U.S. flag

An official website of the United States government

Format
Items per page
Sort by

Send to:

Choose Destination

Links from GEO DataSets

Items: 20

1.

Multiple interactions of the oncoprotein transcription factor MYC with the SWI/SNF chromatin remodeler

(Submitter supplied) We report that even though SNF5 is the most well-documented SWI/SNF subunit to bind MYC, MYC can use multiple interaction surfaces to interact with SWI/SNF subunits independently of SNF5. In line with this, MYC interacts with the pan-SWI/SNF subunit, BAF155, in multiple SNF5-null malignant rhabdoid tumor (MRT) cell lines and almost all of MYC co-localizes with SWI/SNF subunits on chromatin in MRT. In the MRT cell line, G401, MYC binds to essential genes, although for a purpose that appears distinct from chromatin remodeling, and loss of MYC leads to widespread gene expression changes. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing; Expression profiling by high throughput sequencing; Other
Platform:
GPL24676
30 Samples
Download data: BED, TXT
2.

Inhibition of MYC by the SMARCB1 tumor suppressor

(Submitter supplied) We report that the protein encoded by the SMARCB1 gene, SNF5, is capable of inhibiting MYC binding in vitro and in a malignant rhabdoid tumor (MRT) cell line. By comparing the effects of reintroduction of SNF5 with genetic inhibition of MYC (OMOMYC) on multiple aspects of chromatin remodeling and transcription in MRT cells, we show that regulation of MYC binding by SNF5 is not connected to the role of SNF5 in chromatin remodeling, but instead is responsible for controlling RNA polymerase pause release during transcription. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL18573 GPL16791
30 Samples
Download data: NARROWPEAK, TXT
3.

Loss of Snf5 and the formation of an aberrant SWI/SNF complex

(Submitter supplied) Aberrant forms of the SWI/SNF chromatin remodeling complex are associated with human disease. Loss of the Snf5 subunit of SWI/SNF is a driver mutation in pediatric rhabdoid cancers and forms aberrant sub-complexes that are not well characterized. We determined the effects of loss of Snf5 on the composition, nucleosome binding, recruitment and remodeling activities of yeast SWI/SNF. The Snf5 subunit interacts with the ATPase domain of Snf2 and forms a submodule consisting of Snf5, Swp82 and Taf14 as shown by mapping SWI/SNF subunit interactions by crosslinking-mass spectrometry and subunit deletion followed by immunoaffinity chromatography. more...
Organism:
Saccharomyces cerevisiae
Type:
Expression profiling by high throughput sequencing
Platform:
GPL17342
12 Samples
Download data: TXT
Series
Accession:
GSE85460
ID:
200085460
4.

BRD9 defines a novel SWI/SNF sub-complex and constitutes a specific vulnerability in malignant rhabdoid tumors [RNA-seq 2]

(Submitter supplied) Bromodomain-containing protein 9 (BRD9) was recently identified to be associated with the chromatin remodeling SWI/SNF(BAF) complex, yet its function within the complex has remained unclear. Here, using genome-scale CRISPR-Cas9 screens, we found that BRD9 constitutes a specific vulnerability in highly malignant pediatric rhabdoid tumors, which are driven by inactivating mutations of SMARCB1 subunit of SWI/SNF complexes. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL18573
16 Samples
Download data: TXT
5.

BRD9 defines a novel SWI/SNF sub-complex and constitutes a specific vulnerability in malignant rhabdoid tumors

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL18573
31 Samples
Download data: BW, TXT
Series
Accession:
GSE120235
ID:
200120235
6.

BRD9 defines a novel SWI/SNF sub-complex and constitutes a specific vulnerability in malignant rhabdoid tumors [ChIP-seq]

(Submitter supplied) Bromodomain-containing protein 9 (BRD9) was recently identified to be associated with the chromatin remodeling SWI/SNF(BAF) complex, yet its function within the complex has remained unclear. Here, using genome-scale CRISPR-Cas9 screens, we found that BRD9 constitutes a specific vulnerability in highly malignant pediatric rhabdoid tumors, which are driven by inactivating mutations of SMARCB1 subunit of SWI/SNF complexes. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL18573
11 Samples
Download data: BW
Series
Accession:
GSE120234
ID:
200120234
7.

