Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Chromatin accessibility and expression profiling in STAG2 mutant K562 cells

ABSTRACT: Chromatin accessibility and expression profiling in STAG2 mutant K562 cells

PROVIDER: PRJNA543742 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR9090310.fastq.gz	Fastqsanger.gz
	SRR9090320_1.fastq.gz	Fastqsanger.gz
	SRR9090320_2.fastq.gz	Fastqsanger.gz
	SRR9090311_1.fastq.gz	Fastqsanger.gz
	SRR9090311_2.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 39

Similar Datasets

Chromatin accessibility profiling in STAG2 mutant K562 cells

Project description:Chromatin accessibility profiling in STAG2 mutant K562 cells

| PRJNA543744 | ENA

Chromatin accessibility profiling in STAG2 mutant K562 cells

Project description:K562 (female chronic myelogenous leukemia) cells were CRISPR-Cas9 edited to contain STAG2 R614* mutation. STAG2 is encoded on the X-chromosome and normally mutation on one allele is sufficient for complete loss of STAG2 protein due to the wild type allele being mosaically silenced. However, we obtained both heterozygous and homozygous mutant lines that showed partial and complete loss of STAG2 protein respectively. We here examined the impact of STAG2 R614* mutation on gene expression and chromatin acessibilty.

2020-02-03 | GSE131447 | GEO

Expression profiling in STAG2 mutant K562 cells

2020-02-03 | GSE131448 | GEO

Expression profiling in STAG2 mutant K562 cells

Project description:Expression profiling in STAG2 mutant K562 cells

| PRJNA543745 | ENA

Cohesin Members Stag1 and Stag2 Display Distinct Roles in Chromatin Accessibility and Topological Control of HSC Self-Renewal and Differentiation [ChIP_LinNeg_Stag1Stag2CTCF]

Project description:Transcriptional regulators, including the cohesin complex member STAG2, are recurrently mutated in cancer. The role of STAG2 in gene regulation, hematopoiesis, and tumor suppression remains unresolved. We show that Stag2 deletion in hematopoietic stem and progenitor cells (HSPCs) results in altered hematopoietic function, increased self-renewal, and impaired differentiation. Chromatin immunoprecipitation (ChIP) sequencing revealed that, although Stag2 and Stag1 bind a shared set of genomic loci, a component of Stag2 binding sites is unoccupied by Stag1, even in Stag2-deficient HSPCs. Although concurrent loss of Stag2 and Stag1 abrogated hematopoiesis, Stag2 loss alone decreased chromatin accessibility and transcription of lineage-specification genes, including Ebf1 and Pax5, leading to increased self-renewal and reduced HSPC commitment to the B cell lineage. Our data illustrate a role for Stag2 in transformation and transcriptional dysregulation distinct from its shared role with Stag1 in chromosomal segregation.

2019-09-26 | GSE138005 | GEO

Cohesin Members Stag1 and Stag2 Display Distinct Roles in Chromatin Accessibility and Topological Control of HSC Self-Renewal and Differentiation [ATAC_LinNegBM]

2019-09-26 | GSE138004 | GEO

Cohesin Members Stag1 and Stag2 Display Distinct Roles in Chromatin Accessibility and Topological Control of HSC Self-Renewal and Differentiation [ATAC_LSK_GMP_CFUE_Stag2KOWT]

2019-09-26 | GSE138003 | GEO

Cohesin Members Stag1 and Stag2 Display Distinct Roles in Chromatin Accessibility and Topological Control of HSC Self-Renewal and Differentiation [RNA_LinNegBM]

2019-09-26 | GSE138007 | GEO

Cohesin Members Stag1 and Stag2 Display Distinct Roles in Chromatin Accessibility and Topological Control of HSC Self-Renewal and Differentiation [RNA_3populations_LSK_GMP_CFUE]

2019-09-26 | GSE138006 | GEO

STAG2 mutations and 3D genome organization, chromatin loops, and polycomb signaling in glioblastoma multiforme

Project description:Inactivating mutations of genes encoding the cohesin complex are common in a wide range of human cancers. STAG2 is the most commonly mutated subunit. Here we report the impact of stable correction of endogenous, naturally occurring STAG2 mutations on gene expression, 3D genome organization, chromatin loops, and Polycomb signaling in glioblastoma multiforme. Correction of mutant STAG2 significantly altered the expression of ~10% of all expressed genes. The genes most highly regulated by STAG2 (e.g. FGF7, c-KIT, MAGE tumor antigens) were virtually all upregulated in STAG2-mutant cells. Hi-C revealed that ~3% of A/B compartments switched after STAG2 correction, and confirmed prior findings that STAG2 is dispensable for maintenance of Topologically Associating Domains (TADs). The size and strength of thousands of chromatin loops were altered by STAG2 correction, a subset of which controlled the expression of adjacent genes. Loops specific to STAG2-mutant cells and tumors were very large, supporting prior findings that STAG1-containing cohesin complexes have greater loop extrusion processivity than STAG2-containing cohesin complexes, and suggesting that long loops may be a generalizable feature of STAG2-mutant cancers. Finally, STAG2-regulated chromatin loops were enriched for the H3K27me3 Polycomb epigenetic mark, revealing that inactivation of STAG2 can activate Polycomb signaling in GBM. Together these findings illuminate the landscape of STAG2-regulated genes, A/B compartments, chromatin loops, and pathways in GBM, providing important clues into the still mysterious mechanism of STAG2 tumor suppression in human cancer.

2024-05-07 | GSE240343 | 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