human nb4 cell line  (CLS Cell Lines Service GmbH)

Journal: Cell reports

Article Title: ATP7B-maintained copper stores in myeloid progenitors are required for functional maturation of neutrophils

doi: 10.1016/j.celrep.2026.116955

Figure Lengend Snippet: (A) Co-immunostaining of ATP7B (green) with the trans-Golgi marker TGN46 (red) in mouse myelocytes and co-immunostaining of ATP7B (green) with the cis-Golgi marker GM130 (red) in human myeloid NB4 cells. A zoomed view used to demonstrate the ATP7B (green) vesicular pattern. (B) Co-immunostaining of ATP7B (yellow) with TGN46 (cyan), the early endosome marker EEA1 (cyan), the lysosome marker LAMP1 (magenta), and the late endosomal marker Rab8 (magenta) in non-differentiated NB4 cells. There was no significant co-localization of ATP7B with Golgi and endosomal markers, respectively. Scale bar, 5 μm. (C) Live images of CopperGREEN sensor in non-differentiated NB4 cells. DAPI (blue) was used as a nuclear marker. Scale bar, 10 μm. See also – .

Article Snippet: Human NB4 cell line , Cytion , 300299.

Techniques: Immunostaining, Marker

Journal: Cell reports

Article Title: ATP7B-maintained copper stores in myeloid progenitors are required for functional maturation of neutrophils

doi: 10.1016/j.celrep.2026.116955

Figure Lengend Snippet: (A) Schematic representation of ATRA-induced human myeloid NB4 cell differentiation. (B) Western blot analysis reveals that ATP7B protein abundance is significantly reduced and CEBPε is upregulated during ATRA-induced NB4 cell differentiation from day 0 to day 6. β-actin was used as an endogenous loading control. Immunoblotting data represent 4–5 independent experiments. (C) Densitometric analysis demonstrating altered protein abundance of ATP7B and CEBPε was performed using ImageJ by normalizing to β-actin. (D) Western blot analysis reveals that ATP7A protein abundance is upregulated during ATRA-induced NB4 cell differentiation from day 0 to day 6. (E) Densitometric analysis demonstrating altered protein abundance of ATP7A was performed using ImageJ by normalizing to β-actin. (F–L) mRNA expression of CEBPε (F), ATP7B (G), ATP7A (H), CTR1 (I), CTR2 (J), LOXL2 (K), and AOC2 (L) at day 0, day 2, and day 6 of ATRA-induced NB4 cell differentiation. Values represent mean ± SD. * p < 0.05, ** p < 0.01, *** p < 0.001 relative to the undifferentiated control at day 0 or between multiple time points analyzed by ANOVA. Data represent 3–5 independent experiments. The gray color bar denotes day 0, magenta denotes day 2, and blue denotes day 6 NB4 cells, respectively. Abbreviations: ATRA, all-trans retinoic acid. See also .

Article Snippet: Human NB4 cell line , Cytion , 300299.

Techniques: Cell Differentiation, Western Blot, Quantitative Proteomics, Control, Expressing

Journal: Cell reports

Article Title: ATP7B-maintained copper stores in myeloid progenitors are required for functional maturation of neutrophils

doi: 10.1016/j.celrep.2026.116955

Figure Lengend Snippet: (A) Live images of CopperGREEN in ATRA-induced differentiated NB4 cells (day 6). Scale bar, 10 μm. (B) Cellular copper content at day 0, day 2, and day 6 of ATRA-induced NB4 cell differentiation, measured by ICP-MS, and statistical analysis was performed by ordinary one-way ANOVA. Fg denotes femtogram. (C) CopperGREEN staining in isolated BM progenitors (CD117+) and BM neutrophils reveals an increase in intracellular Cu in BM neutrophils. Representative images of one of the CopperGREEN-stained images is shown from progenitors (CD117+) and neutrophils derived from BM. Scale bar, 10 μm. (D) Fluorescence intensity shows increased Cu levels in BM neutrophils compared to progenitors (CD117+). The data represent two independent experiments. **** p < 0.0001 by t test. (E) CopperGREEN staining was lower in blood neutrophils than in BM neutrophils. Treatment with the Cu chelator TTM (10 μM) reduced intracellular Cu staining in BM neutrophils. BM neutrophils without CopperGREEN were used as a negative control. The data represent three independent experiments. Scale bar, 10 μm.