BRD9 defines a novel SWI/SNF sub-complex and constitutes a specific vulnerability in malignant rhabdoid tumors [RNA-seq]

(Submitter supplied) Bromodomain-containing protein 9 (BRD9) was recently identified to be associated with the chromatin remodeling SWI/SNF(BAF) complex, yet its function within the complex has remained unclear. Here, using genome-scale CRISPR-Cas9 screens, we found that BRD9 constitutes a specific vulnerability in highly malignant pediatric rhabdoid tumors, which are driven by inactivating mutations of SMARCB1 subunit of SWI/SNF complexes. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL18573
4 Samples
Download data: TXT
8.

SMARCB1-mediated SWI/SNF complex function is essential for enhancer regulation

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing; Expression profiling by high throughput sequencing
Platforms:
GPL15520 GPL16791 GPL11154
116 Samples
Download data: WIG
Series
Accession:
GSE71506
ID:
200071506
9.

SMARCB1-mediated SWI/SNF complex function is essential for enhancer regulation [cell line_RNA-seq]

(Submitter supplied) SMARCB1 (SNF5/INI1/BAF47), a core subunit of the SWI/SNF (BAF) chromatin remodeling complex, is inactivated in nearly all pediatric rhabdoid tumors. These aggressive cancers are among the most genomically stable, suggesting an epigenetic mechanism by which SMARCB1 loss drives transformation. Here, we show that despite indistinguishable mutational landscapes, human RTs show distinct enhancer H3K27ac signatures, which reveal remnants of differentiation programs. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL11154
34 Samples
Download data: WIG
10.

SMARCB1-mediated SWI/SNF complex function is essential for enhancer regulation [cell line_ChIP-seq]

(Submitter supplied) SMARCB1 (SNF5/INI1/BAF47), a core subunit of the SWI/SNF (BAF) chromatin remodeling complex, is inactivated in nearly all pediatric rhabdoid tumors. These aggressive cancers are among the most genomically stable, suggesting an epigenetic mechanism by which SMARCB1 loss drives transformation. Here, we show that despite indistinguishable mutational landscapes, human RTs show distinct enhancer H3K27ac signatures, which reveal remnants of differentiation programs. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL15520 GPL11154
38 Samples
Download data: WIG
Series
Accession:
GSE71504
ID:
200071504
11.

SMARCB1-mediated SWI/SNF complex function is essential for enhancer regulation [primary tissue_RNA-seq]

(Submitter supplied) SMARCB1 (SNF5/INI1/BAF47), a core subunit of the SWI/SNF (BAF) chromatin remodeling complex, is inactivated in nearly all pediatric rhabdoid tumors. These aggressive cancers are among the most genomically stable, suggesting an epigenetic mechanism by which SMARCB1 loss drives transformation. Here, we show that despite indistinguishable mutational landscapes, human RTs show distinct enhancer H3K27ac signatures, which reveal remnants of differentiation programs. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL11154
3 Samples
Download data: WIG
12.

SMARCB1-mediated SWI/SNF complex function is essential for enhancer regulation [primary tissue_ChIP-seq]

(Submitter supplied) SMARCB1 (SNF5/INI1/BAF47), a core subunit of the SWI/SNF (BAF) chromatin remodeling complex, is inactivated in nearly all pediatric rhabdoid tumors. These aggressive cancers are among the most genomically stable, suggesting an epigenetic mechanism by which SMARCB1 loss drives transformation. Here, we show that despite indistinguishable mutational landscapes, human RTs show distinct enhancer H3K27ac signatures, which reveal remnants of differentiation programs. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL11154 GPL16791
41 Samples
Download data: WIG
Series
Accession:
GSE71502
ID:
200071502
13.

The SWI/SNF ATPase BRG1 facilitates multiple pro-tumorigenic gene expression programs in SMARCB1-deficient cancer cells

(Submitter supplied) Here, we expose the connection between rSWI/SNF and oncogenic processes using a well-characterized chemical degrader to deplete the SWI/SNF ATPase, BRG1. Using a combination of gene expression and chromatin accessibility assays we show that rSWI/SNF complexes facilitate MYC target gene expression. We also find that rSWI/SNF maintains open chromatin at sites associated with hallmark cancer genes linked to the AP-1 transcription factor, suggesting that AP-1 may drive oncogenesis in MRT.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL24676
12 Samples
Download data: BED, TXT
Series
Accession:
GSE198156
ID:
200198156
14.

