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ATCC hl60 cell line
Hl60 Cell Line, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 6401 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Average 99 stars, based on 6401 article reviews

hl60 cell line - by Bioz Stars, 2026-05

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In vitro validation of the Pep@MNP platform for specific capture and identification of thyroid cancer cells. A and B, Immunofluorescence staining of the capture marker EpCAM ( A ) and the identification marker CKmix ( B ) in thyroid cancer cell lines (BHT101 and BCPAP) and a negative control cell line (HL60). Nuclei were counterstained with DAPI. Scale bars, 10 μm. C, Quantitative analysis of the MFI of CKmix in BHT101, BCPAP, and HL60 cells, demonstrating significantly higher expression in thyroid cancer cells. D and E, FCM analysis confirming the surface expression of EpCAM ( D ) and high intracellular expression of CKmix ( E ) in BHT101 and BCPAP cells but not in HL60 cells. F, Scanning electron microscopy images showing the specific binding of Pep@MNPs to target BCPAP cells, whereas bare MNPs show minimal interaction. Both nanoparticle types show negligible binding to the negative control HL60 cells. Scale bars, 5 μm (top row) and 3 μm (bottom row). G, Representative immunofluorescence images defining the criteria for identifying a captured BCPAP cell (CTCs-like phenotype: DAPI+/CKmix+/CD45 − ) and distinguishing it from a co-captured white blood cell (WBC; DAPI+/CKmix − /CD45 + ). H, Capture sensitivity analysis. The graph shows the capture efficiency of the platform for varying numbers of BCPAP cells spiked into a solution. I, Capture specificity analysis. The graph compares the capture efficiency of the platform for cells with high EpCAM expression (BCPAP), low EpCAM expression (BHT101), and negative EpCAM expression (HL60). ****, P value < 0.0001.

Journal: Clinical Cancer Research

Article Title: Clinical Significance for Risk Stratification of Papillary Thyroid Cancer by TUMORFISHER Circulating Tumor Cell Technique

doi: 10.1158/1078-0432.CCR-25-2694

Figure Lengend Snippet: In vitro validation of the Pep@MNP platform for specific capture and identification of thyroid cancer cells. A and B, Immunofluorescence staining of the capture marker EpCAM ( A ) and the identification marker CKmix ( B ) in thyroid cancer cell lines (BHT101 and BCPAP) and a negative control cell line (HL60). Nuclei were counterstained with DAPI. Scale bars, 10 μm. C, Quantitative analysis of the MFI of CKmix in BHT101, BCPAP, and HL60 cells, demonstrating significantly higher expression in thyroid cancer cells. D and E, FCM analysis confirming the surface expression of EpCAM ( D ) and high intracellular expression of CKmix ( E ) in BHT101 and BCPAP cells but not in HL60 cells. F, Scanning electron microscopy images showing the specific binding of Pep@MNPs to target BCPAP cells, whereas bare MNPs show minimal interaction. Both nanoparticle types show negligible binding to the negative control HL60 cells. Scale bars, 5 μm (top row) and 3 μm (bottom row). G, Representative immunofluorescence images defining the criteria for identifying a captured BCPAP cell (CTCs-like phenotype: DAPI+/CKmix+/CD45 − ) and distinguishing it from a co-captured white blood cell (WBC; DAPI+/CKmix − /CD45 + ). H, Capture sensitivity analysis. The graph shows the capture efficiency of the platform for varying numbers of BCPAP cells spiked into a solution. I, Capture specificity analysis. The graph compares the capture efficiency of the platform for cells with high EpCAM expression (BCPAP), low EpCAM expression (BHT101), and negative EpCAM expression (HL60). ****, P value < 0.0001.

Article Snippet: The human thyroid cancer cell lines BCPAP (RRID: CVCL_0153) and BHT101 (RRID: CVCL_1085), and the human promyelocytic leukemia cell line HL60 (RRID: CVCL_0002), were obtained from Procell Life Science & Technology in August 2021.