Article Snippet: Human NB4 cell line , Cytion , 300299.

Techniques: Cell Differentiation, Staining, Isolation, Derivative Assay, Fluorescence, Negative Control

Journal: Cancer Gene Therapy

Article Title: Arsenic trioxide and p97 inhibitor synergize against acute myeloid leukemia by targeting nascent polypeptides and activating the ZAKα–JNK pathway

doi: 10.1038/s41417-024-00818-z

Figure Lengend Snippet: A NB4 cells were treated with different doses of ATO for 24 h, and apoptosis was detected by flow cytometry. B PML-RARα in the NB4 cells was detected by immunoblot after treating with different doses of ATO for 12 h. C ROS level in NB4 induced by ATO for 4 h was detected by using 10 μM DCFH-DA. D Quantification of ROS level in NB4 induced by ATO for 4 h. Normalized to control (0 μM ATO). E NB4 cells were treated with 1.5 μM ATO, 10 or 20 μM H 2 O 2 for 4 h, and then ROS level was detected by using 10 μM DCFH-DA. F Quantification of ROS level in NB4 induced by 1.5 μM ATO, 10 or 20 μM H 2 O 2 for 4 h. Normalized to control. G Quantification of ROS level in NB4 induced by 1.5 μM ATO, 10 or 20 μM H 2 O 2 for 24 h. Normalized to control. H The apoptosis ratio of NB4 cells treated with 1.5 μM ATO or different doses of H 2 O 2 for 24 h was detected by flow cytometry. I NB4 cells were pre-treated with 8 mM NAC or 10 mM GSH for 1 h, and then 2 μM ATO was added for another 24 h. Apoptosis was detected by flow cytometry. Two-tailed Student t test, ** P < 0.01, *** P < 0.001, **** P < 0.0001, the ns indicate no significant difference. Error bars reflect ± SEM of three independent experiments.

Article Snippet: Human AML leukemia cell lines NB4, MV4-11, NOMO-1, MOLM-13, THP-1, U937, HL-60, and Kasumi-1 were purchased from DSMZ.

Techniques: Flow Cytometry, Western Blot, Control, Two Tailed Test

Journal: Cancer Gene Therapy

Article Title: Arsenic trioxide and p97 inhibitor synergize against acute myeloid leukemia by targeting nascent polypeptides and activating the ZAKα–JNK pathway

doi: 10.1038/s41417-024-00818-z

Figure Lengend Snippet: A Ubiquitinated proteins were detected by immunoblot after treatment with 1 or 1.5 μM ATO for 16 h. B , C ProteoStat kit was used to detect protein aggregates in NB4 cells by flow cytometry after treatment with 1 or 1.5 μM ATO ( B ) or 10 or 20 μM H 2 O 2 ( C ) for 16 h. Normalized to control. D Cell viability of indicated AML cell lines with ATO treatment after 24 h. E The global protein synthesis of indicated AML cell lines was detected by Click-iT™ Plus OPP Alexa Fluor™ 647 Protein Synthesis Assay Kit. F Correlation between global protein synthesis and IC 50 . G The global protein synthesis of NB4 cells treated with 0.25 μg/mL cycloheximide, 25 μM rapamycin, 0.2 μg/mL puromycin, or 100 nM anisomycin for 20 h was detected by Click-iT™ HPG Alexa Fluor™ 488 Protein Synthesis Assay Kit. H Quantification of global protein synthesis (Click-iT™ HPG Alexa Fluor™ 488 Protein Synthesis Assay Kit) in NB4 treated with indicated protein synthesis inhibitors for 20 h. Normalized to control. I NB4 cells were pre-treated with 0.25 μg/mL cycloheximide, 25 μM rapamycin, 0.2 μg/mL puromycin, or 100 nM anisomycin for 1 h, and then 1.5 μM ATO was added for another 24 h. Apoptosis was detected by flow cytometry. Two-tailed Student t test, * P < 0.05, ** P < 0.01, *** P < 0.001, the ns indicate no significant difference. Error bars reflect ± SEM of three independent experiments.

