Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Stau2 knockdown in human bcCML cells (K562)"

ABSTRACT: Stau2 knockdown in human bcCML cells (K562)"

PROVIDER: PRJNA557137 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR9853390_1.fastq.gz	Fastqsanger.gz
	SRR9853390_2.fastq.gz	Fastqsanger.gz
	SRR9853391_1.fastq.gz	Fastqsanger.gz
	SRR9853391_2.fastq.gz	Fastqsanger.gz
	SRR9853392_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 12

Similar Datasets

Stau2 knockdown in human bcCML cells (K562)"

Project description:STAU2 knockdown in human K562 cells

2020-04-21 | GSE135012 | GEO

Effect of Stau2 knockdown on H3K4 methylation in human bcCML cells (K562)

Project description:Effect of Stau2 knockdown on H3K4 methylation in human bcCML cells (K562)

| PRJNA596503 | ENA

Effect of Stau2 knockdown on H3K4 methylation in human bcCML cells (K562)

Project description:Evaluating the effect of Stau2 knockdown on H3K4me1, H3K4me2, H3K4me3 in K562 cells

2020-04-21 | GSE142307 | GEO

Effect of Sdc1 knockout in mouse blast crisis chronic myeloid leukemia (bcCML) cells

Project description:Here we report the genomic impact on murine bcCML by Sdc1 loss. We compare bcCML derived from a wildtype cell source to bcCML derived from a Sdc1 knockout mouse. This RNA-seq identifies a number of potential critical regulators of growth, migration, and adhesion.

2020-10-21 | GSE159148 | GEO

Stau2 RIP-Chip in Mouse E13-14 Cortex

Project description:The double-stranded RNA binding protein Staufen2 (Stau2) is asymmetrically localized and segregated during asymmetric cell divisions in the developing mouse cortex and promotes intermediate progenitor cell fate. We carry out RNA immunoprecipitation with a Stau2 specific antibody, followed by microarray analysis to identify Stau2 assoicated RNAs that may be shuttled asymmetrically into one daughter cell thus affecting cell fate.

2012-12-21 | GSE38222 | GEO

Stau2 RIP-Chip in Mouse E13-14 Cortex

2012-12-21 | E-GEOD-38222 | biostudies-arrayexpress

CRISPR RNA-seq from K562 (ENCSR898KNS)

Project description:RNA-seq on K562 cells treated with a CRISPR gRNA against STAU2. (STAU2-BGKcLV11) For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf

2021-06-15 | GSE178044 | GEO

CRISPR-Cas9 knockdown of RBM48 in K562 cells

Project description:CRISPR-Cas9 knockdown of RBM48 in K562 cells

| PRJNA658070 | ENA

An In Vivo Genome-Wide CRISPR Screen Identifies the RNA-Binding Protein Staufen2 as a Key Regulator of Myeloid Leukemia

Project description:While Chronic Myelogenous Leukemia (CML) is generally well controlled with Imatinib and other kinase inhibitors, blast crisis CML (bcCML) continues to be resistant to current therapies and remains highly lethal. In this study, we identify the double stranded RNA binding protein Stau2 as a as key new dependency of bcCML. To define the impact of Staufen2 in myeloid leukemia, we developed a germline knockout with targeted loss of its RNA binding domains. Genetic deletion of Staufen2 led to a profound decrease in bcCML growth and propagation, and markedly improved overall survival in mouse models. Further, Staufen2 was also expressed and required for growth of primary bcCML as well as de novo AML patient samples, indicating a conserved utilization across human disease. Finally, an integrated computational analysis of eCLIP, RNA-Seq analysis and the functional genomic CRISPR screen identified Staufen2 as a regulator of a remarkable network of broad acting chromatin modifiers, resulting in changes in global histone methylation patterns.

2020-04-23 | GSE134971 | GEO

Next Generation Sequencing: in vivo genome-wide CRISPR sgRNA screen in primary cancer-initiating and propagating bcCML stem cells

Project description:While Chronic Myelogenous Leukemia (CML) is generally well controlled with Imatinib and other kinase inhibitors, blast crisis CML (bcCML) continues to be resistant to current therapies and remains highly lethal. Here we report a genome-wide in vivo CRISPR screen to better define the biological determinants of bcCML establishment and propagation in a physiologic context. This screen identified a large number of new genes and programs critically required for bcCML including those essential for chromatin remodeling, spliceosomal assembly, PLK1 and Myc signaling.

2020-04-22 | GSE135300 | 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