Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Stepwise activities of mSWI/SNF family chromatin remodeling complexes direct T cell activation and exhaustion [ATAC-seq]

ABSTRACT: Stepwise activities of mSWI/SNF family chromatin remodeling complexes direct T cell activation and exhaustion [ATAC-seq]

PROVIDER: PRJNA875067 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR21350300_1.fastq.gz	Fastqsanger.gz
	SRR21350300_2.fastq.gz	Fastqsanger.gz
	SRR21350301_1.fastq.gz	Fastqsanger.gz
	SRR21350301_2.fastq.gz	Fastqsanger.gz
	SRR21350302_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 88

Similar Datasets

Stepwise activities of mSWI/SNF family chromatin remodeling complexes direct T cell activation and exhaustion [Cut&Tag]

Project description:This study comprehensively profiles the mSWI/SNF complexes throughout acute and chronic T cell stimulation, with and without small molecular inhibitors and degraders. Specifically, we find pan SWI/SNF and complex specific roles in both activation and exhaustion.

2023-03-21 | GSE212347 | GEO

Stepwise activities of mSWI/SNF family chromatin remodeling complexes direct T cell activation and exhaustion [ATAC-seq]

2023-03-21 | GSE212339 | GEO

Stepwise activities of mSWI/SNF family chromatin remodeling complexes direct T cell activation and exhaustion [RNA-seq]

2023-03-21 | GSE212353 | GEO

Stepwise activities of mSWI/SNF family chromatin remodeling complexes direct T cell activation and exhaustion

Project description:Stepwise activities of mSWI/SNF family chromatin remodeling complexes direct T cell activation and exhaustion

| PRJNA875103 | ENA

Stepwise activities of mSWI/SNF family chromatin remodeling complexes direct T cell activation and exhaustion [Cut&Tag]

Project description:Stepwise activities of mSWI/SNF family chromatin remodeling complexes direct T cell activation and exhaustion [Cut&Tag]

| PRJNA875095 | ENA

Stepwise activities of mSWI/SNF family chromatin remodeling complexes direct T cell activation and exhaustion [RNA-seq]

Project description:Stepwise activities of mSWI/SNF family chromatin remodeling complexes direct T cell activation and exhaustion [RNA-seq]

| PRJNA875107 | ENA

Stepwise activities of mSWI/SNF family chromatin remodeling complexes direct T cell activation and exhaustion.

Project description:Highly coordinated changes in gene expression underlie T cell activation and exhaustion. However, the mechanisms by which such programs are regulated and how these may be targeted for therapeutic benefit remain poorly understood. Here, we comprehensively profile the genomic occupancy of mSWI/SNF chromatin remodeling complexes throughout acute and chronic T cell stimulation, finding that stepwise changes in localization over transcription factor binding sites direct site-specific chromatin accessibility and gene activation leading to distinct phenotypes. Notably, perturbation of mSWI/SNF complexes using genetic and clinically relevant chemical strategies enhances the persistence of T cells with attenuated exhaustion hallmarks and increased memory features in vitro and in vivo. Finally, pharmacologic mSWI/SNF inhibition improves CAR-T expansion and results in improved anti-tumor control in vivo. These findings reveal the central role of mSWI/SNF complexes in the coordination of T cell activation and exhaustion and nominate small-molecule-based strategies for the improvement of current immunotherapy protocols.

| S-EPMC10121856 | biostudies-literature

Stepwise activities of mSWI/SNF family chromatin remodeling complexes direct T cell activation and exhaustion

Project description:This SuperSeries is composed of the SubSeries listed below.

2023-03-21 | GSE212357 | GEO

Shifted assembly and function of mSWI/SNF family subcomplexes underlie targetable dependencies in endometriod carcinomas

Project description:The mammalian SWI/SNF (mSWI/SNF) family of chromatin remodelers govern cell type-specific chromatin accessibility and gene expression and assemble as three distinct complexes: canonical BAF (cBAF), Polybromo-associated BAF (PBAF), and non-canonical BAF (ncBAF). ARID1A and ARID1B are paralog subunits that specifically nucleate the assembly of cBAF complexes and are frequently dual deleted in highly aggressive differentiated endometrial carcinomas (DECs). Here, in cellular models and primary human tumors, we find that ARID1A/B-mediated cBAF loss results in increased ncBAF and PBAF biochemical abundance and function genome-wide to maintain the DEC oncogenic signature. Further, treatment of ARID1A/1B-mutant cell lines and PDX models in vivo with a clinical-grade SMARCA4/2 ATPase inhibitor, FHD-286, markedly attenuates cell proliferation and tumor growth, and synergizes with carboplatin-based chemotherapy. Taken together, these findings reveal the oncogenic contributions of shifted of mSWI/SNF family complex abundance and chromatin-level gene regulatory functions and suggest therapeutic utility of mSWI/SNF complex small molecule inhibitors in dedifferentiated endometrial carcinoma and other cBAF-disrupted cancer types.

2025-08-07 | PXD058236 | Pride

Structural and functional properties of mSWI/SNF chromatin remodeling complexes revealed through single-cell perturbation and genomic profiling

Project description:Mammalian SWI/SNF (mSWI/SNF or BAF) chromatin remodeling complexes play critical roles in regulating DNA accessibility and gene expression and are comprised of three final-form assemblies, cBAF, PBAF, and ncBAF, which exhibit distinct modular organization, chromatin targeting, and roles in disease. However, the contributions of each subcomplex and their constituent subunits to gene expression remain incompletely defined. Here, we performed a large-scale CRISPR-Cas9 knockout screen targeting mSWI/SNF subunits individually and in selected combinations, followed by single-cell RNA-sequencing (Perturb-seq) and SHARE-Seq. We uncover complex- and module-specific contributions across cell regulatory pathways, define paralog subunit relationships, and identify shifted functions upon perturbations. Finally, we superimpose single-cell perturbation signatures over bulk primary human tumor gene expression profiles, defining unique subunit-specific signatures and identifying tumor features that mirror BAF loss-of-function. Taken together, these data highlight the utility of large-scale single-cell genomics to uncover gene expression and chromatin accessibility signatures in human disease states.

2023-04-05 | GSE200201 | 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