on the following biological replicates: N (CTRL) = 6; N (3µM PF‐670462) = 3; N (10µM PF‐670462) = 6; N (3µM MU1742) = 3; and N (10µM MU1742) = 3), tested by the Kruskal–Wallis test with post hoc pairwise Wilcoxon rank sum tests with Benjamini–Hochberg correction. (C) Relative cell counts (% of CTRL) originating from in vitro treated HG‐3 WT cells after 72 h treatment with PF‐670462 or MU1742 (performed on the following biological replicates: N (CTRL) = 4; N (3µM PF‐670462) = 4; N (10µM PF‐670462) = 4; N (3µM MU1742) = 4; and N (10µM MU1742) = 4), tested by the Kruskal–Wallis test with post hoc pairwise Wilcoxon rank sum tests with Benjamini–Hochberg correction. (D) Cell cycle assay setup with initial CK1 inhibitor treatment and mitotic arrest with nocodazole and the representative example of cell cycle alterations between analyzed conditions in MEC‐1 and HG‐3 cell lines. (E) Cell cycle phase distribution in MEC‐1 WT cells upon 9 h pre‐treatment with 3 µM PF‐670462 and 10 µM PF‐670462 and subsequent mitotic arrest with nocodazole (performed on the following biological replicates: N (CTRL) = 11; N (NOCODAZOLE) = 11; N (3µM PF‐670462) = 7; and N (10µM PF‐670462) = 11); for all cases together, the generalized linear mixed‐effects model, followed by estimated marginal means calculation (P‐value < 0.05), was used separately for comparison of CTRL versus NOCODAZOLE and NOCODAZOLE versus PF‐670462 and corrected due to usage of 2 models. (F, G) Cell cycle phase distribution in MEC‐1 WT cells upon 9 h pre‐treatment with 3 and 10 µM concentrations of MU1742 and AH078 (respectively) and subsequent mitotic arrest with nocodazole (performed on the following biological replicates: N (CTRL) = 11; N (NOCODAZOLE) = 11; N (3µM) = 3; and N (10µM) = 3); for all cases together, the generalized linear mixed‐effects model followed by estimated marginal means calculation (P‐value < 0.05), was used separately for comparison of CTRL versus NOCODAZOLE and NOCODAZOLE versus MU1742/AH078 and corrected due to usage of 2 models. (H–J) Cell cycle phase distribution in HG‐3 WT cells upon 9 h pre‐treatment with 3 and 10 µM concentrations of PF‐670462, MU1742, and AH078 (respectively) and subsequent mitotic arrest with nocodazole (performed on the following biological replicates: N (CTRL) = 4; N (NOCODAZOLE) = 4; N (3µM) = 4; and N (10µM) = 4); for all cases together, the generalized linear mixed‐effects model, followed by estimated marginal means calculation (P‐value < 0.05), was used separately for comparison of CTRL versus NOCODAZOLE and NOCODAZOLE versus PF‐670462/MU1742/AH078 and corrected due to usage of 2 models. DMSO, dimethyl sulfoxide; PI, propidium iodide.

    Article Snippet: CLL cell lines MEC‐1 WT (DSMZ, #ACC497) and HG‐3 WT (DSMZ, #ACC765) were treated with PF‐670462 (DC Chemicals, #DC2086), an in‐house CK1δ/ε inhibitor MU1742 or CK1δ/ε degrader AH078, and subjected to cell proliferation tracking and cell cycle tracking via PI staining, EdU Click‐iT assays, and/or western blotting, as described in more detail in the Supporting Information S1: .

    Techniques: Biomarker Discovery, Inhibition, In Vivo, In Vitro, Control, Adoptive Transfer Assay, Cell Cycle Assay, Comparison

