Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Chromatin profiling following SWI/SNF inhibition in H295R or HEK 293T cells [ChIP-seq]

ABSTRACT: To assess the genome-wide effect of acute SWI/SNF inhibition on SF-1/β-catenin chromatin binding, we treated H295R or HEK 293T cells with 1 µM of SWI/SNF inhibitor BRM014 or DMSO vehicle control for 1 hour and performed ChIP-seq. Pronounced loss of chromatin occupancy was observed for SF-1 and β-catenin at enhancer sites bound by ARID1A-containing cBAF complexes.

ORGANISM(S): Homo sapiens

PROVIDER: GSE260867 | GEO | 2025/07/21

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Effect of SWI/SNF inhibition on gene expression in hormone-producing cells [RNA-seq]

Project description:To test the functional dependency of SF-1-dependent gene expression on SWI/SNF catalytic activity, we treated two human steroidogenic adrenocortical carcinoma (ACC) cell lines H295R and CU-ACC1 with 1 μM of SWI/SNF inhibitor BRM014 or equal volume of DMSO for 72 hours and performed RNA-seq. SWI/SNF inhibition strongly reduced the expression of steroidogenic genes targeted by the transcription factor SF-1, as well SF-1 (NR5A1) and β-catenin (CTNNB1) themselves.

2025-07-21 | GSE261006 | GEO

β-catenin functions as a molecular adapter for disordered cBAF interactions

Project description:BAF (SWI/SNF) chromatin remodelers engage binding partners to generate sitespecific DNA accessibility. However, the basis for interactions between BAF and divergent binding partners has remained unclear. Here we tested the hypothesis that scaffold proteins augment BAF’s binding repertoire by examining β-catenin and steroidogenic factor-1 (SF-1, NR5A1), a β-catenin–dependent transcription factor central to steroid production. In steroidogenic cell lines, BAF inhibition rapidly opposed overlapping SF-1/β-catenin enhancer occupancy, thereby impairing SF-1 target activation, steroid production, and SF-1/β-catenin autoregulation. These effects arise due to β-catenin’s role as an adapter between SF-1 and an intrinsically disordered region (IDR) of the canonical BAF (cBAF) subunit ARID1A. In contrast to exclusively IDR-driven mechanisms, folded Armadillo repeats on β-catenin were required to bind cBAF. β-catenin similarly linked cBAF to SOX2, FOXO3, YAP1, and CBP/p300. Visualization of contacts highlighted β-catenin’s central role in IDR-dependent interaction of cBAF with diverse transcription factors and chromatin regulators. The cross-linking dataset was used to validate the interaction interface obtained with computational modelling.

2025-07-11 | PXD063603 | Pride

DNA accessibility sites requiring SWI/SNF or β-catenin activity [ATAC-seq]

Project description:To reveal the effects of β-catenin knockout or acute SWI/SNF (BAF) inhibition on chromatin accessibility, we performed knockout of β-catenin or treated cells with 1 µM of BAF inhibitor BRM014 or DMSO vehicle control and performed ATAC-seq. Analysis of altered DNA accessibility in H295R cells revealed that sites with Steroidogenic Factor-1 (SF-1) motifs had the strongest loss of DNA accessibility. In HEK 293T cells, sites with motifs belonging to β-catenin binding partners (specifically YAP binding-partner TEAD, SOX, or FOXO motifs) had loss of DNA accessibility upon either BAF inhibition or β-catenin knockout.

2025-07-21 | GSE260866 | GEO

Expression data from human adrenocortical H295R cells expressing a doxycyclin-inducible shRNA targeting CTNNB1

Project description:We used the H295R cell line, human adrenocortical cells, harboring a heterozygous CTNNB1 (beta-catenin) gene mutation affecting the GSK3 beta-phosphorylation site (S45P) and leading to constitutive transcriptional activity of beta-catenin-LEF/TCF. Whole-transcript gene expression was analyzed in three stable clones of H295R cells expressing a doxycycline-inducible shRNA targeting CTNNB1 mRNA and in a control clone, without or with doxycycline for 5 days.

