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cll cell lines mec 1 wt  (DSMZ)


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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
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    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

    Related Articles

    Cell Culture:

    Article Title: Deficiency of miR-155 in leukemic B-cells results in cell cycle arrest and deregulation of MIR155HG/TP53INP1/CDKN1A/CCND1 network.
    Article Snippet: The MEC-1 cell line was cultured in IMDM medium (#LM-I1090, Biosera) supplemented with 10% of fetal bovine serum (#FB-1090, Biosera), 1% of P/S (#P4333, Sigma Aldrich) at 37 °C in 5% CO2 incubator. .. We followed the DSMZ-recommended cell culture protocol for MEC-1 cells (ACC-497). ..

    Article Title: Coupled miR-155 Deficiency and Hypoxia Lead to the Upregulation of SLC2A3 (GLUT3) and VEGFA in the Leukemic B-cells
    Article Snippet: MEC-1 cell line was cultured in IMDM medium (#LM-I1090, Biosera) supplemented with 10 % of fetal bovine serum (#FB-1090, Biosera), 1 % of P/S (#P4333, Sigma Aldrich) at 37°C in 5 % CO2 incubator. .. We followed the recommended protocol for cell culturing from DSMZ for MEC-1 cells (ACC-497). .. In case of hypoxia MEC-1 cell line was incubated in hypoxic chamber (Coy O2 Controlled InVitro Glove-Box - Hypoxia Chamber, Genetica) in IMDM medium supplemented with 10 % of fetal bovine, 1 % of P/S at 37°C, 1 % O2 (for optimizing experiments we used 0.2 %, 1 % and 5 % O2) and 5 % CO2 for 24, and 48 hours (for optimizing experiments also 72, 96 and 120 h).

    Article Title: MiR-155 deficiency and hypoxia results in metabolism switch in the leukemic B-cells
    Article Snippet: More information about the creation and validation of miR-155 deficient MEC-1 clone #48 are in the Supplemental Fig. . MEC-1 cell line was cultured in IMDM medium (#LM-I1090, Biosera) supplemented with 10% of fetal bovine serum (#FB-1090, Biosera), 1% of P/S (#P4333, Sigma Aldrich) at 37 °C in 5% CO 2 incubator. .. We followed the recommended protocol for cell culturing from DSMZ for MEC-1 cells (#ACC-497). .. The hypoxic MEC-1 cell line was incubated in hypoxic glove box (Coy O 2 Controlled InVitro Glove-Box–Hypoxia Chamber, Genetica) in IMDM medium supplemented with 10% of fetal bovine serum, 1% of P/S at 37 °C, 1% O 2 (for optimizing experiments we used 0.2%, 1% and 5% O 2 ) and 5% CO 2 for 24 h, and 48 h (for optimizing experiments also 72 h, 96 h and 120 h).

    Modification:

    Article Title: Inhibition of p38 MAPK or immunoproteasome overcomes resistance of chronic lymphocytic leukemia cells to Bcl-2 antagonist venetoclax.
    Article Snippet: Recombinant human sCD40 ligand (sCD40L; 310-02) was from PeproTech (London, UK). .. MEC-1 cells were from Deutsche Sammlung von Mikroorganismen und Zellkulturen GmbH (Braunschweig, Germany) and were maintained in Iscove’s modified Dulbecco’s medium (Gibco; Grand Island, NY, USA) supplemented with 10% heat-inactivated fetal bovine serum, 100 U/mL penicillin, and 100 μg/mL streptomycin. ..

    other:

    Article Title: Combination of anti CD19 antibody with a BCL-2 inhibitor and uses thereof
    Article Snippet: NKs: RPMI1640, with GlutaMAX, Invitrogen, Cat No.: 31870, 10% FCS; Biocoll: Biochrome AG CAT No.: L6115 LOT No.: 0034D; MACS NK cell isolation kit: Miltenyi Biotec CAT No.: 130-092-657 LOT No.: 5150402327; venetoclax: Selleck Chem.



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    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.
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    95
    DSMZ research cell line source s mec1
    (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 <t>MEC1</t> 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.
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    human leukemia mec1 cell line  (DSMZ)
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    DSMZ human leukemia mec1 cell line
    (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 <t>MEC1</t> 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.
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    DSMZ hg3 cll cell lines
    (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 <t>MEC1</t> 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.
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    cll cell line mec1  (DSMZ)
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    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.
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    mec-1 cells dsmz# acc497  (DSMZ)
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    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.
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    mec-1 cells  (DSMZ)
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    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.
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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