Genome-wide maps of histone modification and chromatin remodeler binding in acute myeloid leukemia blast cells and normal hematopoietic cells

(Submitter supplied) We have used chromatin immunoprecipitation followed by high throughput sequencing to map regions of chromatin remodeler binding accompanied by histone modification state. We have used this data to distinguish between the transcriptional state of regulatory genes in leukemic and normal hematopoietic cells, and thus understand contribution of the chromatin remodeler towards leukemogenesis.
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL16791
24 Samples
Download data: BED
Series
Accession:
GSE108976
ID:
200108976
15.

mSWI/SNF functional genomic characterization of SMARCB1 mutants in SMARCB1-null and heterozygous settings

(Submitter supplied) Chromatin remodeling complexes regulate gene expression by shifting, evicting, and exchanging nucleosomes along the chromosomes of eukaryotic organisms. The mammalian SWI/SNF chromatin remodeling complex (mSWI/SNF or BAF) is mutated in over 20% of human cancers and loss of the SMARCB1 gene, encoding the BAF47 protein subunit, results in one of the most aggressive and lethal pediatric cancers. An accumulation of point mutations occurs at the C-terminal end of the protein, for which the functional ramifications are unknown. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL24676 GPL18573
102 Samples
Download data: BW
Series
Accession:
GSE124903
ID:
200124903
16.

Next Generation Sequencing Facilitates Quantitative Analysis of in 14-day-old wt, syd-5 and swi3d-1 seedlings [RNA-seq]

(Submitter supplied) To investigate the cooperative function swi3d-1 and syd-5 in regulating plant development. We then performed gene expression profiling analysis using data obtained from RNA-seq of 14-day-old wt, syd-5 and swi3d-1 seedlings under long day condition.
Organism:
Arabidopsis
Type:
Expression profiling by high throughput sequencing
Platform:
GPL27784
9 Samples
Download data: XLSX
Series
Accession:
GSE218842
ID:
200218842
17.

Organization, genomic targeting and assembly of three distinct SWI/SNF chromatin remodeling complexes in Arabidopsis [ChIP-seq]

(Submitter supplied) Switch defective/sucrose non-fermentable (SWI/SNF) complexes are evolutionarily conserved multi-subunit machines that play vital roles in chromatin architecture regulation for modulating gene expression via sliding or ejection of nucleosomes in eukaryotes. In plants, perturbations of SWI/SNF subunits often result in severe developmental disorders. However, the subunit composition, pathways of assembly, and genomic targeting of the plant SWI/SNF complexes remain undefined. more...
Organism:
Arabidopsis
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL27784
26 Samples
Download data: BED, BIGWIG, NARROWPEAK
Series
Accession:
GSE218841
ID:
200218841
18.

The SWI/SNF chromatin remodeling complex is required for lineage specific enhancer activity

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing; Expression profiling by high throughput sequencing
Platform:
GPL13112
41 Samples
Download data: WIG
Series
Accession:
GSE71509
ID:
200071509
19.

The SWI/SNF chromatin remodeling complex is required for lineage specific enhancer activity [MEF_RNA-seq]

(Submitter supplied) Genes encoding subunits of SWI/SNF (BAF) chromatin remodeling complexes are collectively altered in over 20% of all human malignancies, but the mechanisms by which these complexes alter chromatin to modulate transcription and control cell fate are poorly understood. Utilizing both loss-of-function and gain-of-function approaches, here we show that SWI/SNF complexes are preferentially targeted to distal enhancers and interact with p300 to regulate transcription via modulation of histone H3 lysine 27 acetylation. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL13112
6 Samples
Download data: WIG
Series
Accession:
GSE71508
ID:
200071508
20.

The SWI/SNF chromatin remodeling complex is required for lineage specific enhancer activity [MEF_ChIP]

(Submitter supplied) Genes encoding subunits of SWI/SNF (BAF) chromatin remodeling complexes are collectively altered in over 20% of all human malignancies, but the mechanisms by which these complexes alter chromatin to modulate transcription and control cell fate are poorly understood. Utilizing both loss-of-function and gain-of-function approaches, here we show that SWI/SNF complexes are preferentially targeted to distal enhancers and interact with p300 to regulate transcription via modulation of histone H3 lysine 27 acetylation. more...
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL13112
35 Samples
Download data: BED, WIG
Series
Accession:
GSE71507
ID:
200071507
Format
Items per page
Sort by

Send to:

Choose Destination

Supplemental Content

db=gds|term=|query=1|qty=5|blobid=MCID_674ccb6130e6852f8a881ef7|ismultiple=true|min_list=5|max_list=20|def_tree=20|def_list=|def_view=|url=/Taxonomy/backend/subset.cgi?|trace_url=/stat?
   Taxonomic Groups  [List]
Tree placeholder
    Top Organisms  [Tree]

Find related data

Recent activity

Your browsing activity is empty.

Activity recording is turned off.

Turn recording back on

See more...
Support Center