2015-08-03 | E-MTAB-3330 | biostudies-arrayexpress

The TRIP12 E3 Ligase Induces Interaction Between the SWI/SNF Component BRG1 and Beta-catenin to Promote Wnt Signaling

Project description:SWItch/Sucrose Non-Fermentable (SWI/SNF) chromatin remodeling complexes displace nucleosomes to promote the access of transcription factors to enhancers and promoters. Despite the critical roles of SWI/SNF in animal development and tumorigenesis, how signaling pathways recruit SWI/SNF complexes to their target genes is unclear. Here, we demonstrate that target gene activation mediated by Beta-catenin, the essential transcriptional coactivator in the Wnt signal transduction pathway, requires ubiquitylation of the SWI/SNF component Brahma-related gene-1 (BRG1) by the E3 ubiquitin ligase Thyroid Hormone Receptor Interactor 12 (TRIP12). TRIP12 depletion in Drosophila, zebrafish, mouse organoids, and human cells attenuates Wnt signaling. Genetic epistasis experiments place TRIP12 activity downstream of the Beta-catenin destruction complex. TRIP12 interacts with and ubiquitylates BRG1, and BRG1 depletion blocks TRIP12-mediated Wnt pathway activation. TRIP12 promotes BRG1 binding to Beta-catenin in the presence of Wnt. Our findings support a model in which TRIP12 ubiquitylates BRG1 in the presence of Wnt and promotes its interaction with Beta-catenin, thereby bringing SWI/SNF to Wnt target genes. Our studies suggest a general mechanism by which cell signaling induces the interaction between BRG1 and pathway-specific transcription factors to recruit SWI/SNF complexes to their appropriate target genes.

2024-01-06 | MSV000093784 | MassIVE

Chromatin profiling following SWI/SNF inhibition in H295R or HEK 293T cells [ChIP-seq]

Project description:Chromatin profiling following SWI/SNF inhibition in H295R or HEK 293T cells [ChIP-seq]

| PRJNA1083884 | ENA

Expression data from H295R cells in basal conditions/overexpressing SF-1

2013-08-01 | GSE43032 | GEO

Expression data from H295R cells in basal conditions/overexpressing SF-1

Project description:SF-1 is a nuclear receptor transcription factor playing a key role in adrenogonadal development and in adrenocortical tumorigenesis when overexpressed. We studied gene expression profiles using Affymetrix microarrays in the H295R/TR SF-1 adrenocortical cancer cell line, where SF-1 expression can be increased in a doxycycline-dependent manner (Mol. Endocrinol. 21: 2968–2987, 2007) H295R/TR SF-1 cells were cultured either in basal conditions or with doxycycline (Dox) added to the culture medium for 72 hours. RNA was extracted and hybridized to HG-U133 Plus 2.0 Affymetrix microarrays.

2013-08-01 | E-GEOD-43032 | biostudies-arrayexpress

SWI/SNF-dependent genes are defined by their chromatin landscape [ChIP-seq_2]

Project description:The SWI/SNF complex was the first chromatin remodeling machinery discovered. Although it has been extensively investigated, numerous aspects of its regulation and activity are still poorly understood, especially in higher eukaryotes. In mammals, there is not a single SWI/SNF complex (also called BRM or BRG1 associated factors, BAF, complex) but rather a polymorphic family of complexes, with three main subtypes called canonical BAF (cBAF), polybromo-associated BAF (PBAF), and non-canonical BAF (ncBAF), with relatively different specificities. The enzymatic motors of the complexes are two mutually exclusive ATPases of the SNF2 family called BRAHMA (BRM, also called SMARCA2) and BRAHMA RELATED GENE 1 (BRG1, also called SMARCA4). Recently, an specific inhibitor of BRM and BRG1 ATPase activity, called BRM014, has been developed. We have extensively investigated the effect of BRM014 on the transcriptome and the chromatin landscape of non-tumoral normal murine mammary (NMuMG) epithelial cells.

2024-03-08 | GSE249211 | GEO

SWI/SNF-dependent genes are defined by their chromatin landscape [RNA-seq]

2024-03-08 | GSE226953 | GEO