Article Snippet: Human AML leukemia cell lines NB4, MV4-11, NOMO-1, MOLM-13, THP-1, U937, HL-60, and Kasumi-1 were purchased from DSMZ.

Techniques: Western Blot, Flow Cytometry, Control, Two Tailed Test

Journal: Cancer Gene Therapy

Article Title: Arsenic trioxide and p97 inhibitor synergize against acute myeloid leukemia by targeting nascent polypeptides and activating the ZAKα–JNK pathway

doi: 10.1038/s41417-024-00818-z

Figure Lengend Snippet: A The NB4 cells were pre-treated with 0.1 μg/mL puromycin for 1 h, and then 4 μM Biotin-As was added for another 16 h. Immunofluorescence visualized the localization of puromycin, Biotin-As, and aggresome in the cells. Scale bar, 25 μm. B The NB4 cells were treated with 1 μM Biotin-As for 4 h, and then 20 μM puromycin was added for another 30 min. Cell fractions were prepared for the Co-IP assays using the streptavidin magnetic beads and indicated antibodies. C Immunoblot of indicated proteins in the NB4 cells at 0, 4, 8, 12, and 24 h with 0.5 or 2 μM ATO treatment. D The NB4 cells were pre-treated with 0.5 μM PERKi (GSK2656157) or 10 μM GCN2iB for 1 h, and then 2 μM ATO was added for another 4 h. Immunoblot of indicated proteins in the NB4 cells.

Article Snippet: Human AML leukemia cell lines NB4, MV4-11, NOMO-1, MOLM-13, THP-1, U937, HL-60, and Kasumi-1 were purchased from DSMZ.

Techniques: Immunofluorescence, Co-Immunoprecipitation Assay, Magnetic Beads, Western Blot

Journal: Cancer Gene Therapy

Article Title: Arsenic trioxide and p97 inhibitor synergize against acute myeloid leukemia by targeting nascent polypeptides and activating the ZAKα–JNK pathway

doi: 10.1038/s41417-024-00818-z

Figure Lengend Snippet: A Polysome profiles from NB4 cells with or without 1.5 μM ATO treatment for 6 h. B Immunoblot of indicated proteins in the NB4 cells at 0, 4, 20 h with 0.5 or 2 μM ATO treatment. C NB4 cells were pre-treated with 5 μM JNK inhibitor (JNK-IN-8) for 1 h, and then 2.5 μM ATO was added for another 24 h. Apoptosis was detected by flow cytometry. D Immunoblot of ZAKα and p-ZAKα in the NB4 cells at 4 or 20 h with 0.5 or 2 μM ATO treatment. The phosphorylated proteins in the cell lysate were enriched by Phos-tag TM Agarose. E The apoptosis ratio of ZAKα-knockdown NB4 cells with or without ATO treatment for 24 h. F Immunoblot of ZAKα in the ZAKα-knockdown NB4 cells. G The NB4 cells were treated with 1 μM Biotin-As for 4 h, and then cell fractions were prepared for the Co-IP assays using the streptavidin magnetic beads and indicated antibodies. H The NB4 cells were treated with 1 μM Biotin-As for 4 h, and then 20 μM puromycin was added for another 30 min. Cell fractions were prepared for the Co-IP assays using the NEMF, p97, and puromycin antibodies. I The NB4 cells were pre-treated with or without 1 μM NMS873 for 1 h and then indicated doses of ATO were added for another 24 h. The apoptosis ratio was detected by flow cytometry. Two-tailed Student t test, * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001. Error bars reflect ± SEM of three independent experiments.

