Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Mus musculus

ABSTRACT: Effects of dominant-negative Smarca4 mutations on the DNA accessibility landscape [ATAC-seq]

PROVIDER: PRJNA385199 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR5499350_1.fastq.gz	Fastqsanger.gz
	SRR5499350_2.fastq.gz	Fastqsanger.gz
	SRR5499351_1.fastq.gz	Fastqsanger.gz
	SRR5499351_2.fastq.gz	Fastqsanger.gz
	SRR5499352_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 28

Similar Datasets

Dominant-negative SMARCA4 mutants alter the accessibility landscape of tissue-unrestricted enhancers

Project description:Dominant-negative SMARCA4 mutants alter the accessibility landscape of tissue-unrestricted enhancers

| PRJNA385658 | ENA

Mus musculus

Project description:Transcriptional effects of dominant-negative G784E Smarca4 mutation in mouse embryonic stem cells [RNA-seq]

| PRJNA385176 | ENA

Re-expression of SMARCA4/BRG1 in Small Cell Carcinoma of Ovary, Hypercalcemic Type (SCCOHT) promotes an epithelial-like gene signature through an AP-1-dependent mechanism

Project description:Small cell carcinoma of the ovary, hypercalcemic type (SCCOHT) is a rare and aggressive form of ovarian cancer. SCCOHT tumors have inactivating mutations in SMARCA4 (BRG1), one of the two mutually exclusive ATPases of the SWI/SNF chromatin remodeling complex. To address the role that BRG1 loss plays in SCCOHT tumorigenesis, we performed integrative multi-omic analyses in SCCOHT cell lines +/- BRG1 re-expression. BRG1 re-expression induced a gene and protein signature similar to an epithelial cell and gained chromatin accessibility sites correlated with other epithelial originating TCGA tumors. Furthermore, AP-1 motifs were enriched at the promoters of highly upregulated epithelial genes. Using a dominant negative AP-1 cell line, we found that both AP-1 DNA binding activity and BRG1 re-expression are necessary for the gene and protein expression of epithelial genes. Our study demonstrates that BRG1 re-expression drives an epithelial-like gene and protein signature in SCCOHT cells that depends upon AP-1 activity.

2021-01-15 | PXD014134 | Pride

Chromatin accessibility of lung cancer cells reconstituted with SMARCA4 WT or SMARCA4 mutants with and without SMARCA2 depletion

Project description:Using ATAC-seq, we identified the accessibility changes in lung cancer cells (NCI-H1944) reconstituted with SMARCA4 WT or SMARCA4 mutants. We also determined the SMARCA2-regulated accessibility program in NCI-H1944 after SMARCA2 depletion. Lastly, we identified the SMARCA2 accessibility program that is rescued by SMARCA4 WT and mutants. The "SAMPLE_ID" sample characteristic is a sample identifier internal to Genentech.

2020-09-10 | GSE144840 | GEO

DNA accessibility sites requiring SMARCA4 activity in neuroblastoma cells [ATAC-seq]

Project description:To reveal the genome-wide targets of SWI/SNF complexes in neuroblastoma cells, we performed ATAC-seq in IMR-32 cells with or without SMARCA4 inactivation. To identify changes in DNA accessibility following SMARCA4 inactivation, we used either the small-molecule catalytic inhibitor BRM014, auxin-induced degradation of IMR-32 cells engineered with SMARCA4 tagged to the minimal auxin-induced degron (SMARCA4-mAID), or the corresponding vehicle controls. Analysis of these locations reveal that SMARCA4-dependent sites are located at enhancers used by the neuroblastoma core regulatory circuitry.

2023-10-24 | GSE190706 | GEO

Mus musculus

Project description:Effects of dominant-negative G784E Smarca4 mutation on enhancer marks and factors in mouse embryonic stem cells [ChIP-seq]

| PRJNA385663 | ENA

DNA accessibility sites requiring SMARCA4 activity in neuroblastoma cells [ATAC-seq]

Project description:DNA accessibility sites requiring SMARCA4 activity in neuroblastoma cells [ATAC-seq]

| PRJNA788139 | ENA

DNase-seq profile of mES cells treated with PFA/Noco/5aza, at different timepoints within in vitro mouse differentiation protocols, or in the presence of a NFYA dominant negative construct

Project description:The aim of this experiment was to profile the DNase-I accessibility landscape in mES when treated with various factors effecting genomic methylation, at day 5 of a non-standard in vitro mouse differentiation protocol, and at days 2, 3, 5, 6, 7 within our in vitro pancreas mouse differentiation protocol, as well as day 6 along an intestinal branch (int) and day 7 along an anterior endoderm branch (ae). The profiles surrounding the binding sites of NFYA were studied in the presence of a NFYA dominant negative construct. Separate fractions were taken for DNA cleavages of length 50-100bp and 175-400bp.

2015-03-30 | E-MTAB-3465 | biostudies-arrayexpress

Drosophila photoreceptor chromatin accessibility landscape upon disruption of Clock activity [ClkATACseq]

Project description:We report the chromatin accessibility landscape of Drosophila photoreceptor neurons obtained using a tissue-specific approach at different time points after eclosion upon expression of a Clock dominant negative mutant

2021-12-31 | GSE183746 | GEO

Systematic characterization of BAF mutations explains intra-complex synthetic lethalities

Project description:Aberrations in genes coding for subunits of the BAF chromatin remodeling complex are highly abundant in human cancers. Currently, it is not understood how these loss-of-function mutations contribute to cancer development and how they can be targeted therapeutically. The cancer type specific occurrence patterns of certain subunit mutations suggest subunit-specific effects on BAF complex function, possibly by the formation of aberrant residual complexes. Here, we systematically characterize the effects of individual subunit loss on complex composition, chromatin accessibility and gene expression in a panel of knock-out cell lines deficient for 22 targetable BAF subunits. We observe strong, specific and often discordant alterations dependent on the targeted subunit and show that these explain intra-complex co-dependencies, including the novel synthetic lethal interactions SMARCA4-ARID2, SMARCA4-ACTB and SMARCC1-SMARCC2. These data provide insights into the role of different BAF subcomplexes in genome-wide chromatin organization and suggest novel approaches to therapeutically target BAF mutant cancers.

2019-08-01 | PXD013102 | Pride

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