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human set 2 cell line  (DSMZ)


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    DSMZ human set 2 cell line
    Human Set 2 Cell Line, supplied by DSMZ, used in various techniques. Bioz Stars score: 94/100, based on 129 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/human+set+2+cell+line/SET-2/pm38646919-36-1-18
    Average 94 stars, based on 129 article reviews
    human set 2 cell line - by Bioz Stars, 2026-09
    94/100 stars

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    Article Title: miR-146a -/- mice model reveals that NF-κB inhibition reverts inflammation-driven myelofibrosis-like phenotype.
    Article Snippet: Funding information Ministerio de Ciencia, Innovación y Universidades, Grant/Award Number: FPU18/03189; Next Generation EU, Grant/Award Number: PMP21/00052; Fundación Séneca, Grant/Award Number: 20644/JLI/18; Instituto de Salud Carlos III, Grant/Award Numbers: PI18/00316, PI20/00136, PI21/00347; UCAM, Grant/Award Numbers: GE/FE/14-21, GE/FE/15-23, GE/FE/14-24 Abstract Emerging evidence shows the crucial role of inflammation (particularly NF-κB pathway) in the development and progression of myelofibrosis (MF), becoming a promising therapeutic target.. Furthermore, tailoring treatment with currently available JAK inhibitors (such as ruxolitinib or fedratinib) does not modify the natural history of the disease and has important limitations, including cytopenias.. Since recent studies have highlighted the role of miR-146a, a negative regulator of the NF-κB pathway, in the pathogenesis of MF; here we used miR-146a / (KO) mice, a MF-like model lacking driver mutations, to investigate whether pharmacological inhibition of JAK/STAT and/or NF-κB pathways may reverse the myelofibrotic phenotype of these mice.



