Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Transcriptome profiling of NE-4C cells and NE-4C cells with knockdown of Setdb1 by RNA-sequencing

ABSTRACT: Transcriptome profiling of NE-4C cells and NE-4C cells with knockdown of Setdb1 by RNA-sequencing

PROVIDER: PRJNA791301 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR17290119_1.fastq.gz	Fastqsanger.gz
	SRR17290119_2.fastq.gz	Fastqsanger.gz
	SRR17290120_1.fastq.gz	Fastqsanger.gz
	SRR17290120_2.fastq.gz	Fastqsanger.gz

Items per page:

1 - 4 of 4

Similar Datasets

Transcriptome profiling of NE-4C cells and NE-4C cells with knockdown of Setdb1 by RNA-sequencing

Project description:NE-4C is a mouse neural stem cell line used for study of neuronal differentiation. Setdb1 is an epigenetic modification factor responsible for catalyzing the histone modification H3K9me3. Transcription of Setdb1 gene is enriched in embryonic neural cells during vertebrate embryogenesis. Setdb1 is upregulated in cancer cells and promotes cancers. We found that knockdown of Setdb1 in NE-4C cells led to neuronal differentiation.

2022-06-30 | GSE192373 | GEO

Proteomic profile of NE-4C cells after radiofrequency elecromagnetic field exposure and sham-exposure

Project description:NE-4C cells were randomly devided into sham group and RF exposure group, after 48 h 1950 MHz RF exposure at a SAR of 2W/kg, cells were harvested and proteomic profile was detected by liquid chromatography-tandem mass spectrometric approach.

2022-01-26 | PXD031285 |

Transcriptome profiling of HCT116 cells and HCT116 cells with knockdown of SETDB1 by RNA-sequencing

Project description:HCT116 is a colorectal cancer cell line. SETDB1 is an epigenetic modification factor responsible for catalyzing the histone modification H3K9me3. Transcription of SETDB1 gene is enriched in embryonic neural cells during vertebrate embryogenesis. SETDB1 is upregulated in cancer cells and promotes cancers. We found that knockdown of SETDB1 in HCT116 cells led to a neuronal-like differentiation phenotype.

2022-06-30 | GSE192372 | GEO

Identification of Setdb1 interaction proteins in neural stem cells

Project description:Setdb1 is an epigenetic factors catalyzing modification of H3K9me3. Expression of its gene is localized to embryonic neural cells during vertebrate embryogenesis, suggesting its role in regulating neural stemness. The project is to identify the interaction partners of Setdb1, by which Setdb1 regulates neural stemness in neural stem cells.

2022-08-12 | PXD030453 | Pride

SOX2 promoter 4C-seq of H9-hESC derived human neural stem cells with mutant IDH1-R132H overexpression, P53 shRNA knockdown and ATRX shRNA knockdown

Project description:4C-seq was performed to assess genomic contacts with the SOX2 protmoter, human neural stem cells with no oncogenic alterations were compared to those with concurrent IDH1-R132H overexpression, P53 shRNA knockdown and ATRX shRNA knockdown.

2017-11-09 | GSE94961 | GEO

Effect of inhibition of Setdb1 on gene expression in AML12 cells

Project description:To investigate the mRNA expression regulated by Setdb1, we established AML12 knockdown cell model by infecting Setdb1 siRNA for 72 hours

2023-03-05 | GSE225723 | GEO

Setdb1-mediated H3K9 methylation is enriched on the inactive X and plays a role in its epigenetic silencing

