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Links from GEO DataSets

Items: 20

1.

SWI/SNF inactivation in the endometrial epithelium leads to loss of epithelial integrity [12Z RNA-seq]

(Submitter supplied) Although ARID1A mutations are a hallmark feature, mutations in other SWI/SNF (SWItch/Sucrose Non-Fermentable) chromatin remodeling subunits are also observed in endometrial neoplasms. Here, we interrogated the roles of Brahma/SWI2-related gene 1 (BRG1, SMARCA4), the SWI/SNF catalytic subunit, in the endometrial epithelium. BRG1 loss affects more than one-third of all active genes and highly overlaps with the ARID1A gene regulatory network. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platforms:
GPL24676 GPL18573
6 Samples
Download data: CSV, TAB
2.

SWI/SNF inactivation in the endometrial epithelium leads to loss of epithelial integrity

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens; Mus musculus
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
4 related Platforms
16 Samples
Download data: BROADPEAK, TAB
Series
Accession:
GSE152663
ID:
200152663
3.

SWI/SNF inactivation in the endometrial epithelium leads to loss of epithelial integrity [Mouse EPCAM]

(Submitter supplied) Although ARID1A mutations are a hallmark feature, mutations in other SWI/SNF (SWItch/Sucrose Non-Fermentable) chromatin remodeling subunits are also observed in endometrial neoplasms. Here, we interrogated the roles of Brahma/SWI2-related gene 1 (BRG1, SMARCA4), the SWI/SNF catalytic subunit, in the endometrial epithelium. BRG1 loss affects more than one-third of all active genes and highly overlaps with the ARID1A gene regulatory network. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platforms:
GPL19057 GPL24247
7 Samples
Download data: CSV, TAB
Series
Accession:
GSE152662
ID:
200152662
4.

SWI/SNF inactivation in the endometrial epithelium leads to loss of epithelial integrity [ChIP-seq]

(Submitter supplied) Although ARID1A mutations are a hallmark feature, mutations in other SWI/SNF (SWItch/Sucrose Non-Fermentable) chromatin remodeling subunits are also observed in endometrial neoplasms. Here, we interrogated the roles of Brahma/SWI2-related gene 1 (BRG1, SMARCA4), the SWI/SNF catalytic subunit, in the endometrial epithelium. BRG1 loss affects more than one-third of all active genes and highly overlaps with the ARID1A gene regulatory network. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL24676
3 Samples
Download data: BROADPEAK
Series
Accession:
GSE152660
ID:
200152660
5.

Co-regulation of transcription by BRG1 and Brm, two mutually exclusive SWI/SNF ATPase subunits

(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:
GPL20301 GPL18573
53 Samples
Download data: BW
Series
Accession:
GSE102561
ID:
200102561
6.

Expression analysis of genes responding to ARID1A knockdown

(Submitter supplied) Illumina array was employed to analyze the genes whose expression are altered when ARID1A gene is downregulated by shRNA in normal ovarian surface epithelial cells OSE4 and IOSE80pc. This leads to discovery of p53-regulated genes such as p21 and SMAD3.
Organism:
Homo sapiens
Type:
Expression profiling by array
Dataset:
GDS4826
Platform:
GPL10558
4 Samples
Download data: TXT
Series
Accession:
GSE37684
ID:
200037684
7.
Full record GDS4826

ARID1A depletion effect on ovarian surface epithelial cell lines

Analysis of OSE4 and IOSE80pc ovarian surface epithelial cells depleted for ARID1A, which encodes large nuclear protein p270. ARID1A depletion enhances OSE4 and IOSE80pc proliferation. OSE4 cells become highly tumorigenic upon ARID1A depletion. Results suggest a tumor-suppressor role for ARID1A.
Organism:
Homo sapiens
Type:
Expression profiling by array, transformed count, 2 cell line, 2 protocol sets
Platform:
GPL10558
Series:
GSE37684
4 Samples
Download data
8.