    (a) Flow cytometric analysis of cell-surface high-affinity CD16 (FcγRIIIA; V158) expression on Jurkat-Lucia™ NFAT-CD16 cells. Fluorescence histograms show isotype control mAb (blue) and CD16-FITC (red). (b) Jurkat-Lucia™ NFAT-CD16 effector cells (e) were co-cultured with MEC1 or MEC1-ROR1 target cells (T) (E:T = 20:1; 6 h; 37°C) in the presence or absence of anti-CD20 (rituximab) or anti-ROR1 mAbs (GE-zilovertamab, zilovertamab; 100 ng/ml). Data are mean ± SD; unpaired two-tailed Student’s t test, P < .01. (c) Dose-dependent activation of CLL target cells (T) co-cultured with Jurkat-Lucia™ NFAT-CD16 effector cells (E:T = 20:1; 6 h; 37°C) and exposed to serial dilutions of anti-ROR1 mAbs (GE-zilovertamab, zilovertamab). Luminescence was measured after 6 h. data are mean ± SD; one-way ANOVA, P < .01. (d) Flow cytometric detection of CD16A on NK92-CD16 (FcγRIIIa; F176V/S197P mutated). Isotype control mAb (red) and CD16-FITC (blue) are shown. (e) 51 Cr-labeled MEC1 or MEC1-ROR1 target cells (T) were co-cultured with NK92-CD16 effector cells (E:T = 2:1; 6 h; 37°C) with or without rituximab or anti-ROR1 mAbs (GE-zilovertamab, zilovertamab; 100 ng/ml). Percent lysis was calculated from 51 Cr release relative to TCA-treated cells. Data are mean ± SD; two-tailed Student’s t test, P < .01. (f) 51 Cr-labeled primary CLL cells (T) were co-cultured with NK92-CD16 effector cells (E:T = 10:1; 6 h; 37°C) with or without rituximab or anti-ROR1 mAbs (GE-zilovertamab, zilovertamab; 100 ng/ml). Percent specific lysis was calculated as in panel e. Data are mean ± SD; two-tailed Student’s t test, P < .05.

    Journal: Antibody Therapeutics

    Article Title: A glycoengineered anti-ROR1 antibody, GE-zilovertamab, selectively enhances antibody-dependent cellular cytotoxicity against chronic lymphocytic leukemia

    doi: 10.1093/abt/tbag001

    Figure Lengend Snippet: (a) Flow cytometric analysis of cell-surface high-affinity CD16 (FcγRIIIA; V158) expression on Jurkat-Lucia™ NFAT-CD16 cells. Fluorescence histograms show isotype control mAb (blue) and CD16-FITC (red). (b) Jurkat-Lucia™ NFAT-CD16 effector cells (e) were co-cultured with MEC1 or MEC1-ROR1 target cells (T) (E:T = 20:1; 6 h; 37°C) in the presence or absence of anti-CD20 (rituximab) or anti-ROR1 mAbs (GE-zilovertamab, zilovertamab; 100 ng/ml). Data are mean ± SD; unpaired two-tailed Student’s t test, P < .01. (c) Dose-dependent activation of CLL target cells (T) co-cultured with Jurkat-Lucia™ NFAT-CD16 effector cells (E:T = 20:1; 6 h; 37°C) and exposed to serial dilutions of anti-ROR1 mAbs (GE-zilovertamab, zilovertamab). Luminescence was measured after 6 h. data are mean ± SD; one-way ANOVA, P < .01. (d) Flow cytometric detection of CD16A on NK92-CD16 (FcγRIIIa; F176V/S197P mutated). Isotype control mAb (red) and CD16-FITC (blue) are shown. (e) 51 Cr-labeled MEC1 or MEC1-ROR1 target cells (T) were co-cultured with NK92-CD16 effector cells (E:T = 2:1; 6 h; 37°C) with or without rituximab or anti-ROR1 mAbs (GE-zilovertamab, zilovertamab; 100 ng/ml). Percent lysis was calculated from 51 Cr release relative to TCA-treated cells. Data are mean ± SD; two-tailed Student’s t test, P < .01. (f) 51 Cr-labeled primary CLL cells (T) were co-cultured with NK92-CD16 effector cells (E:T = 10:1; 6 h; 37°C) with or without rituximab or anti-ROR1 mAbs (GE-zilovertamab, zilovertamab; 100 ng/ml). Percent specific lysis was calculated as in panel e. Data are mean ± SD; two-tailed Student’s t test, P < .05.

    Article Snippet: MEC1 cells derived from CLL were obtained from DSMZ and maintained in RPMI-1640 medium with 10% FBS and 1% penicillin–streptomycin at 37°C in 5% CO 2 .

    Techniques: Expressing, Fluorescence, Control, Cell Culture, Two Tailed Test, Activation Assay, Labeling, Lysis

    (a) Flow cytometric analysis of CD16 expression in peripheral blood mononuclear cells (PBMCs). Isotype control and CD16-FITC staining are shown. (b) 51 Cr-labeled MEC1 or MEC1-ROR1 target cells (T) were co-cultured with PBMCs (E:T = 20:1; 6 h; 37°C; ≥25% CD16 + ) with or without anti-ROR1 mAbs (GE-zilovertamab, zilovertamab; 100 ng/ml). Percent lysis was calculated relative to TCA-treated controls. Data are mean ± SD; two-tailed Student’s t test, P < .01. (c) 51 Cr-labeled primary CLL cells (T) were co-cultured with PBMCs (E:T = 50:1; 6 h; 37°C; ≥25% CD16 + ) with or without anti-CD16 or anti-ROR1 mAbs (GE-zilovertamab, zilovertamab; 100 ng/ml). Percent specific lysis was calculated. Data are mean ± SD; two-tailed Student’s t test, P < .05. (d) 51 Cr-labeled MEC1-ROR1 cells were pre-treated for 1 h with DMSO or prochlorperazine (PCZ; 50 nM), then co-cultured with PBMCs (E:T = 20:1; 6 h; 37°C) with or without rituximab or anti-ROR1 mAbs (GE-zilovertamab, zilovertamab; 100 ng/ml). Percent lysis was calculated as in panel b. Data are mean ± SD; two-tailed Student’s t test, P < .01.

