Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Effect of depletion of TFII-I or TRIM24 on Jurkat T cell activation.

ABSTRACT: Effect of depletion of TFII-I or TRIM24 on Jurkat T cell activation.

PROVIDER: PRJNA915097 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR22873721_1.fastq.gz	Fastqsanger.gz
	SRR22873721_2.fastq.gz	Fastqsanger.gz
	SRR22873722_1.fastq.gz	Fastqsanger.gz
	SRR22873722_2.fastq.gz	Fastqsanger.gz
	SRR22873723_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 96

Similar Datasets

Effect of depletion of TFII-I or TRIM24 on Jurkat T cell activation.

Project description:To investigate the cooperative function TFII-I and TRIM24 in the regulation of T cell activation regulated genes, we established Jurkat Tat cells in which TFII-I was depleted by shRNA and TRIM24 was knocked out by CRISPR-Cas9. We then performed gene expression profiling analysis using data obtained from RNA-seq of cell lines stimulated by PMA and Ionomycin.

2022-12-28 | GSE221633 | GEO

PolyA-sequencing in Jurkat cells upon CDK12 depletion.

Project description:PolyA-sequencing in Jurkat cells upon CDK12 depletion.

| PRJNA679028 | ENA

ATAC-seq analysis after dTAG-mediated MYB depletion in Jurkat cells

Project description:ATAC-seq analysis was performed in a T-ALL cell line (Jurkat) with FKBP knock-in at MYB locus to analyze chromatin accessibility after dTAG-mediated depletion.

2024-11-10 | GSE267359 | GEO

RNA-seq analysis after dTAG-mediated MYB depletion in Jurkat cells

Project description:RNA-seq analysis was performed in a T-ALL cell line (Jurkat) with FKBP tag knock-in at the MYB locus to analyze gene expression changes after dTAG-mediated MYB depletion.

2024-11-10 | GSE267370 | 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

Mammary-specific expression of Trim24 establishes a mouse model of human metaplastic breast cancer and nominates c-Met and TRIM24 as therapeutic targets

Project description:Conditional overexpression of histone reader Tripartite motif containing protein 24 (TRIM24) in mouse mammary epithelia (Trim24COE) drives spontaneous development of carcinosarcoma tumors, lacking ER, PR and HER2. Human carcinosarcomas or metaplastic breast cancers (MpBC) are a rare, chemorefractory subclass of triple-negative breast cancers (TNBC). Comparison of Trim24COE carcinosarcoma morphology, TRIM24 protein levels and a derived Trim24COE gene signature revealed strong correlation with human MpBC tumors and MpBC xenograft (PDX) models. Global and single-cell tumor profiling revealed Met as a direct oncogenic target of TRIM24, leading to aberrant PI3K/mTOR activation. Pharmacological inhibition of these pathways in primary Trim24COE tumor cells and TRIM24-PROTAC treatment of MpBC PDX tumorspheres revealed the therapeutic potential of targeting TRIM24. Altogether, global expression, single-cell immunophenotyping and mechanistic studies of tumors and MpBC PDX nominated TRIM24-activated c-MET/PI3K/mTOR pathways and TRIM24, which were validated as potential MpBC therapeutic targets.

2021-06-25 | GSE165407 | GEO

Cyclic LSD1 recruitment and dynamic H3K4 methylation establish TRIM24-activated estrogen response

Project description:The role of histone lysine methylation in estrogen receptor-alpha (ERα)-activated transcription is highly context-specific and poorly understood. Here, we show that lysine demethylase 1 (LSD1) mediates loss of H3 lysine 4 dimethylation (H3K4me2) in coordination with tripartite-motif-containing protein 24 (TRIM24)- regulated growth of breaset cancer-derived cells. We performed global profiling of histone H3K4me2 in comparison to genome-wide binding of TRIM24 in MCF7 cells when estrogen is depleted or added. We found specific subsets of genes with functions in transcription and cell proliferation are depleted of H3K4me2 at TRIM24 binding sites. Chromatin immunoprecipitation (ChIP) analyses over a time course of estrogen induction revealed cyclic demethylation of H3K4me2, LSD1, TRIM24 and ERα binding. Inhibition of LSD1 enzymatic activity led to increased H3K4me2 and decreased estrogen response of TRIM24-dependent genes. Additon of a small molecule inhibitor of the TRIM24 bromodomain or depletion of TRIM24 expression amplified the impact of LSD1 inhbition as measured by survival and proliferation of MCF7 cells, suggesting that combinatorial inhibition of LSD1 and TRIM24 may be effective in targeting ER-positive breast cancers.

2019-12-01 | GSE113654 | GEO

VL30 retro-transposons are TRIM24-repressed enhancers that generate non-coding RNA to regulate gene expression in mouse hepatocytes. [RNA-Seq]

Project description:TRIM24 and TRIM33 interact to form a corepressor complex that suppresses murine hepatocellular carcinoma (HCC). TRIM24 and TRIM33 cooperatively repress retinoic acid receptor dependent activity of VL30 retro-transposons in hepatocytes in vivo. In TRIM24 knockout hepatocytes, VL30 long terminal repeats (LTRs) generate enhancer (e)RNAs and act as surrogate promoter and enhancer elements deregulating expression of neighbouring genes. We show that a VL30 LTR-derived eRNA is essential to activate the lipocalin 13 gene in hepatocytes in vivo. A further consequence of VL30 de-repression is the accumulation of retro-transcribed VL30 DNA in the cytoplasm of TRIM24-mutant hepatocytes and activation of the viral defence/interferon response. VL30 activation therefore modulates gene expression via the enhancer activity of the LTRs and by activation of the interferon response. Both of these processes are genetically linked to HCC development suggesting that VL30 repression by TRIM24 plays an important role in tumour suppression. RNA profiles in liver of wild type (WT) and Trim24-/- mice by deep sequencing using Illumina GAIIx.

2013-01-01 | E-GEOD-39851 | biostudies-arrayexpress

Expression data from NR2F2(COUP-TFII) depleted mouse MA-10 Leydig cells

Project description:In males, Leydig cells are the main producers of testosterone and insulin-like 3, hormones which are both essential for sex differentiation and reproductive functions. Nuclear receptor chicken ovalbumin upstream promoter-transcription factors II (COUP-TFII) is expressed in the cells committed to give rise to the fully functional steroidogenic adult Leydig cells and has a major role in their function and differentiation. Up to date, only handful of COUP-TFII gene targets have been reported. A transcriptomic approach was used to identify additional genes affected by depletion of COUP-TFII in mouse MA-10 Leydig cell line.

2021-07-01 | GSE163283 | GEO

Genes regulated by COUP-TFII inhibitor

Project description:The orphan nuclear receptor COUP-TFII is expressed at a low level in adult tissues, but its expression is increased and shown to promote progression of multiple diseases including prostate cancer, heart failure and muscular dystrophy. Suppression of COUP-TFII slows disease progression, making it an intriguing therapeutic target. Here, we identified a potent and specific COUP-TFII inhibitor through high-throughput screening. The inhibitor specifically suppressed COUP-TFII activity to regulate its target genes.

2020-05-12 | GSE142475 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

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