Techniques: In Vitro, Biomarker Discovery, Immunofluorescence, Staining, Marker, Negative Control, Expressing, Electron Microscopy, Binding Assay

The aryl hydrocarbon receptor (AhR) activation directly suppresses the NETosis. (a-f) The neutrophils were treated with FICZ (100 nM), DIM (10 μM) or CH223191 (10 μM) in the present or absence of LPS (10 μg/mL) or PMA (50 nM). The release of dsDNA was stained, and measured using fluorescence microscope (scale bar: 50 μm) (a) and microplate reader (b, c) . The formation of NETs were detected by staining for NE/CitH3 (red), MPO (green) and DNA (blue) (scale bar: 20 μm) (d) . The levels of histone H4 (e) as well as the nucleus morphology (f) was detected (scale bar = 5 μm). (g) The HL60 cells were pre-transfected with shAhR, incubated with 1.25 % dimethyl sulfoxide, and treated with FICZ (100 nM) or DIM (10 μM) at the present or absence of LPS (10 μg/mL) or PMA (50 nM). The release of dsDNA was stained (scale bar: 50 μm). The data were presented as the means ± S.E.M. of three or five independent experiments. ## p < 0.01 vs. Control group; ** p < 0.01 vs. LPS or PMA group. (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)

Journal: Journal of Advanced Research

Article Title: Aryl hydrocarbon receptor impairs HK2-controlled flux of the hexosamine biosynthesis pathway to suppress NETosis in an N -glycosylation-dependent manner

doi: 10.1016/j.jare.2025.06.078

Figure Lengend Snippet: The aryl hydrocarbon receptor (AhR) activation directly suppresses the NETosis. (a-f) The neutrophils were treated with FICZ (100 nM), DIM (10 μM) or CH223191 (10 μM) in the present or absence of LPS (10 μg/mL) or PMA (50 nM). The release of dsDNA was stained, and measured using fluorescence microscope (scale bar: 50 μm) (a) and microplate reader (b, c) . The formation of NETs were detected by staining for NE/CitH3 (red), MPO (green) and DNA (blue) (scale bar: 20 μm) (d) . The levels of histone H4 (e) as well as the nucleus morphology (f) was detected (scale bar = 5 μm). (g) The HL60 cells were pre-transfected with shAhR, incubated with 1.25 % dimethyl sulfoxide, and treated with FICZ (100 nM) or DIM (10 μM) at the present or absence of LPS (10 μg/mL) or PMA (50 nM). The release of dsDNA was stained (scale bar: 50 μm). The data were presented as the means ± S.E.M. of three or five independent experiments. ## p < 0.01 vs. Control group; ** p < 0.01 vs. LPS or PMA group. (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)

Article Snippet: The human promyelocytic leukaemia cell line HL60 was obtained from Procell Life Science & Technology Co., Ltd. (Wuhan, China) and cultured in Iscove’s Modified Dulbecco’s Medium supplemented with 20 % fetal bovine serum at 37 °C.

Techniques: Activation Assay, Staining, Fluorescence, Microscopy, Transfection, Incubation, Control

The aryl hydrocarbon receptor (AhR) activation inhibits NETosis with the help of neutrophil elastase (NE). (a) The HL60 cells were pre-transfected with pcDNA-NE or pcDNA-PAD4 , differentiated for 5 days by incubation of 1.25 % dimethyl sulfoxide (DMSO), and treated with FICZ (100 nM) or DIM (10 μM) at the present or absence of lipopolysaccharide (LPS, 10 μg/mL) or phorbol-12-myristate-13-acetate (PMA, 50 nM). The release of dsDNA was stained (scale bar: 50 μm). (b-d) The HL60 cells were differentiated for 0, 1, 3 and 5 days, and incubated with 1.25 % DMSO in the presence of FICZ (100 nM), DIM (10 μM) or CH223191 (10 μM). The mRNA level of NE (b) and protein level of CTSC (c, d) was detected. ( e-h) The neutrophils were treated with FICZ (100 nM), DIM (10 μM) or CH223191 (10 μM) at the present or absence of LPS (10 μg/mL) or PMA (50 nM), and the protein level (e) and activity (f) of NE was detected. The NE (red) and DNA (blue) was stained for detecting the nuclear localisation of NE (scale bar = 20 μm) (g) . The NE (green) and F-actin (red) was stained for detecting the cutting capacity of NE (scale bar: 5 μm) (h) . (i) The HL60 cells were pre-transfected with shAhR, incubated with 1.25 % DMSO, and treated with FICZ (100 nM) and DIM (10 μM) at the present or absence of LPS (10 μg/mL) or PMA (50 nM). The NE activity was determined. The data were presented as the means ± S.E.M. of three or five independent experiments. ## p < 0.01 vs. Control group; ** p < 0.01 vs. LPS or PMA group; $$ p < 0.01 vs. LPS/PMA + FICZ group; ++ p < 0.01 vs. LPS/PMA + DIM group. (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)