Article Snippet: Human AML leukemia cell lines NB4, MV4-11, NOMO-1, MOLM-13, THP-1, U937, HL-60, and Kasumi-1 were purchased from DSMZ.

Techniques: Western Blot, Flow Cytometry, Knockdown, Co-Immunoprecipitation Assay, Magnetic Beads, Two Tailed Test

Journal: Cancer gene therapy

Article Title: Arsenic trioxide and p97 inhibitor synergize against acute myeloid leukemia by targeting nascent polypeptides and activating the ZAKα-JNK pathway.

doi: 10.1038/s41417-024-00818-z

Figure Lengend Snippet: Fig. 3 ATO targets nascent polypeptides while activating the GCN2–ATF4 pathway. A The NB4 cells were pre-treated with 0.1 μg/mL puromycin for 1 h, and then 4 μM Biotin-As was added for another 16 h. Immunofluorescence visualized the localization of puromycin, Biotin- As, and aggresome in the cells. Scale bar, 25 μm. B The NB4 cells were treated with 1 μM Biotin-As for 4 h, and then 20 μM puromycin was added for another 30 min. Cell fractions were prepared for the Co-IP assays using the streptavidin magnetic beads and indicated antibodies. C Immunoblot of indicated proteins in the NB4 cells at 0, 4, 8, 12, and 24 h with 0.5 or 2 μM ATO treatment. D The NB4 cells were pre-treated with 0.5 μM PERKi (GSK2656157) or 10 μM GCN2iB for 1 h, and then 2 μM ATO was added for another 4 h. Immunoblot of indicated proteins in the NB4 cells.

Article Snippet: Cell lines and cell culture Human AML leukemia cell lines NB4, MV4-11, NOMO-1, MOLM-13, THP-1, U937, HL-60, and Kasumi-1 were purchased from DSMZ.

Techniques: Co-Immunoprecipitation Assay, Magnetic Beads, Western Blot

Journal: Cancer gene therapy

Article Title: Arsenic trioxide and p97 inhibitor synergize against acute myeloid leukemia by targeting nascent polypeptides and activating the ZAKα-JNK pathway.

doi: 10.1038/s41417-024-00818-z

Figure Lengend Snippet: Fig. 4 ATO causes ribosome stalling and p97 inhibitor increases the sensitivity of APL to ATO. A Polysome profiles from NB4 cells with or without 1.5 μM ATO treatment for 6 h. B Immunoblot of indicated proteins in the NB4 cells at 0, 4, 20 h with 0.5 or 2 μM ATO treatment. C NB4 cells were pre-treated with 5 μM JNK inhibitor (JNK-IN-8) for 1 h, and then 2.5 μM ATO was added for another 24 h. Apoptosis was detected by flow cytometry. D Immunoblot of ZAKα and p-ZAKα in the NB4 cells at 4 or 20 h with 0.5 or 2 μM ATO treatment. The phosphorylated proteins in the cell lysate were enriched by Phos-tagTM Agarose. E The apoptosis ratio of ZAKα-knockdown NB4 cells with or without ATO treatment for 24 h. F Immunoblot of ZAKα in the ZAKα-knockdown NB4 cells. G The NB4 cells were treated with 1 μM Biotin-As for 4 h, and then cell fractions were prepared for the Co-IP assays using the streptavidin magnetic beads and indicated antibodies. H The NB4 cells were treated with 1 μM Biotin-As for 4 h, and then 20 μM puromycin was added for another 30 min. Cell fractions were prepared for the Co-IP assays using the NEMF, p97, and puromycin antibodies. I The NB4 cells were pre-treated with or without 1 μM NMS873 for 1 h and then indicated doses of ATO were added for another 24 h. The apoptosis ratio was detected by flow cytometry. Two-tailed Student t test, *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001. Error bars reflect ± SEM of three independent experiments.

