Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

ARID5B ChIP-seq in Jurkat

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

ORGANISM(S): Homo sapiens

PROVIDER: GSE97512 | GEO | 2018/01/12

SECONDARY ACCESSION(S): PRJNA382152

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

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

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

RNA-seq analysis in Jurkat cells

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

2016-12-31 | GSE81712 | 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

Changes in genetic transcription patterns in Jurkat cells treated with Tamoxifen

Project description:In this research, we use DNA microarray analysis to clarify the gene expression responses in Jurkat cells after Tamoxifen treatment. Jurkat cells are a dexamethasone-resistant cell line derived from a T-cell Acute Lymphoblastic Leukaemia sample in relapse

2019-09-02 | GSE122852 | GEO

Expression data from Jurkat cells treated with SB225002 for 6h and 9h.

Project description:In our efforts to evaluate the function of the IL-8 receptor CXCR2 in Acute Lymphoblastic Leukemia (ALL) cells, we made use of SB225002 (N-(2-hydroxy-4-nitrophenyl)-N’-(2-bromophenyl)urea), a drug initially described as a CXCR2 antagonist. Although the CXCR2 receptor was found to be non-functional in ALL, B- and T-ALL cell lines were sensitive to SB225002. We used microarray analysis to identify a transcriptional profile of genes that mediate SB225002's effects in acute lymphoblastic leukemia cells. Jurkat cells were treated for 6h or 9h with SB225002 [12.5 uM] or 0.1% DMSO (vehicle control).

2015-07-23 | E-GEOD-71212 | biostudies-arrayexpress

ChIP-seq analysis for TAL1-FKBP12 Jurkat cells

Project description:ChIP-seq analysis was performed in a Jurkat cell line to analyze DNA bindings of TAL1-FKBP12 protein using an anti-HA antibody after DMSO or dTAG-13 treatment.

2023-11-20 | GSE226197 | GEO

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

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

RNAseq of Jurkat_control and Jurkat_shPPM1A-AS

Project description: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.

2021-10-19 | GSE182998 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data