Journal: Journal of Advanced Research

Article Title: Aryl hydrocarbon receptor impairs HK2-controlled flux of the hexosamine biosynthesis pathway to suppress NETosis in an N -glycosylation-dependent manner

doi: 10.1016/j.jare.2025.06.078

Figure Lengend Snippet: The aryl hydrocarbon receptor (AhR) activation inhibits NETosis with the help of neutrophil elastase (NE). (a) The HL60 cells were pre-transfected with pcDNA-NE or pcDNA-PAD4 , differentiated for 5 days by incubation of 1.25 % dimethyl sulfoxide (DMSO), and treated with FICZ (100 nM) or DIM (10 μM) at the present or absence of lipopolysaccharide (LPS, 10 μg/mL) or phorbol-12-myristate-13-acetate (PMA, 50 nM). The release of dsDNA was stained (scale bar: 50 μm). (b-d) The HL60 cells were differentiated for 0, 1, 3 and 5 days, and incubated with 1.25 % DMSO in the presence of FICZ (100 nM), DIM (10 μM) or CH223191 (10 μM). The mRNA level of NE (b) and protein level of CTSC (c, d) was detected. ( e-h) The neutrophils were treated with FICZ (100 nM), DIM (10 μM) or CH223191 (10 μM) at the present or absence of LPS (10 μg/mL) or PMA (50 nM), and the protein level (e) and activity (f) of NE was detected. The NE (red) and DNA (blue) was stained for detecting the nuclear localisation of NE (scale bar = 20 μm) (g) . The NE (green) and F-actin (red) was stained for detecting the cutting capacity of NE (scale bar: 5 μm) (h) . (i) The HL60 cells were pre-transfected with shAhR, incubated with 1.25 % DMSO, and treated with FICZ (100 nM) and DIM (10 μM) at the present or absence of LPS (10 μg/mL) or PMA (50 nM). The NE activity was determined. The data were presented as the means ± S.E.M. of three or five independent experiments. ## p < 0.01 vs. Control group; ** p < 0.01 vs. LPS or PMA group; $$ p < 0.01 vs. LPS/PMA + FICZ group; ++ p < 0.01 vs. LPS/PMA + DIM group. (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)

Techniques: Activation Assay, Transfection, Incubation, Staining, Activity Assay, Control

The aryl hydrocarbon receptor (AhR) activation prevents the N- glycosylation of alpha-1 antitrypsin (AAT) and alpha-2-macroglobulin (A2M) to down-regulate the neutrophil elastase (NE) activity. (a) The recombinant protein of NE was incubated with FICZ (100 nM), DIM (10 μM) or CH223191 (10 μM), and NE activity was determined. (b, c) The neutrophils were treated with FICZ (100 nM), DIM (10 μM) or CH223191 (10 μM) at the present or absence of lipopolysaccharide (LPS, 10 μg/mL) or phorbol-12-myristate-13-acetate (PMA, 50 nM). The cytoplasmic proteins in each group were isolated and co-incubated with the recombinant protein of NE, and NE activity was determined (b) . The association of AAT, A2M or secretory leukocyte protease inhibitor (SLPI) with NE was detected (c) . (d) The HL60 cells were pre-transfected with shAAT or shA2M, incubated with 1.25 % dimethyl sulfoxide, treated with FICZ (100 nM) and DIM (10 μM) at the present or absence of LPS (10 μg/mL) or PMA (50 nM), and NE activity was determined. (e-h) The neutrophils were treated with FICZ (100 nM), DIM (10 μM) or CH223191 (10 μM) at the present or absence of LPS (10 μg/mL) or PMA (50 nM). The levels of AAT, A2M, SLPI (e) , ROS (f) , N- glycosylation (g) and neutral lipid content (h) were detected. ( i, j) The neutrophils were treated with FICZ (100 nM), DIM (10 μM) or CH223191 (10 μM), and tunicamycin (TM; 1 μM) or MK-8719 (21 nM) were jointly given at the present or absence of LPS (10 μg/mL) or PMA (50 nM). The association of AAT or A2M with NE (i) and release of dsDNA (scale bar: 50 μm) (j) were detected. The data were presented as the means ± S.E.M. of three or five independent experiments. # p < 0.05, ## p < 0.01 vs. Control group; * p < 0.05, ** p < 0.01 vs. LPS group; $$ p < 0.01 vs. LPS + FICZ group; ++ p < 0.01 vs. LPS + DIM or CH223191 group.

