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RNAseq of Jurkat_control and Jurkat_shPPM1A-AS

ABSTRACT: To study the effect of PPM1A-AS on T-cell acute lymphoblastic leukemia (T-ALL) cells, we conducted shRNA-mediated knockdown of PPM1A-AS in Jurkat and performed RNA-seq.

ORGANISM(S): Homo sapiens

PROVIDER: GSE182998 | GEO | 2021/10/19

REPOSITORIES: GEO

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Core transcriptional regulatory circuit controlled by the TAL1 complex in human T-cell acute lymphoblastic leukemia

Project description:This SuperSeries is composed of the following subset Series: GSE29179: Identification of differentially expressed genes upon shRNA knockdown of TAL1 and its regulatory partners in T-ALL cells (Jurkat) GSE29180: ChIP-Seq of TAL1 and its regulatory partners in T-ALL cells (Jurkat) GSE33850: Core transcriptional regulatory circuit controlled by the tal1 complex in human t-cell acute lymphoblastic leukemia (Subseries) Refer to individual Series

2012-08-16 | E-GEOD-29181 | biostudies-arrayexpress

ARID5B ChIP-seq in Jurkat

Project description:ChIP-seq analysis was performed in Jurkat cells (T-cell acute lymphoblastic leukemia cell line)

2018-01-12 | GSE97512 | GEO

H3K4me1 ChIP-seq analysis in Jurkat cells

Project description:ChIP-seq analysis was performed in Jurkat cells (T-cell acute lymphoblastic leukemia cell line)

2018-09-05 | GSE119439 | GEO

Gene expression changes in REH following STAT3 inhibition by shRNA

Project description:STAT3 (Signal transducer and activator of transcription 3) expression is associated with with t(12;21) acute lymphoblastic leukaemia (ALL) and it is crucial for the survival of the t(12;21) ALL . Our study investigated the STAT3 regulated pathways and discovered a novel STAT3-TP53 axis in B-ALL. In order to determine the STAT3 regulated pathways in t(12;21) ALL cells, we performed RNAseq analysis on the Pre-B Acute Lymphoblastic Leukemia (ALL) cell line REH following shRNA-mediated STAT3 knockdown

2024-01-31 | GSE179332 | GEO

Genome wide screen reveals WNT11, a noncanonical WNT gene, as a target of ETS transcription factor ERG

Project description:ERG is a transcription factor that is involved in leukomogenesis and its mRNA overexpression has been associated with poor prognosis in a subset of patients with T-cell acute lymphoblastic leukemia (T-ALL) and acute myeloid leukemia (AML). Herein, a genome-wide screen of ERG target genes was conducted by chromatin immunoprecipitation-on-chip (ChIP-chip) in Jurkat cells. 342 significant annotated regions were derived from ChIP-chip experiments. Seventeen candidate promoter regions resulted in at least two-fold enrichment by quantitative PCR. Notably, ERG potential targets included WNT signaling genes: WNT2, WNT9A, WNT11, CCND1, and FZD7. Functionally, expression of WNT11 was downregulated with siRNA ERG knockdown and substantially upregulated in a tet-on ERG-inducible assay in K562 cells. To investigate a role for ERG in WNT signaling, a WNT agonist was used to inhibit glycogen synthase kinase (GSK-3). This treatment resulted in an ERG-dependent proliferative growth advantage in the tet-on ERG-inducible system. Lastly, chromatin immunoprecipitation assays of primary leukemia blasts confirmed WNT11 promoter enrichment dependent on ERG mRNA expression. In conclusion, ERG transcriptional networks in leukemia are revealed. Specifically, WNT11 emerged as a target of ERG. We propose that overexpression of ERG in acute leukemia may lead to a proliferative advantage upon activation of WNT signals. ChIP-chip with ERG antibody C20 and combined C17/20 and nonspecificic IgG in Jurkat

2010-12-10 | E-GEOD-21495 | biostudies-arrayexpress

RNA-seq analysis after depletion of ALDH1A2 by enhancer blocking in Jurkat cells

Project description:RNA-seq analysis was performed in a T-cell acute lymphoblastic leukemia cell line (Jurkat) to analyze gene expression changes after ALDH1A2 depletion.

2020-12-31 | GSE136416 | GEO

Glucocorticoids induced transcriptional regulation in acute lymphoblastic leukemia

Project description:Four acute lymphoblastic leukemia cell lines SUP-B15, JURKAT, MOLT-3, and CCRF-CEM cells were treated with glucocorticoids such as dexamethasone and prednisolone for six hours before RNA extraction.

2020-12-18 | E-MTAB-9250 | biostudies-arrayexpress

RNA-seq analysis after PIK75 treatment in T-ALL cells

Project description:RNA-seq analysis was performed in two T-cell acute lymphoblastic leukemia (T-ALL) cell lines (Jurkat and DND-41) to analyze gene expression changes after the treatment with PIK-75.

2022-09-15 | GSE181435 | GEO

ChIP-seq of cyclin-dependent kinases

Project description:Several cyclin-dependent kinases (CDKs) are known to have roles in transcriptional regulation. The datasets presented here are ChIP-seq experiments for different CDKs and RNA polymerase II in murine embryonic stem cells and Jurkat cells. ChIP-Seq of cyclin-dependent kinases in mouse embryonic stem cells and Jurkat human T cell acute lymphoblastic leukemia cell line

2014-08-03 | E-GEOD-60027 | biostudies-arrayexpress

Metabolomics identifies the intersection of phosphoethanolamine with menaquinone- triggered apoptosis in an in vitro model of leukemia

Project description:Altered metabolism is increasingly acknowledged as an important aspect of cancer, and thus serves as a potentially fertile area for the identification of therapeutic targets or leads. Our recent work using transcriptional data to predict metabolite levels in cancer cells led to preliminary evidence of the antiproliferative role of menaquinone (vitamin K2) in the Jurkat cell line model of acute lymphoblastic leukemia. However, nothing is known about the direct metabolic impacts of menaquinone in cancer, which could provide insights into its mechanism of action. Here, we used metabolomics to investigate the process by which menaquinone exerts antiproliferative activity on Jurkat cells. We first validated the dose-dependent, semi-selective, pro-apoptotic activity of menaquinone treatment on Jurkat cells relative to non-cancerous lymphoblasts. We then used mass spectrometry-based metabolomics to identify systems-scale changes in metabolic dynamics that are distinct from changes induced in noncancerous cells or by other chemotherapeutics. One of the most significantly affected metabolites was phosphoethanolamine, which exhibited a two-fold increase in menaquinone-treated Jurkat cells compared to vehicle-treated cells at 24 h, growing to a five-fold increase at 72 h. Phosphoethanolamine elevation was observed prior to the induction of apoptosis, and was not observed in menaquinonetreated lymphoblasts or chemotherapeutic-treated Jurkat cells. We also validated the link between menaquinone and phosphoethanolamine in an ovarian cancer cell line, suggesting potentially broad applicability of their relationship. This metabolomics-based work is the first detailed characterization of the metabolic impacts of menaquinone treatment and the first identified link between phosphoethanolamine and menaquinone-induced apoptosis.

2015-10-19 | MTBLS226 | MetaboLights

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