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    Fig. 1 Ruxolitinib increases autophagy <t>in</t> <t>JAK2V617F</t> cells. A, B <t>HEL</t> and SET-2 cells were treated with ruxolitinib (1 µM) for 2 hours in the presence or absence of bafilomycin (25 nM) to monitor the autophagy flux. A Cells were processed for western blot analysis of P-STAT5, STAT5 and LC3B. Actin was used as a loading control. Graphs represent the LC3B-II/actin ratio obtained by densitometric analysis (n = 4 ± sem). B Cells were stained for LC3B and analyzed by confocal microscopy. Graphs represent the number of LC3B dots per cell (n = 4 ± sem). Scale bar: 10 µm. C Mononuclear cells from peripheral blood samples from JAK2V617F-positive MPN patients were separated by Ficoll-Hypaque density gradient centrifugation. CD34+ progenitors were then sorted using an immunomagnetic positive selection kit and processed for further experiments. D Patients’ cells obtained in C were treated or not with chloroquine (20 µM) over 16 hours to monitor autophagy flux in combination with ruxolitinib (1 µM) for 2 h and stained for LC3B. Representative confocal pictures are shown and histograms represent the number of LC3B dots per cell (n = 8 ± sem). Scale bar: 10 µm. E, F JAK2WT HL-60 cells were treated with ruxolitinib (1 µM) for 2 hours in the presence or absence of bafilomycin (25 nM) to monitor autophagy flux. E Cells were processed for western blot analysis of P-STAT5, STAT5 and LC3B. Actin was used as a loading control. Graphs represent the LC3B-II/actin ratio obtained by densitometric analysis (n = 3 ± sem). F Cells were stained for LC3B and analyzed by confocal microscopy. Graphs represent the number of LC3B dots per cell (n = 3). Scale bar: 10 µm.
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    Fig. 1 Ruxolitinib increases autophagy <t>in</t> <t>JAK2V617F</t> cells. A, B <t>HEL</t> and SET-2 cells were treated with ruxolitinib (1 µM) for 2 hours in the presence or absence of bafilomycin (25 nM) to monitor the autophagy flux. A Cells were processed for western blot analysis of P-STAT5, STAT5 and LC3B. Actin was used as a loading control. Graphs represent the LC3B-II/actin ratio obtained by densitometric analysis (n = 4 ± sem). B Cells were stained for LC3B and analyzed by confocal microscopy. Graphs represent the number of LC3B dots per cell (n = 4 ± sem). Scale bar: 10 µm. C Mononuclear cells from peripheral blood samples from JAK2V617F-positive MPN patients were separated by Ficoll-Hypaque density gradient centrifugation. CD34+ progenitors were then sorted using an immunomagnetic positive selection kit and processed for further experiments. D Patients’ cells obtained in C were treated or not with chloroquine (20 µM) over 16 hours to monitor autophagy flux in combination with ruxolitinib (1 µM) for 2 h and stained for LC3B. Representative confocal pictures are shown and histograms represent the number of LC3B dots per cell (n = 8 ± sem). Scale bar: 10 µm. E, F JAK2WT HL-60 cells were treated with ruxolitinib (1 µM) for 2 hours in the presence or absence of bafilomycin (25 nM) to monitor autophagy flux. E Cells were processed for western blot analysis of P-STAT5, STAT5 and LC3B. Actin was used as a loading control. Graphs represent the LC3B-II/actin ratio obtained by densitometric analysis (n = 3 ± sem). F Cells were stained for LC3B and analyzed by confocal microscopy. Graphs represent the number of LC3B dots per cell (n = 3). Scale bar: 10 µm.
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    Fig. 1 Ruxolitinib increases autophagy <t>in</t> <t>JAK2V617F</t> cells. A, B <t>HEL</t> and SET-2 cells were treated with ruxolitinib (1 µM) for 2 hours in the presence or absence of bafilomycin (25 nM) to monitor the autophagy flux. A Cells were processed for western blot analysis of P-STAT5, STAT5 and LC3B. Actin was used as a loading control. Graphs represent the LC3B-II/actin ratio obtained by densitometric analysis (n = 4 ± sem). B Cells were stained for LC3B and analyzed by confocal microscopy. Graphs represent the number of LC3B dots per cell (n = 4 ± sem). Scale bar: 10 µm. C Mononuclear cells from peripheral blood samples from JAK2V617F-positive MPN patients were separated by Ficoll-Hypaque density gradient centrifugation. CD34+ progenitors were then sorted using an immunomagnetic positive selection kit and processed for further experiments. D Patients’ cells obtained in C were treated or not with chloroquine (20 µM) over 16 hours to monitor autophagy flux in combination with ruxolitinib (1 µM) for 2 h and stained for LC3B. Representative confocal pictures are shown and histograms represent the number of LC3B dots per cell (n = 8 ± sem). Scale bar: 10 µm. E, F JAK2WT HL-60 cells were treated with ruxolitinib (1 µM) for 2 hours in the presence or absence of bafilomycin (25 nM) to monitor autophagy flux. E Cells were processed for western blot analysis of P-STAT5, STAT5 and LC3B. Actin was used as a loading control. Graphs represent the LC3B-II/actin ratio obtained by densitometric analysis (n = 3 ± sem). F Cells were stained for LC3B and analyzed by confocal microscopy. Graphs represent the number of LC3B dots per cell (n = 3). Scale bar: 10 µm.
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    Fig. 1 Ruxolitinib increases autophagy <t>in</t> <t>JAK2V617F</t> cells. A, B <t>HEL</t> and SET-2 cells were treated with ruxolitinib (1 µM) for 2 hours in the presence or absence of bafilomycin (25 nM) to monitor the autophagy flux. A Cells were processed for western blot analysis of P-STAT5, STAT5 and LC3B. Actin was used as a loading control. Graphs represent the LC3B-II/actin ratio obtained by densitometric analysis (n = 4 ± sem). B Cells were stained for LC3B and analyzed by confocal microscopy. Graphs represent the number of LC3B dots per cell (n = 4 ± sem). Scale bar: 10 µm. C Mononuclear cells from peripheral blood samples from JAK2V617F-positive MPN patients were separated by Ficoll-Hypaque density gradient centrifugation. CD34+ progenitors were then sorted using an immunomagnetic positive selection kit and processed for further experiments. D Patients’ cells obtained in C were treated or not with chloroquine (20 µM) over 16 hours to monitor autophagy flux in combination with ruxolitinib (1 µM) for 2 h and stained for LC3B. Representative confocal pictures are shown and histograms represent the number of LC3B dots per cell (n = 8 ± sem). Scale bar: 10 µm. E, F JAK2WT HL-60 cells were treated with ruxolitinib (1 µM) for 2 hours in the presence or absence of bafilomycin (25 nM) to monitor autophagy flux. E Cells were processed for western blot analysis of P-STAT5, STAT5 and LC3B. Actin was used as a loading control. Graphs represent the LC3B-II/actin ratio obtained by densitometric analysis (n = 3 ± sem). F Cells were stained for LC3B and analyzed by confocal microscopy. Graphs represent the number of LC3B dots per cell (n = 3). Scale bar: 10 µm.
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    Fig. 1 Ruxolitinib increases autophagy in JAK2V617F cells. A, B HEL and SET-2 cells were treated with ruxolitinib (1 µM) for 2 hours in the presence or absence of bafilomycin (25 nM) to monitor the autophagy flux. A Cells were processed for western blot analysis of P-STAT5, STAT5 and LC3B. Actin was used as a loading control. Graphs represent the LC3B-II/actin ratio obtained by densitometric analysis (n = 4 ± sem). B Cells were stained for LC3B and analyzed by confocal microscopy. Graphs represent the number of LC3B dots per cell (n = 4 ± sem). Scale bar: 10 µm. C Mononuclear cells from peripheral blood samples from JAK2V617F-positive MPN patients were separated by Ficoll-Hypaque density gradient centrifugation. CD34+ progenitors were then sorted using an immunomagnetic positive selection kit and processed for further experiments. D Patients’ cells obtained in C were treated or not with chloroquine (20 µM) over 16 hours to monitor autophagy flux in combination with ruxolitinib (1 µM) for 2 h and stained for LC3B. Representative confocal pictures are shown and histograms represent the number of LC3B dots per cell (n = 8 ± sem). Scale bar: 10 µm. E, F JAK2WT HL-60 cells were treated with ruxolitinib (1 µM) for 2 hours in the presence or absence of bafilomycin (25 nM) to monitor autophagy flux. E Cells were processed for western blot analysis of P-STAT5, STAT5 and LC3B. Actin was used as a loading control. Graphs represent the LC3B-II/actin ratio obtained by densitometric analysis (n = 3 ± sem). F Cells were stained for LC3B and analyzed by confocal microscopy. Graphs represent the number of LC3B dots per cell (n = 3). Scale bar: 10 µm.

