Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Global change of RNA expression upon silencing TET1 in PDX2 B-ALL cells

ABSTRACT: Global change of RNA expression upon silencing TET1 in PDX2 B-ALL cells

PROVIDER: PRJNA788631 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR17223843.fastq.gz	Fastqsanger.gz
	SRR17223845.fastq.gz	Fastqsanger.gz
	SRR17223847.fastq.gz	Fastqsanger.gz
	SRR17223849.fastq.gz	Fastqsanger.gz

Items per page:

1 - 4 of 4

Similar Datasets

Global change of RNA expression upon silencing TET1 in PDX2 B-ALL cells

Project description:Here we report that TET1 has a critical role in B-ALL development. TET1-depleted cells delayed the onset of B-ALL. To investigate the mechanisms, we first generate the patient-derived xenograft cells (PDX2) and transduce with inducible-Cas9 and sgRNA targeting TET1. After treatment with doxycycline, we observe the expression of Cas9 and a depletion of TET1 protein. By using the high throughput sequencing RNA-seq, we check the potential targets of TET1 in B-ALL cells. Finally, we validate that CD72 and JCHAIN are two essential targets of TET1 signaling in B-ALL cells.

2023-02-13 | GSE190851 | GEO

Global change of RNA expression upon silencing TET1 in PDX2 B-ALL cells Landscapes of TET1 and STAT5B binding on DNA across the entire genome in PDX2 B-ALL cells

Project description:Global change of RNA expression upon silencing TET1 in PDX2 B-ALL cells Landscapes of TET1 and STAT5B binding on DNA across the entire genome in PDX2 B-ALL cells

| PRJNA788624 | ENA

TET1 interactome in mESCs (via ChIP-MS)

Project description:Precise regulation of DNA methylation in mammals is critical for genome stability and epigenetic regulation. The discovery of the ten-eleven translocation (TET) proteins catalyzing the oxidation from 5-methylcytosine (5mC) to 5-hydroxymethylcytosine (5hmC), 5-formylcytosine (5fC), and 5-carboxylcytosine (5caC) revolutionized the perspective on the complexity and regulation of DNA modifications. Despite accumulating knowledge about the role of TET1, it remains unclear to what extent these can be attributed to its catalytic activity. Here, we use genome engineering and quantitative multi-omics approaches to dissect the role and mechanism of TET1 in mESCs. Our study identifies TET1 as an essential interaction hub for multiple chromatin modifying complexes and as a global regulator of histone modifications. Strikingly, we find that the majority of transcriptional regulation depends on non-catalytic functions of TET1. Moreover, we show that the establishment of H3K9me3 and H4K20me3 at ERV1, ERVK, and ERVL is mediated by TET1 independent of DNA demethylation. We provide evidence that repression of endogenous retroviruses depends on the interaction between TET1 and SIN3A. In summary, we demonstrate that the non-catalytic functions of TET1 are critical for regulation of gene expression and the silencing of endogenous retroviruses in mESCs.

2022-08-31 | PXD028850 | Pride

Jasper Ridge Global Change Experiment

Project description:Jasper Ridge Global Change Experiment

| PRJNA419199 | ENA

Transcriptome analysis upon REXO2 silencing

Project description:Transcriptome analysis upon REXO2 silencing

| PRJNA564828 | ENA

Transcriptome analysis upon C6orf203 silencing

Project description:Transcriptome analysis upon C6orf203 silencing

| PRJNA509589 | ENA

Oncogenic EGFR Represses the TET1 DNA Demethylase to Induce Silencing of Tumor Suppressors in Cancer Cells

Project description:Oncogene-induced DNA methylation-mediated transcriptional silencing of tumor suppressors frequently occurs in cancer, but the mechanism and functional role of this silencing in oncogenesis is not fully understood. Here, we show that oncogenic epidermal growth factor receptor (EGFR) induces silencing of multiple unrelated tumor suppressors in lung adenocarcinomas and glioblastomas by inhibiting DNA demethylase TET oncogene family member 1 (TET1) via the C/EBPα transcription factor. After oncogenic EGFR inhibition, TET1 binds to tumor suppressor promoters and induces their re-expression via active DNA demethylation. Ectopic expression of TET1 potently inhibits lung and glioblastoma tumor growth, and TET1 knockdown confers resistance to EGFR inhibitors in lung cancer cells. Lung cancer samples exhibited reduced TET1 expression or TET1 cytoplasmic localization in a majority of cases. Collectively, these results identify a conserved pathway of oncogenic EGFR-induced DNA methylation-mediated transcriptional silencing of tumor suppressors, which may have therapeutic benefit for oncogenic EGFR-mediated lung cancers and glioblastomas.

2016-06-23 | GSE39292 | GEO

Oncogenic EGFR Represses the TET1 DNA Demethylase to Induce Silencing of Tumor Suppressors in Cancer Cells

Project description:Oncogene-induced DNA methylation-mediated transcriptional silencing of tumor suppressors frequently occurs in cancer, but the mechanism and functional role of this silencing in oncogenesis is not fully understood. Here, we show that oncogenic epidermal growth factor receptor (EGFR) induces silencing of multiple unrelated tumor suppressors in lung adenocarcinomas and glioblastomas by inhibiting DNA demethylase TET oncogene family member 1 (TET1) via the C/EBPÎ± transcription factor. After oncogenic EGFR inhibition, TET1 binds to tumor suppressor promoters and induces their re-expression via active DNA demethylation. Ectopic expression of TET1 potently inhibits lung and glioblastoma tumor growth, and TET1 knockdown confers resistance to EGFR inhibitors in lung cancer cells. Lung cancer samples exhibited reduced TET1 expression or TET1 cytoplasmic localization in a majority of cases. Collectively, these results identify a conserved pathway of oncogenic EGFR-induced DNA methylation-mediated transcriptional silencing of tumor suppressors, which may have therapeutic benefit for oncogenic EGFR-mediated lung cancers and glioblastomas. HCC827-Del (EGFR L747-S752) and HCC827-Del-TM (EGFR L747-S752/T790M) cell lines were treated with Decitibine (2.5 Î¼M) and Vorinostat (1Î¼M) or as a control cells that were treated with DMSO for 72 hrs. Expression profiling was performed using 3 biological replicates for each condition for a total of 12 samples analyzed.

2016-06-23 | E-GEOD-39292 | biostudies-arrayexpress

Change of the mRNA level upon Puromycin treatment

Project description:Change in the levels of mRNAs upon Puromycin treatment were examined to analyze the mRNA population(s) affected directly or indirectly by global translation

2025-07-21 | GSE85794 | GEO

TET1 KO affects Sox9 function [cell line]

Project description:Ten eleven translocation 1 (Tet1) directs chondrogenic differentiation in the mouse embryonic growth plate. We have characterized the global exon array analysis upon Tet1 knockdown induced by two different shRNAs. In this dataset, we include the expression data obtained from in vitro differentiation of ATDC5 chondroprogenitor cells for 15 days in presence (non-target) and absence (Tet1 sh1 and Tet1 sh2) of Tet1. These data are used to obtain the genes which are differentially expressed in absence of Tet1 and to identify the altered signaling pathways.

2020-11-05 | GSE61855 | 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