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human tumor cell lines hl 60  (ATCC)


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    ATCC human tumor cell lines hl 60
    Human Tumor Cell Lines Hl 60, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 6483 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/cell+lines+human+hl+60+hl+60/pm42034196-89-0-13?v=ATCC
    Average 99 stars, based on 6483 article reviews
    human tumor cell lines hl 60 - by Bioz Stars, 2026-08
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    ATCC human cell lines hl60
    Pacritinib blocks HIV latency reversal in an IRF7-dependent manner. (A) Left panel, WB of a representative experiment of <t>HL60</t> 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.
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    ATCC human acute myeloid leukemia aml cell line hl60
    Pacritinib blocks HIV latency reversal in an IRF7-dependent manner. (A) Left panel, WB of a representative experiment of <t>HL60</t> 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.
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    ATCC human aml cell line hl
    Pacritinib blocks HIV latency reversal in an IRF7-dependent manner. (A) Left panel, WB of a representative experiment of <t>HL60</t> 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.
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    Pacritinib blocks HIV latency reversal in an IRF7-dependent manner. (A) Left panel, WB of a representative experiment of <t>HL60</t> 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.
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    Pacritinib blocks HIV latency reversal in an IRF7-dependent manner. (A) Left panel, WB of a representative experiment of <t>HL60</t> 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.
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    Image Search Results


    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