Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Genome binding of SMARCA2 and SMARCA4 in lung cancer cells reconstituted with SMARCA4 WT with and without SMARCA2 depletion

ABSTRACT: Using ChIP-seq, we identified the genome-wide occupancy of SMARCA2 and SMARCA4 in lung cancer cells (NCI-H1944) reconstituted with SMARCA4 WT. We also determined how SMARCA4 occupancy changed in NCI-H1944 after SMARCA2 depletion.

ORGANISM(S): Homo sapiens

PROVIDER: GSE147201 | GEO | 2020/09/10

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

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

Expression profiling of lung cancer cells reconstituted with SMARCA4 WT and mutant K785R after SMARCA2 knockdown

Project description:Using RNA-seq, we identified the expression changes in lung cancer cells (NCI-H1944) transduced with control or SMARCA2-targeting hairpins. We also identified the SMARCA2 program that is rescued by SMARCA4 WT and SMARCA4 K785R transduced. The "SAMPLE_ID" sample characteristic is a sample identifier internal to Genentech. The ID of this project in Genentech's ExpressionPlot database is PRJ0034746

2020-09-10 | GSE144843 | GEO

Genome binding of SMARCA2 and SMARCA4 in lung cancer cells reconstituted with SMARCA4 WT with and without SMARCA2 depletion

Project description:Genome binding of SMARCA2 and SMARCA4 in lung cancer cells reconstituted with SMARCA4 WT with and without SMARCA2 depletion

| PRJNA613396 | ENA

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

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

| PRJNA605115 | ENA

Selective PROTAC-mediated degradation of SMARCA2 is efficacious in SMARCA4 mutant cancers

Project description:The mammalian SWI/SNF helicase SMARCA4 is frequently mutated in cancer and inactivation results in a cellular dependence on its paralog, SMARCA2, thus making SMARCA2 an attractive synthetic lethal target. However, published data indicates that achieving a high degree of SMARCA2 selectivity is likely essential to afford an acceptable therapeutic index and this has been a considerable challenge due to the homology between paralogs. Herein we report the discovery of the first potent and selective SMARCA2 proteolysis-targeting chimera (PROTAC) molecule. Selective degradation was achieved in the absence of selective PROTAC binding and translated to potent in vitro growth inhibition and in vivo efficacy in SMARCA4 mutant models, compared to wild type models. Global ubiquitin mapping and proteome profiling revealed no unexpected off-target degradation. Our study thus highlights the ability to transform a non-selective SMARCA2-binding ligand into a selective and efficacious in vivo SMARCA2 PROTAC, providing a potential therapeutic opportunity for SMARCA4 mutant patients.

2022-09-22 | PXD036865 | Pride

Gene expression profiling on isogenic lines expressing wild-type and mutant forms of SMARCA2 and SMARCA4

Project description:SMARCA2 and SMARCA4 are two mutually exclusive ATPase subunits of SWI/SNF complex. SMARCA4 deficient lung cancer population selectively depend on SMARCA2 for cancer growth phenotype. Rescue experiments with ectopic expression of wild-type, bromodomain mutant and ATPase dead SMARCA2 and SMARCA4 highlight that ATPase domain is the drug target. In this study, we performed genome-wide microarray and differential gene expression profiling on isogenic lung cancer lines expressing cDNA rescue constructs for wild-type, bromodomain mutant and ATPase dead SMARCA2 and SMARCA4

2015-07-21 | GSE69088 | GEO

Heterozygous mutations in SMARCA2 lead to impaired neurogenesis due to global retargeting of SMARCA4

Project description:Mammalian SWI/SNF complexes are multi-subunit chromatin remodeling complexes associated with an ATPase, either SMARCA4 or SMARCA2. Heterozygous mutations in the SMARCA2 ATPase cause Nicolaides-Baraitser Syndrome (NCBRS), an intellectual disability syndrome associated with delayed speech onset. We engineered human embryonic stem cells (hESCs) to carry NCBRS-associated heterozygous SMARCA2 K755R or R1159Q mutations. While SMARCA2 mutant hESCs were phenotypically normal, differentiation to neural progenitors cells (NPCs) was severely impaired. We find that SMARCA2 mutations cause enhancer reorganization with loss of SOX3-dependent neural enhancers and prominent emergence of astrocyte-specific de novo enhancers. Changes in chromatin accessibility at enhancers were associated with an increase in SMARCA2 binding and retargeting of SMARCA4. We show that AP-1 family member FRA2 is aberrantly overexpressed in SMARCA2 mutant NPCs, where it functions as a pioneer factor at de novo enhancers. Together, our results demonstrate SMARCA2 mutations cause impaired differentiation through enhancer reprogramming via inappropriate targeting of SMARCA4.

2019-07-30 | GSE122631 | GEO

Selective PROTAC-mediated degradation of SMARCA2 is efficacious in SMARCA4 mutant cancers

2022-03-31 | MSV000089176 | MassIVE

Expression profiling of lung cancer cells reconstituted with SMARCA4 WT and mutant K785R after SMARCA2 knockdown

Project description:Expression profiling of lung cancer cells reconstituted with SMARCA4 WT and mutant K785R after SMARCA2 knockdown

| PRJNA605123 | ENA

ATAC-seq analysis for OVSAHO cells with upregulated SMARCA2 and downregulated SMARCA4 expression

Project description:The goal of this study is to explore the underlying mechanism which contributes to chemoresistance in high-grade serous carcinoma (HGSC) with low SMARCA4 and high SMARCA2 expression.

2023-02-07 | GSE212885 | 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