Project description:Purpose: The aim of this study is (1) to identify the chromatin occupancy of the epigenetic regulator Setdb1 in mouse embryonic fibroblasts (MEF); (2) to profile key epigenetic marks H3K9me2, H3K9me3 and H3K27me3; utilizing wildtype cells with nonsilencing shRNA mediated knockdown and Setdb1 geneTrap heterozygous cells with Setdb1 shRNA mediated knockdown. Methods: Chromatin immunoprecipitation for Setdb1, H3K9me2, H3K9me3 and H3K27me3 was performed essentially as in (Nelson et al. 2006). Briefly, nuclei were isolated from formaldehyde crosslinked MEFs and chromatin was fragmented by sonication. Chromatin immunoprecipitation was performed with corresponding antibodies for Setdb1, H3K9me2, H3K9me3 and H3K27me3. DNA was extracted from the immunoprecipitated fraction following reverse-crosslinking. Isolated DNA was used to generate sequencing libraries with Illumina's TruSeq DNA Sample Preparation Kit according to manufacturer's instruction. Libraries were pooled and sequenced on the Illumina HiSeq 2000 platform for 100 bp single-end reads. Image analysis was performed in real time by the HiSeq Control Software (HCS) v1.4.8 and Real Time Analysis (RTA) v1.12.4.2, running on the instrument computer. Real-time base calling on the HiSeq instrument computer was performed with the RTA software. Illumina CASAVA1.8 pipeline was used to generate the sequence data. Chromatin occupancy of the epigenetic regulator Setdb1, H3K9me2, H3K9me3 and H3K27me3 in mouse embryonic fibroblasts (MEFs) with wildtype MEFs and nonsilencing shRNA mediated knockdown or Setdb1 geneTrap heterozygous MEFs with Setdb1 shRNA mediated knockdown was determined by Setdb1, H3K9me2, H3K9me3 and H3K27me3 ChIP-seq, respectively.

2016-05-18 | E-GEOD-66522 | biostudies-arrayexpress

Transcriptome profiling of HCT116 cells and HCT116 cells with knockdown of SETDB1 by RNA-sequencing

Project description:Transcriptome profiling of HCT116 cells and HCT116 cells with knockdown of SETDB1 by RNA-sequencing

| PRJNA791302 | ENA

Hypoxia stabilizes SETDB1 to maintain genome stability

Project description:Von Hippel-Lindau (VHL) is a tumor suppressor that functions as the substrate recognition subunit of the CRL2VHL E3 complex. While substrates of VHL have been identified, its tumor suppressive role remains to be fully understood. For further determination of VHL substrates, we analyzed the physical interactome of VHL and identified the histone H3K9 methyltransferase SETBD1 as a novel target. SETDB1 undergoes oxygen-dependent hydroxylation by prolyl hydroxylase domain proteins (PHD) and the CRL2VHL complex recognizes hydroxylated SETDB1 for ubiquitin-mediated degradation. Under hypoxic conditions, SETDB1 accumulates by escaping CRL2VHL activity. Loss of SETDB1 in hypoxia compared with that in normoxia escalates the production of transposable element (TE)-derived double-stranded RNAs (dsRNAs), thereby hyperactivating the immune-inflammatory response. In addition, strong derepression of TEs in hypoxic cells lacking SETDB1 triggers DNA damage-induced death. Our collective results support a molecular mechanism of oxygen-dependent SETDB1 degradation by the CRL2VHL E3 complex and reveal a role of SETDB1 in genome stability under hypoxia.

2024-01-26 | PXD037104 | Pride

Setdb1-mediated H3K9 methylation is enriched on the inactive X and plays a role in its epigenetic silencing

Project description:Purpose: The aim of this study was to determine the DNA methylation state of wildtype female mouse embryonic fibroblasts with nonsilencing shRNA mediated knockdown and Setdb1 geneTrap heterozygous cells with Setdb1 shRNA mediated knockdown. Methods: Enhanced Reduced Representation Bisulfite Libraries (eRRBS) were produced as previously descirbed (Akalin et al. 2012). Libraries were pooled and sequenced on the Illumina HiSeq 2000 platform for 100 bp single-end reads with dark cycle parameters (Boyle et al. 2012). Image analysis was performed in real time by the HiSeq Control Software (HCS) v1.4.8 and Real Time Analysis (RTA) v1.12.4.2, running on the instrument computer. Real-time base calling on the HiSeq instrument computer was performed with the RTA software. Illumina CASAVA1.8 pipeline was used to generate the sequence data. Determine the DNA methylation state of mouse embryonic fibroblasts (MEFs) with wildtype MEFs and nonsilencing shRNA mediated knockdown or Setdb1 geneTrap heterozygous MEFs with Setdb1 shRNA mediated knockdown. Single-end with dark cycle protocol (Boyle et al. 2012)

2016-05-18 | E-GEOD-66524 | biostudies-arrayexpress

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