Journal: Journal of Advanced Research

Article Title: Aryl hydrocarbon receptor impairs HK2-controlled flux of the hexosamine biosynthesis pathway to suppress NETosis in an N -glycosylation-dependent manner

doi: 10.1016/j.jare.2025.06.078

Figure Lengend Snippet: The aryl hydrocarbon receptor (AhR) activation prevents the N- glycosylation of alpha-1 antitrypsin (AAT) and alpha-2-macroglobulin (A2M) to down-regulate the neutrophil elastase (NE) activity. (a) The recombinant protein of NE was incubated with FICZ (100 nM), DIM (10 μM) or CH223191 (10 μM), and NE activity was determined. (b, c) The neutrophils were treated with FICZ (100 nM), DIM (10 μM) or CH223191 (10 μM) at the present or absence of lipopolysaccharide (LPS, 10 μg/mL) or phorbol-12-myristate-13-acetate (PMA, 50 nM). The cytoplasmic proteins in each group were isolated and co-incubated with the recombinant protein of NE, and NE activity was determined (b) . The association of AAT, A2M or secretory leukocyte protease inhibitor (SLPI) with NE was detected (c) . (d) The HL60 cells were pre-transfected with shAAT or shA2M, incubated with 1.25 % dimethyl sulfoxide, treated with FICZ (100 nM) and DIM (10 μM) at the present or absence of LPS (10 μg/mL) or PMA (50 nM), and NE activity was determined. (e-h) The neutrophils were treated with FICZ (100 nM), DIM (10 μM) or CH223191 (10 μM) at the present or absence of LPS (10 μg/mL) or PMA (50 nM). The levels of AAT, A2M, SLPI (e) , ROS (f) , N- glycosylation (g) and neutral lipid content (h) were detected. ( i, j) The neutrophils were treated with FICZ (100 nM), DIM (10 μM) or CH223191 (10 μM), and tunicamycin (TM; 1 μM) or MK-8719 (21 nM) were jointly given at the present or absence of LPS (10 μg/mL) or PMA (50 nM). The association of AAT or A2M with NE (i) and release of dsDNA (scale bar: 50 μm) (j) were detected. The data were presented as the means ± S.E.M. of three or five independent experiments. # p < 0.05, ## p < 0.01 vs. Control group; * p < 0.05, ** p < 0.01 vs. LPS group; $$ p < 0.01 vs. LPS + FICZ group; ++ p < 0.01 vs. LPS + DIM or CH223191 group.

Techniques: Activation Assay, Glycoproteomics, Activity Assay, Recombinant, Incubation, Isolation, Protease Inhibitor, Transfection, Control