ARID-DNA interactions are required for promoter occupancy by SWI/SNF

(Submitter supplied) Every known SWI/SNF chromatin-remodeling complex incorporates an ARID DNA binding domain-containing subunit. Despite being a ubiquitous component of the complex, physiological roles for this domain remain undefined. Here we show that disruption of ARID1a-DNA binding in mice results in embryonic lethality, with mutant embryos manifesting prominent defects in the heart and extraembryonic vasculature. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL7202
12 Samples
Download data: TXT
Series
Accession:
GSE32116
ID:
200032116
9.

Loss of SWI/SNF Chromatin Remodeling Alters NRF2 Signaling in Non-Small Cell Lung Carcinoma

(Submitter supplied) Purpose: RNA-seq of CRISPR Knockout of SMARCA4 and SMARCA2 in H358 focused on examining the effects of the knockouts on NRF2 signaling
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24676
9 Samples
Download data: TXT
10.

Signal-dependent incorporation of MyoD-BAF60c into Brg1-based SWI/SNF chromatin-remodeling complex

(Submitter supplied) Tissue-specific transcription factors initiate differentiation toward a specialized cell type by inducing transcription-permissive chromatin modifications at target gene promoters, through the recruitment of the SWI/SNF chromatin-remodeling complex (1, 2). The molecular mechanism that regulates the chromatin re-distribution of SWI/SNF in response to differentiation signals is currently unknown. Here we show that the muscle determination factor MyoD and the SWI/SNF structural sub-unit, BAF60c (SMARCD3), form a complex on the regulatory elements of MyoD-target genes in undifferentiated myoblasts, prior to the activation of gene expression. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL6887
12 Samples
Download data: TXT
Series
Accession:
GSE24573
ID:
200024573
11.

ARID1A deficiency weakens BRG1-RAD21 interaction that jeopardizes chromatin compactness and drives HCC metastasis

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL17021
20 Samples
Download data: TXT
Series
Accession:
GSE152052
ID:
200152052
12.

ARID1A deficiency weakens BRG1-RAD21 interaction that jeopardizes chromatin compactness and drives HCC metastasis [RNA-seq]

(Submitter supplied) ARID1A, encoding a subunit of SWI/SNF chromatin remodeling complex, is widely recognized as a tumor suppressor gene in multiple tumor types including hepatocellular carcinoma (HCC). Previous studies have demonstrated that ARID1A deficiency can cause HCC metastasis, possibly due to the altered chromatin organization, however the underlying mechanisms of which remain poorly understood. Whether and how SWI/SNF complex could function as an architectural cooperator to synergistically stabilize chromatin organization should be explored, particular in tumorigenesis. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL17021
6 Samples
Download data: TXT
Series
Accession:
GSE152050
ID:
200152050
13.

ARID1A deficiency weakens BRG1-RAD21 interaction that jeopardizes chromatin compactness and drives HCC metastasis [ChIP-seq]

(Submitter supplied) ARID1A, encoding a subunit of SWI/SNF chromatin remodeling complex, is widely recognized as a tumor suppressor gene in multiple tumor types including hepatocellular carcinoma (HCC). Previous studies have demonstrated that ARID1A deficiency can cause HCC metastasis, possibly due to the altered chromatin organization, however the underlying mechanisms of which remain poorly understood. Whether and how SWI/SNF complex could function as an architectural cooperator to synergistically stabilize chromatin organization should be explored, particular in tumorigenesis. more...
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL17021
14 Samples
Download data: TXT
Series
Accession:
GSE152049
ID:
200152049
14.

ARID1A maintains transcriptionally repressive H3.3 through CHD4-ZMYND8 chromatin interactions [12Z_shARID1A_CHD4_H3.1_ChIP]

(Submitter supplied) Background: SWI/SNF (BAF) chromatin remodeling complexes regulate lineage-specific enhancer activity by promoting accessibility for diverse DNA-binding factors and chromatin regulators. Additionally, they are known to modulate the function of the epigenome through regulation of histone post-translational modifications and nucleosome composition, although the way SWI/SNF complexes govern the epigenome remains poorly understood. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL24676
10 Samples
Download data: BROADPEAK, TXT
Series
Accession:
GSE210201
ID:
200210201
15.