    Journal: Antibody Therapeutics

    Article Title: A glycoengineered anti-ROR1 antibody, GE-zilovertamab, selectively enhances antibody-dependent cellular cytotoxicity against chronic lymphocytic leukemia

    doi: 10.1093/abt/tbag001

    Figure Lengend Snippet: (a) Flow cytometric analysis of CD16 expression in peripheral blood mononuclear cells (PBMCs). Isotype control and CD16-FITC staining are shown. (b) 51 Cr-labeled MEC1 or MEC1-ROR1 target cells (T) were co-cultured with PBMCs (E:T = 20:1; 6 h; 37°C; ≥25% CD16 + ) with or without anti-ROR1 mAbs (GE-zilovertamab, zilovertamab; 100 ng/ml). Percent lysis was calculated relative to TCA-treated controls. Data are mean ± SD; two-tailed Student’s t test, P < .01. (c) 51 Cr-labeled primary CLL cells (T) were co-cultured with PBMCs (E:T = 50:1; 6 h; 37°C; ≥25% CD16 + ) with or without anti-CD16 or anti-ROR1 mAbs (GE-zilovertamab, zilovertamab; 100 ng/ml). Percent specific lysis was calculated. Data are mean ± SD; two-tailed Student’s t test, P < .05. (d) 51 Cr-labeled MEC1-ROR1 cells were pre-treated for 1 h with DMSO or prochlorperazine (PCZ; 50 nM), then co-cultured with PBMCs (E:T = 20:1; 6 h; 37°C) with or without rituximab or anti-ROR1 mAbs (GE-zilovertamab, zilovertamab; 100 ng/ml). Percent lysis was calculated as in panel b. Data are mean ± SD; two-tailed Student’s t test, P < .01.

    Article Snippet: MEC1 cells derived from CLL were obtained from DSMZ and maintained in RPMI-1640 medium with 10% FBS and 1% penicillin–streptomycin at 37°C in 5% CO 2 .

    Techniques: Expressing, Control, Staining, Labeling, Cell Culture, Lysis, Two Tailed Test

    The disease model (A) Recirculation of MEC1 CLL cells in the “niche” conformation with the microenvironment. Immunofluorescence images showing CD45 + (green) MEC1 cells in the LN and BM microenvironments. Z Stacks were acquired using a 20× (a, d), a 30× (c), a 60× (e, f), and a 60× with 1.5 zoom (b) objective lens. Scale bars, 50 μm. (B) Flow cytometry analysis of CLL-specific markers on circulating cells in the LN model. (C) Flow cytometry analysis of CLL-specific markers on circulating cells in the BM model. For all the markers, data are represented by fold change relative to the 2D condition. All data are represented by mean ± SEM. For each model (LN and BM) two independent experiments (EXP.1 in black, EXP.2 in pink), with four replicates each were performed.

    Journal: Cell Reports Methods

    Article Title: Dynamic stimulation promotes functional tissue-like organization of a 3D human lymphoid microenvironment model in vitro

    doi: 10.1016/j.crmeth.2025.101105

    Figure Lengend Snippet: The disease model (A) Recirculation of MEC1 CLL cells in the “niche” conformation with the microenvironment. Immunofluorescence images showing CD45 + (green) MEC1 cells in the LN and BM microenvironments. Z Stacks were acquired using a 20× (a, d), a 30× (c), a 60× (e, f), and a 60× with 1.5 zoom (b) objective lens. Scale bars, 50 μm. (B) Flow cytometry analysis of CLL-specific markers on circulating cells in the LN model. (C) Flow cytometry analysis of CLL-specific markers on circulating cells in the BM model. For all the markers, data are represented by fold change relative to the 2D condition. All data are represented by mean ± SEM. For each model (LN and BM) two independent experiments (EXP.1 in black, EXP.2 in pink), with four replicates each were performed.

    Article Snippet: The CLL cell line MEC1 was obtained from DSMZ (Cat. No. ACC 497; DSMZ, Braunschweig, Germany).

    Techniques: Immunofluorescence, Flow Cytometry