The aryl hydrocarbon receptor (AhR) acts as an E3 ligase to promote the ubiquitination of hexokinase-2 (HK2) and restrain glucose metabolism. (a-c) The neutrophils were treated with FICZ (100 nM), DIM (10 μM) or CH223191 (10 μM) at the present or absence of lipopolysaccharide (LPS, 10 μg/mL) or phorbol-12-myristate-13-acetate (PMA, 50 nM). The relative activity (a) as well as protein levels ( b, c ) of hexokinase 2 (HK2) and phosphofructokinase (PFK) were detected. (d-f) The HL60 cells were pre-transfected with pcDNA -HK2, incubated with 1.25 % dimethyl sulfoxide (DMSO), and treated with FICZ (100 nM) and DIM (10 μM) at the present or absence of LPS (10 μg/mL) or PMA (50 nM). The activity of NE (d) and levels of UDP-GlcNAc (e) , HK2, PFK (f) were detected. (g) The neutrophils were treated with FICZ (100 nM) or DIM (10 μM) before receiving LPS (10 μg/mL) and CHX (15 μg/mL) for 0, 0.5, 1, 1.5 h, and the protein level of HK2 was detected. (h, i) The neutrophils were treated with FICZ (100 nM), DIM (10 μM) or CH223191 (10 μM), and MG132 (25 μg/mL) or hydroxychloroquine (HCQ; 10 μM) were jointly given at the present or absence of LPS (10 μg/mL) or PMA (50 nM). The protein level (h) and ubiquitination (i) of HK2 was detected. (j, k) The neutrophils were treated with FICZ (100 nM), DIM (10 μM) or CH223191 (10 μM) at the present or absence of LPS (10 μg/mL). The co-localization of HK2 and PSMD2 was stained (scale bar: 5 μm) (j) . The mRNA levels of CYP1A1 and CYP1B1 was detected (k) . (l) The HL60 cells were pre-transfected with shARNT, incubated with 1.25 % DMSO, treated with FICZ (100 nM) or DIM (10 μM) at the present or absence of LPS (10 μg/mL), and release of dsDNA was stained (scale bar = 50 μm). (m, n) The association of AhR and HK2 was simulated using molecular docking and the association of AhR and HK2 was detected. (o) The neutrophils were treated with FICZ (100 nM), DIM (10 μM) or CH223191 (10 μM) at the present or absence of LPS (10 μg/mL), and the association of ubiquitination at Lys 48 and Lys 63 of HK2 protein was detected. The data were presented as the means ± S.E.M. of three or five independent experiments. # p < 0.05, ## p < 0.01 vs. Control group; * p < 0.05, ** p < 0.01 vs. LPS group; $ p < 0.05, $$ p < 0.01 vs. LPS + FICZ group; + p < 0.01, ++ p < 0.01 vs. LPS + DIM group.

Journal: Journal of Advanced Research

Article Title: Aryl hydrocarbon receptor impairs HK2-controlled flux of the hexosamine biosynthesis pathway to suppress NETosis in an N -glycosylation-dependent manner

doi: 10.1016/j.jare.2025.06.078

Figure Lengend Snippet: The aryl hydrocarbon receptor (AhR) acts as an E3 ligase to promote the ubiquitination of hexokinase-2 (HK2) and restrain glucose metabolism. (a-c) The neutrophils were treated with FICZ (100 nM), DIM (10 μM) or CH223191 (10 μM) at the present or absence of lipopolysaccharide (LPS, 10 μg/mL) or phorbol-12-myristate-13-acetate (PMA, 50 nM). The relative activity (a) as well as protein levels ( b, c ) of hexokinase 2 (HK2) and phosphofructokinase (PFK) were detected. (d-f) The HL60 cells were pre-transfected with pcDNA -HK2, incubated with 1.25 % dimethyl sulfoxide (DMSO), and treated with FICZ (100 nM) and DIM (10 μM) at the present or absence of LPS (10 μg/mL) or PMA (50 nM). The activity of NE (d) and levels of UDP-GlcNAc (e) , HK2, PFK (f) were detected. (g) The neutrophils were treated with FICZ (100 nM) or DIM (10 μM) before receiving LPS (10 μg/mL) and CHX (15 μg/mL) for 0, 0.5, 1, 1.5 h, and the protein level of HK2 was detected. (h, i) The neutrophils were treated with FICZ (100 nM), DIM (10 μM) or CH223191 (10 μM), and MG132 (25 μg/mL) or hydroxychloroquine (HCQ; 10 μM) were jointly given at the present or absence of LPS (10 μg/mL) or PMA (50 nM). The protein level (h) and ubiquitination (i) of HK2 was detected. (j, k) The neutrophils were treated with FICZ (100 nM), DIM (10 μM) or CH223191 (10 μM) at the present or absence of LPS (10 μg/mL). The co-localization of HK2 and PSMD2 was stained (scale bar: 5 μm) (j) . The mRNA levels of CYP1A1 and CYP1B1 was detected (k) . (l) The HL60 cells were pre-transfected with shARNT, incubated with 1.25 % DMSO, treated with FICZ (100 nM) or DIM (10 μM) at the present or absence of LPS (10 μg/mL), and release of dsDNA was stained (scale bar = 50 μm). (m, n) The association of AhR and HK2 was simulated using molecular docking and the association of AhR and HK2 was detected. (o) The neutrophils were treated with FICZ (100 nM), DIM (10 μM) or CH223191 (10 μM) at the present or absence of LPS (10 μg/mL), and the association of ubiquitination at Lys 48 and Lys 63 of HK2 protein was detected. The data were presented as the means ± S.E.M. of three or five independent experiments. # p < 0.05, ## p < 0.01 vs. Control group; * p < 0.05, ** p < 0.01 vs. LPS group; $ p < 0.05, $$ p < 0.01 vs. LPS + FICZ group; + p < 0.01, ++ p < 0.01 vs. LPS + DIM group.