Article Snippet: Cell lines and cell culture Human AML leukemia cell lines NB4, MV4-11, NOMO-1, MOLM-13, THP-1, U937, HL-60, and Kasumi-1 were purchased from DSMZ.

Techniques: Western Blot, Cytometry, Knockdown, Co-Immunoprecipitation Assay, Magnetic Beads, Two Tailed Test

Journal: Cell Death Discovery

Article Title: USP22 regulates APL differentiation via PML-RARα stabilization and IFN repression

doi: 10.1038/s41420-024-01894-8

Figure Lengend Snippet: A Western blot analysis of basal PML-RARα and USP22 expression in wild-type (wt), control (non-human target; n.h.t) and USP22 knockout (KO) NB4 acute promyelocytic leukemia (APL) cells. β-Actin served as loading control. Representative blots of at least two different independent experiments are shown. B Densitometric quantification of gray level intensities of the major (130 kDa) PML-RARα isoform detected by Western blot analysis in wt, n.h.t and USP22 KO NB4 APL cells, normalized against loading control intensities. Mean and SEM of three independent experiments are shown. C Basal mRNA expression levels of the PML-RARα long isoform in wt, n.h.t. and USP22 KO NB4 APL cells using qRT-PCR. Gene expression was normalized against 28S mRNA and is presented as x-fold mRNA expression compared to n.h.t. Mean and SEM of three independent experiments are shown. D Western blot analysis of wt, n.h.t and USP22 KO NB4 APL cells treated with 20 μg/ml CHX for the indicated timepoints. GAPDH served as loading control. Representative blots of at least two different independent experiments are shown. Red dashed line indicates protein stability at 50% compared to untreated controls. E Densitometric quantification of gray level intensities of the major (130 kDa) PML-RARα isoform detected by Western blot analysis in wt, n.h.t and USP22 KO NB4 APL cells treated with 20 μg/ml CHX for the indicated timepoints, normalized against loading control intensities. Mean and SEM of three independent experiments are shown. F Western blot analysis of n.h.t and USP22 KO HEK293T cells, transiently transfected with plasmids encoding the long isoform of PML-RARα and treated with 20 μg/ml CHX for the indicated timepoints. Co-transfection with GFP plasmid served as transfection control. GAPDH served as loading control. Representative blots of at least two different independent experiments are shown. Red dashed line indicates protein stability at 50% compared to untreated controls. G Densitometric quantification of gray level intensities of the long isoform of PML-RARα transiently transfected in n.h.t and USP22 KO HEK293T cells treated with 20 μg/ml CHX for the indicated timepoints, normalized against loading control intensities. Mean and SEM of three independent experiments are shown. H Western blot analysis of HEK293T cells, transiently transfected with plasmids encoding the long isoform of wt (PML-RARα) and K394R (KR) PML-RARα (PML-K394R-RARα) and treated with 20 μg/ml CHX for the indicated timepoints. Co-transfection with GFP plasmid served as transfection control. GAPDH served as loading control. Representative blots of at least two different independent experiments are shown. Red dashed line indicates protein stability at 50% compared to untreated controls. I Densitometric quantification of gray level intensities of the long isoform of wt (PML-RARα) and K394R (KR) PML-RARα (PML-K394R-RARα) transiently transfected in HEK293T cells treated with 20 μg/ml CHX for the indicated timepoints, normalized against loading control intensities. Mean and SEM of three independent experiments are shown.

Article Snippet: Human colon carcinoma HT-29, human embryonic kidney HEK293T and human APL NB4 cell lines were obtained from and authenticated by DSMZ (Braunschweig, Germany).