    Journal: Blood cancer journal

    Article Title: Targeting PP2A-dependent autophagy enhances sensitivity to ruxolitinib in JAK2 V617F myeloproliferative neoplasms.

    doi: 10.1038/s41408-023-00875-x

    Figure Lengend Snippet: Fig. 1 Ruxolitinib increases autophagy in JAK2V617F cells. A, B HEL and SET-2 cells were treated with ruxolitinib (1 µM) for 2 hours in the presence or absence of bafilomycin (25 nM) to monitor the autophagy flux. A Cells were processed for western blot analysis of P-STAT5, STAT5 and LC3B. Actin was used as a loading control. Graphs represent the LC3B-II/actin ratio obtained by densitometric analysis (n = 4 ± sem). B Cells were stained for LC3B and analyzed by confocal microscopy. Graphs represent the number of LC3B dots per cell (n = 4 ± sem). Scale bar: 10 µm. C Mononuclear cells from peripheral blood samples from JAK2V617F-positive MPN patients were separated by Ficoll-Hypaque density gradient centrifugation. CD34+ progenitors were then sorted using an immunomagnetic positive selection kit and processed for further experiments. D Patients’ cells obtained in C were treated or not with chloroquine (20 µM) over 16 hours to monitor autophagy flux in combination with ruxolitinib (1 µM) for 2 h and stained for LC3B. Representative confocal pictures are shown and histograms represent the number of LC3B dots per cell (n = 8 ± sem). Scale bar: 10 µm. E, F JAK2WT HL-60 cells were treated with ruxolitinib (1 µM) for 2 hours in the presence or absence of bafilomycin (25 nM) to monitor autophagy flux. E Cells were processed for western blot analysis of P-STAT5, STAT5 and LC3B. Actin was used as a loading control. Graphs represent the LC3B-II/actin ratio obtained by densitometric analysis (n = 3 ± sem). F Cells were stained for LC3B and analyzed by confocal microscopy. Graphs represent the number of LC3B dots per cell (n = 3). Scale bar: 10 µm.

    Article Snippet: MATERIALS AND METHODS Cell lines culture and treatments The human cell lines HEL (expressing JAK2V617F), SET-2 (expressing both JAK2V617F and JAK2WT) and HL-60 (expressing JAK2WT) were purchased from the Leibniz Institute DSMZ-German Collection of Microorganisms and Cell Cultures (Braunschweig, Germany).

    Techniques: Western Blot, Control, Staining, Confocal Microscopy, Gradient Centrifugation, Selection