Techniques: Ubiquitin Proteomics, Activity Assay, Transfection, Incubation, Staining, Control

Pacritinib blocks HIV latency reversal in an IRF7-dependent manner. (A) Left panel, WB of a representative experiment of HL60 cells treated with PMA or with a dose response of pacritinib (Pac) immunoblotted with anti-pJAK2, anti-pSTAT1, anti-IRF7 and anti-GAPDH antibodies. Middle panel, bar plots represent the mean quantification of IRF7 bands obtained by densitometry analysis of three independent experiments. Values were normalized to that of GAPDH used as a loading control and relativized to the untreated condition (ND). Right panel, relative mRNA expression of IRF7 gene expression measured by quantitative RT-PCR and normalized to GAPDH. (B, C) WB of a representative experiment in J-HIG (B) and HL-HIG (C) cells treated with PMA, pacritinib or fedratinib (Fed), alone or in combination, and immunoblotted with anti-IRF7 and anti-GAPDH antibodies. Bar plots represent the mean quantification of bands obtained by densitometry analysis of 3 independent experiments. (D, E) Correlation plots of IRF7 and gene expression versus HIV-1 latency reversal capacity of PMA or JAK2i-treated J-HIG and HL-HIG cells. (F) Transactivation assay as measured by luciferase expression in TZM-bl cells transfected to overexpress IRF7 protein and 24 hours after drug treatment. Luciferase values were normalized within each transfection condition (mock or IRF7 overexpression, left panel), and overexpression of IRF7 confirmed by WB ( right panel). PMA: phorbol 12-myristate 13-acetate (0,1µg/mL); Pac: pacritinib (1µM); Fed: fedratinib (5µM); Vor: vorinostat (5µM). Data expressed as means ± SD values from at least three independent experiments normalized to the no drug (ND) condition *p<0.05; **p<0.005; ***p<0.0001.

Journal: Frontiers in Immunology

Article Title: Modulation of IRF7-driven transcription as a strategy to control HIV-1 latency

doi: 10.3389/fimmu.2026.1735192

Figure Lengend Snippet: Pacritinib blocks HIV latency reversal in an IRF7-dependent manner. (A) Left panel, WB of a representative experiment of HL60 cells treated with PMA or with a dose response of pacritinib (Pac) immunoblotted with anti-pJAK2, anti-pSTAT1, anti-IRF7 and anti-GAPDH antibodies. Middle panel, bar plots represent the mean quantification of IRF7 bands obtained by densitometry analysis of three independent experiments. Values were normalized to that of GAPDH used as a loading control and relativized to the untreated condition (ND). Right panel, relative mRNA expression of IRF7 gene expression measured by quantitative RT-PCR and normalized to GAPDH. (B, C) WB of a representative experiment in J-HIG (B) and HL-HIG (C) cells treated with PMA, pacritinib or fedratinib (Fed), alone or in combination, and immunoblotted with anti-IRF7 and anti-GAPDH antibodies. Bar plots represent the mean quantification of bands obtained by densitometry analysis of 3 independent experiments. (D, E) Correlation plots of IRF7 and gene expression versus HIV-1 latency reversal capacity of PMA or JAK2i-treated J-HIG and HL-HIG cells. (F) Transactivation assay as measured by luciferase expression in TZM-bl cells transfected to overexpress IRF7 protein and 24 hours after drug treatment. Luciferase values were normalized within each transfection condition (mock or IRF7 overexpression, left panel), and overexpression of IRF7 confirmed by WB ( right panel). PMA: phorbol 12-myristate 13-acetate (0,1µg/mL); Pac: pacritinib (1µM); Fed: fedratinib (5µM); Vor: vorinostat (5µM). Data expressed as means ± SD values from at least three independent experiments normalized to the no drug (ND) condition *p<0.05; **p<0.005; ***p<0.0001.

Article Snippet: The human cell lines HL60, Jurkat, MOLT-4 and U937 were obtained from ATCC (Gaithersburg, MD).

Techniques: Control, Expressing, Gene Expression, Quantitative RT-PCR, Transactivation Assay, Luciferase, Transfection, Over Expression

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