Techniques: Western Blot, Expressing, Control, Knock-Out, Quantitative RT-PCR, Gene Expression, Transfection, Cotransfection, Plasmid Preparation

Journal: Cell Death Discovery

Article Title: USP22 regulates APL differentiation via PML-RARα stabilization and IFN repression

doi: 10.1038/s41420-024-01894-8

Figure Lengend Snippet: A Western blot analysis of RARα and USP22 in wild-type (wt), control (non-human target; n.h.t) and USP22 knockout (KO) NB4 APL cells treated with the indicated concentrations of all- trans retinoic acid (ATRA) for 120 h. β-actin served as loading control. Representative blots of at least two different independent experiments are shown. B Basal and ATRA-induced mRNA expression levels of PML-RARα in wt, n.h.t and USP22 KO NB4 APL cells incubated with the indicated ATRA concentrations for 120 h using qRT-PCR. UT, untreated. Gene expression was normalized against 28S mRNA and is presented as x-fold mRNA expression compared to UT of wt NB4 cells Mean and SEM of three independent biological replicates are shown. C FACS analysis of wt, n.h.t., and USP22 KO NB4 APL cells incubated with the indicated ATRA concentrations for 120 h. Shown is the cell count per fluorescence intensity of PE-labeled CD11b. D Mean fluorescence intensities (MFIs) of CD11b-PE signals on wt, n.h.t., and USP22 KO NB4 APL cells incubated with the indicated ATRA concentrations for 120 h. UT, untreated. Mean and SEM of four independent biological replicates are shown. E Basal and ATRA-induced mRNA expression levels of CD11b in wt, n.h.t and USP22 KO NB4 APL cells incubated with the indicated ATRA concentrations for for 120 h using qRT-PCR. UT, untreated. Gene expression was normalized against 28S mRNA and is presented as x-fold mRNA expression compared to UT of wt NB4 cells Mean and SEM of three independent biological replicates are shown.

Article Snippet: Human colon carcinoma HT-29, human embryonic kidney HEK293T and human APL NB4 cell lines were obtained from and authenticated by DSMZ (Braunschweig, Germany).

Techniques: Western Blot, Control, Knock-Out, Expressing, Incubation, Quantitative RT-PCR, Gene Expression, Cell Counting, Fluorescence, Labeling

Journal: Cell Death Discovery

Article Title: USP22 regulates APL differentiation via PML-RARα stabilization and IFN repression

doi: 10.1038/s41420-024-01894-8

Figure Lengend Snippet: A Basal and ATRA-induced mRNA expression levels of IRF1 in wild-type (wt), control (non-human target; n.h.t) and USP22 knockout (KO) NB4 APL cells incubated with the indicated ATRA concentrations for 120 h using qRT-PCR. UT, untreated. Gene expression was normalized against 28S mRNA and is presented as x-fold mRNA expression compared to UT of wt NB4 cells. Mean and SEM of three independent biological replicates are shown. B Basal mRNA expression levels of USP22 and the indicated ISGs in n.h.t and USP22 KO NB4 APL cells using qRT-PCR. Gene expression was normalized against 28S mRNA and is presented as x-fold mRNA expression compared to n.h.t. Mean and SEM of three independent biological replicates are shown. C Model of USP22-mediated effects on PML-RARα and IFN signaling in APL.

Article Snippet: Human colon carcinoma HT-29, human embryonic kidney HEK293T and human APL NB4 cell lines were obtained from and authenticated by DSMZ (Braunschweig, Germany).

Techniques: Expressing, Control, Knock-Out, Incubation, Quantitative RT-PCR, Gene Expression

Journal: Biochemical pharmacology

Article Title: The clinically relevant CHK1 inhibitor MK-8776 induces the degradation of the oncogenic protein PML-RARα and overcomes ATRA resistance in acute promyelocytic leukemia cells.

