Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Expression data from fibroblasts with knock-down of Brg1 and Brm

ABSTRACT: Expression data from fibroblasts with knock-down of Brg1 and Brm

PROVIDER: PRJNA595866 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

Expression data from fibroblasts with knock-down of Brg1 and Brm

Project description:We used microarrays to asses gene expression in 3T3 fibroblasts, after knock-down of Brg1 and Brm using stable shRNA interference. Cells were treated with 5ng/ml mouse TNF-alpha to stimulate inducible gene activation.

2020-02-04 | GSE142076 | GEO

Profiling of Polyadenylated RNAs after Brg1/Smarca4 knock-down in murine bone marrow-derived macrophages after LPS or LPS plus Dex stimulation [RNA-seq]

Project description:We performed Brg1 (Smarac4) knock-down by siRNA in murine primary bone marrow-derived macrophages and profiled the effect on gene expression by RNAseq after lipopolysaccharide (LPS) or LPS plus dexamethasone (Dex) treatment. Brg1 knock-down cells are compared to cells treated with a control siRNA. We analysed the requirement of Brg1/Smarca4 for the expression of inflammatory and glucocorticoid receptor target genes.

2023-10-31 | GSE186513 | GEO

Expression of SWI/SNF subunits BRG1 and BRM in C33A cells

Project description:We exogenously expressed the SWI/SNF ATPase catalytic subunits BRG1 and BRM in the lacking cell line C33A, and compared the differences with mock transfected cell at gene expression and alternative splicing level.

2022-03-17 | GSE140474 | GEO

FGFR3 knock-down

Project description:FGFR3 knock-down

| PRJNA330963 | ENA

SPARC knock down

Project description:SPARC knock down

| PRJNA327124 | ENA

Gene expression changes in adult mouse cardiomyocytes when Brg1 and Brm are knocked out

Project description:Identification of gene expression changes in wild type versus mutant mouse hearts where Brg1 and Brm were knocked out in adult cardiomyocytes.

2017-04-11 | GSE97593 | GEO

Protein-protein interactions of BRG1 or BRG1-HSA in SW13 cells

Project description:The SWI/SNF complex remodels chromatin in an ATP-dependent manner through the ATPase subunits BRG1 and BRM. Chromatin remodeling alters nucleosome structure to change gene expression, however aberrant remodeling and gene expression can result in cancer. The function and localization on chromatin of the SWI/SNF complex depends on the protein makeup of the complex. Here we report the protein-protein interactions of wild-type BRG1 or mutant BRG1 in which the HSA domain has been deleted (BRG1-HSA). We demonstrate the interaction of BRG1 with most SWI/SNF complex members and a failure of a number of these members to interact with BRG1-HSA. These results demonstrate that the HSA domain of BRG1 is a critical interaction platform for the correct formation of SWI/SNF remodeling complexes.

2023-02-15 | PXD029647 | Pride

BRG1-dependent regulation of Wnt signaling pathway during skeletal muscle differentiation

Project description:RNA-seq analysis for C2C12 myoblasts knocked down for either only-BRG1 or only-BRM or both BRG1 and BRM. Cells were treated with an siRNA SMARTpools of four oligos each targeting either BRG1 (siGENOME mouse Smarca4 pool #M-041135-01-0020) or BRM (siGENOME mouse Smarca2 pool #M-056591-00-0020) or both. Control samples were treated with non-targeting scrambled oligos (siRNA SMARTpool ON-TARGETplus scrambled non-targeting pool # D-001810-10-20). siRNA pools were purchased from Dharmacon, Horizon Discovery Ltd., USA.

2023-06-24 | GSE196283 | GEO

CRISPR/Cas9 knock down line

Project description:CRISPR/Cas9 knock down line

| PRJNA521684 | ENA

BRG1/BRM inhibitor targets AML stem cells and exerts superior preclinical efficacy combined with BET or Menin inhibitor (scRNA-Seq)

Project description:BRG1 (SMARCA4) and BRM (SMARCA2) are the mutually exclusive core ATPases of the chromatin remodeling BAF (BRG1/BRM-associated factor) complexes. They enable transcription factors/co-factors to access enhancers/promoter and modulate gene-expressions responsible for cell growth and differentiation of AML stem/progenitor cells. In AML with MLL1r (MLL1 rearrangement) or mutant (mt) NPM1, although Menin inhibitor (MI) treatment induces clinical remissions, most patients either fail to respond or relapse, some harboring Menin mutations. FHD-286 is an orally bioavailable, selective inhibitor of BRG1/BRM under clinical development in AML. Present studies show that FHD-286 induces differentiation and lethality in AML cells with MLL1r or mtNPM1, concomitantly causing perturbed chromatin accessibility and repression of c-Myc, PU.1 and CDK4/6. Co-treatment with FHD-286 and decitabine, BET inhibitor (BETi) or MI, or venetoclax synergistically induced in vitro lethality in AML cells with MLL1r or mtNPM1. In patient-derived xenograft (PDX) models of AML with MLL1r or mtNPM1, FHD-286 treatment reduced AML burden, improved survival, and attenuated AML-initiating potential of stem-progenitor cells. Compared to each drug, co-treatment with FHD-286 and BETi, MI, decitabine or venetoclax significantly reduced AML burden and improved survival, without inducing significant toxicity. These findings highlight the FHD-286-based combinations as promising therapy of AML with MLL1r or mtNPM1.

2024-03-01 | GSE252937 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

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