ARID1A-dependent maintenance of H3.3 is required for repressive CHD4-ZMYND8 chromatin interactions at super-enhancers

(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
Platform:
GPL24676
69 Samples
Download data: BROADPEAK, NARROWPEAK, TAB
Series
Accession:
GSE190557
ID:
200190557
16.

ARID1A-dependent maintenance of H3.3 is required for repressive CHD4-ZMYND8 chromatin interactions at super-enhancers [12Z_siH3F3B_siZMYND8_RNA]

(Submitter supplied) Background: SWI/SNF (BAF) chromatin remodeling complexes regulate lineage-specific enhancer activity by promoting accessibility for diverse DNA-binding factors and chromatin regulators. Additionally, they are known to modulate the function of the epigenome through regulation of histone post-translational modifications and nucleosome composition, although the way SWI/SNF complexes govern the epigenome remains poorly understood. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24676
9 Samples
Download data: CSV, TAB
17.

ARID1A-dependent maintenance of H3.3 is required for repressive CHD4-ZMYND8 chromatin interactions at super-enhancers [12Z_siCHD4_siARID1A_RNA]

(Submitter supplied) Background: SWI/SNF (BAF) chromatin remodeling complexes regulate lineage-specific enhancer activity by promoting accessibility for diverse DNA-binding factors and chromatin regulators. Additionally, they are known to modulate the function of the epigenome through regulation of histone post-translational modifications and nucleosome composition, although the way SWI/SNF complexes govern the epigenome remains poorly understood. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24676
12 Samples
Download data: CSV, TAB
18.

ARID1A-dependent maintenance of H3.3 is required for repressive CHD4-ZMYND8 chromatin interactions at super-enhancers [12Z_ZMYND8_ChIP]

(Submitter supplied) Background: SWI/SNF (BAF) chromatin remodeling complexes regulate lineage-specific enhancer activity by promoting accessibility for diverse DNA-binding factors and chromatin regulators. Additionally, they are known to modulate the function of the epigenome through regulation of histone post-translational modifications and nucleosome composition, although the way SWI/SNF complexes govern the epigenome remains poorly understood. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL24676
3 Samples
Download data: BROADPEAK
Series
Accession:
GSE190554
ID:
200190554
19.

ARID1A-dependent maintenance of H3.3 is required for repressive CHD4-ZMYND8 chromatin interactions at super-enhancers [12Z_shCHD4_H3.3_ChIP]

(Submitter supplied) Background: SWI/SNF (BAF) chromatin remodeling complexes regulate lineage-specific enhancer activity by promoting accessibility for diverse DNA-binding factors and chromatin regulators. Additionally, they are known to modulate the function of the epigenome through regulation of histone post-translational modifications and nucleosome composition, although the way SWI/SNF complexes govern the epigenome remains poorly understood. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL24676
6 Samples
Download data: BROADPEAK, TXT
Series
Accession:
GSE190553
ID:
200190553
20.

ARID1A-dependent maintenance of H3.3 is required for repressive CHD4-ZMYND8 chromatin interactions at super-enhancers [12Z_shARID1A_H4K16ac_ChIP]

(Submitter supplied) Background: SWI/SNF (BAF) chromatin remodeling complexes regulate lineage-specific enhancer activity by promoting accessibility for diverse DNA-binding factors and chromatin regulators. Additionally, they are known to modulate the function of the epigenome through regulation of histone post-translational modifications and nucleosome composition, although the way SWI/SNF complexes govern the epigenome remains poorly understood. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL24676
6 Samples
Download data: BROADPEAK, TXT
Series
Accession:
GSE190552
ID:
200190552
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