doi: 10.1016/j.bcp.2023.115675

Figure Lengend Snippet: Fig. 1. Effects of CHK1 inhibition by MK-8776 in APL cells. Sensitivity of NB4, R4, R2, and THP1 cells to the MK-8776 inhibitor. Each cell line was treated with 0–32 µM MK-8776 for 24, 48, 72, and 96 h. Cells were counterstained with propidium iodide (PI) and acquired for volumetric absolute counting. Approximately 10.000 useful events were acquired for each experimental point, and the absolute number of live cells (A) and death cells (B) were analyzed. (A) Graphs represent the percentage of cells surviving fractions normalized to untreated cells for each concentration of MK-8776. For each cell line and for each time point the IC50 values were calculated. (B) Graphs represent the percentage of PI-positive cells, which corresponds to death cells. (C) CD11b expression in NB4, R4, and R2 cells treated with MK- 8776. NB4 cells were treated with 1.6 µM MK-8776 for 72 h, R4 cells were treated with 4 µM MK-8776 for 96 h, and R2 cells were treated with 4 µM MK-8776 for 48 h. Cells were hybridized with the anti-CD11b antibody labeled with phycoerythrin (PE). In orange, the population of cells expressing the CD11b surface antigen. All the cell lines were also tested also for their responsiveness to 1 μM ATRA for 96 h. (D) NBT assay performed in R4 cells treated with 4 μM MK-8776 for 96 or with the only vehicle as control. Absorbance was measured at 570 nm. Mean values were derived from repeated experiments ± SD (Student’s t-test, **p ≤0.01). (E) Morphological changes induced in R4 cells treated with 4 μM MK-8776 for 96 h, as revealed by the May-Grünwald/Giemsa staining (scale bar: 10 μm). (F) R4 and R2 cells were treated with 4 μM MK-8776 for 48, 72, and 96 h. Protein lysates were analyzed by immunoblot using the anti-RARα antibody, which allows the detection of PML-RARα protein. As positive control to evaluate PML-RARα degradation, NB4 cells were treated with 1 μM ATRA for 96 h. (G) Synergy map of R4 cells treated for 96 h with MK-8776 (0, 0.5, 1, 2, and 4 μM) and ATO (0, 0.01, 0.1, and 1 μM). The effect of the treatments was measured by the NBT assay and the synergy index was calculated with the Combenefit freeware software [31]. (H) The graph reports the synergic effect of the most effective combination of R4 cells treatment with 4 μM MK-8776 and 0.01 μM ATO. Mean values were derived from repeated experiments ± SD (Student’s t-test, *p ≤0.05, ***p ≤0.001, and ****p ≤0.0001).

Article Snippet: The human APL-derived NB4 cell line bears the t(15;17) translocation and expresses the fusion protein PML-RARα [46] (DSMZ, Braunschweig, Germany).

Techniques: Inhibition, Concentration Assay, Expressing, Labeling, Control, Derivative Assay, Staining, Western Blot, Positive Control, Software

Journal: Cell Reports

Article Title: Chromatin accessibility governs the differential response of cancer and T cells to arginine starvation

doi: 10.1016/j.celrep.2021.109101

Figure Lengend Snippet:

Article Snippet: Human tumor cell lines NB4 (female; Cancer Research UK; RRID CVCL_0005), MOLM13 (male; DSMZ, ACC-554; RRID CVCL_2119), RT112 (female; CRUK; RRID CVCL_1670), LNCaP (male; CRUK; RRID CVCL_0395), OCI-AML3 (male; DSMZ, ACC-582; RRID CVCL_1844), THP1 (male; ATCC, TIB-202; RRID CVCL_0006), HL60 (female; ATCC, CCL-240; RRID CVCL_0002) and RS4;11 (female; ATCC, CRL-1873; RRID CVCL_0093) cells were cultured in RPMI-1640 supplemented with 10% fetal calf serum and GlutaMAX (ThermoFisher Scientific).

Techniques: Recombinant, Multiplex sample analysis, Cell Isolation, Activation Assay, Staining, Flow Cytometry, Expressing, Reverse Transcription, Transfection, TA Cloning, Plasmid Preparation, Methylation, Immunoprecipitation, Purification, DNA Library Preparation, Library Quantification, Control, Sequencing, Methylation Sequencing, Amplification, Software