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Ro, GSK-591 and combination treatment in Z-138 cells

ABSTRACT: Ro, GSK-591 and combination treatment in Z-138 cells

PROVIDER: PRJNA800369 | ENA |

REPOSITORIES: ENA

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RNA-seq datasets of Ro, GSK-591 and combination treatment in Z-138 cells

Project description:Dual targeting of PRMT5 and MSI2 inhibited synergisticly B-cells proliferation. Thus, next-generation sequencing was performed to evaluate the effect of the inhibitors of PRMT5 and MSI2, GSK-591 and Ro, respectively, in the global transcriptome of the mantle cell lymphoma cell line, Z-138.

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HyperTRIBE uncovers MSI2 RNA binding activity and the effect of Ro, GSK-591 and combination in Z-138 cells

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RNA-seq datasets of Ro, GSK-591 and combination treatment in Z-138 cells

Project description:RNA-seq datasets of Ro, GSK-591 and combination treatment in Z-138 cells

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HyperTRIBE uncovers MSI2 RNA binding activity and the effect of Ro, GSK-591 and combination in Z-138 cells

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Ro, GSK-591 and combination treatment in Z-138 cells

Project description:This SuperSeries is composed of the SubSeries listed below.

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Gene expression in astrocytes upon sustained GSK-3 inhibition by small molecule

Project description:In order to identify molecular targets that mediates the stimulation of astrocyte's migration upon sustained specific inhibition of GSK-3, we have employed whole genome microarray expression profiling. Murine cortical-striatal astrocytes grown in primary culture were treated in vitro for 48 h with either 1 micromolar Ro3303544, or control medium (final equivalent concentration of DMSO), or washed-out for 48h in control medium after an initial 48h treatment with 1 micromolar Ro3303544. The three different conditions: Ctrl, Ro and wash-out (each in duplicate) were compared.

2011-08-31 | E-GEOD-25770 | biostudies-arrayexpress

A comparison of GS-5759, a bifunctional Î²2-adrenoceptor agonist and PDE4 inhibitor, and indacaterol and GSK 256066 in combination on gene expression changes in the BEAS-2B human airway epithelial cell line

Project description:GS-5759 is a bifunctional ligand composed of a quinolinone-containing pharmacophore found in several Î²2-adrenoceptor agonists linked covalently to a phosphodiesterase 4 inhibitor (PDE4) related to GSK 256066 by a pent-1-yn-1-ylbenzene spacer. The object of the study was to detemine if gene expression changes induced by GS-5759 were replicated by a Î²2-adrenoceptor agonist (indacaterol; Ind) and a PDE4 inhibitor (GSK 256066; GSK) in combination. Microarray analysis was performed on RNA from BEAS-2B cells treated with GS-5759 and a combination of indacaterol and GSK 256066 to identify differentialy expressed genes. Confluent BEAS-2B cells were treated with vehicle, Ind/GSK or GS-5759 for 1h, 2h, 6h or 18h. Total RNA was extracted, quantified (NanoDrop 2000) and the quality of each sample determined by using the Agilent 2100 Lab-on-a-Chip system before being processed for gene expression chnages by Expression Analysis Inc (Dunham, NC, USA).

2016-07-27 | E-GEOD-84880 | biostudies-arrayexpress

A comparison of GS-5759, a bifunctional β2-adrenoceptor agonist and PDE4 inhibitor, and indacaterol and GSK 256066 in combination on gene expression changes in the BEAS-2B human airway epithelial cell line

Project description:GS-5759 is a bifunctional ligand composed of a quinolinone-containing pharmacophore found in several β2-adrenoceptor agonists linked covalently to a phosphodiesterase 4 inhibitor (PDE4) related to GSK 256066 by a pent-1-yn-1-ylbenzene spacer. The object of the study was to detemine if gene expression changes induced by GS-5759 were replicated by a β2-adrenoceptor agonist (indacaterol; Ind) and a PDE4 inhibitor (GSK 256066; GSK) in combination. Microarray analysis was performed on RNA from BEAS-2B cells treated with GS-5759 and a combination of indacaterol and GSK 256066 to identify differentialy expressed genes.

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An analysis of the effect of indacaterol and GSK 256066 alone and in combination on gene expression changes in the BEAS-2B human airway epithelial cell line.

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Project description:Gene expression data from AML cell lines, MOLM-14, U937, THP-1 and HL-60, that were infected with a scrambled control hairpin (shControl), two shRNAs directed against GSK-3B (shGSK3B_1 and shGSK3B_2), or two shRNAs directed against GSK-3A (shGSK3A_5 and shGSK3A_6). Acute myeloid leukemia (AML) is the most common form of acute leukemia in adults. Long-term survival of patients with AML has changed little over the past decade, necessitating the identification and validation of new AML targets. Integration of genomic approaches with small-molecule and genetic-based high-throughput screening holds the promise of improved discovery of candidate targets for cancer therapy. Here, we identified a role for glycogen synthase kinase 3A (GSK-3A) in AML by performing two independent small-molecule library screens and an shRNA screen for perturbations that induced a differentiation expression signature in AML cells. GSK-3 is a serine-threonine kinase involved in diverse cellular processes including differentiation, signal transduction, cell cycle regulation, and proliferation. We demonstrated that specific loss of GSK-3A induced differentiation in AML by multiple measurements, including induction of gene expression signatures, morphological changes, and cell surface markers consistent with myeloid maturation. GSK-3AM-bM-^@M-^Sspecific suppression also led to impaired growth and proliferation in vitro, induction of apoptosis, loss of colony formation in methylcellulose, and anti-AML activity in vivo. Although the role of GSK-3B has been well studied in cancer development, these studies support a role for GSK-3A in AML. The AML cell lines, MOLM-14, U937, THP-1 and HL-60, were infected with a scrambled control hairpin (shControl), two shRNAs directed against GSK-3B (shGSK3B_1 and shGSK3B_2), and two shRNAs directed against GSK-3A (shGSK3A_5 and shGSK3A_6).

2012-02-27 | E-GEOD-35200 | biostudies-arrayexpress

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