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Links from GEO DataSets

Items: 20

1.

The ARID1A tumor suppressor controls global transcription via pausing of RNA Polymerase II

(Submitter supplied) We investigated the genomic consequences of the depletion of the SWI/SNF subumit ARID1A, in an ovarian cancer derived model. We produced genome wide data for nascent RNA (GRO-seq) and steady state RNA (total RNA-seq). Further, we used ChIP-seq to examine genome-wide distribution of ARID1A, as well as the changes in occupancy of RNAPII, H3K4me3 and H3K36me3. Finally we used ATAC-seq to investigate chromatin accessibility.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing; Other
Platform:
GPL18573
37 Samples
Download data: BW, TXT
2.

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
3.
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
4.

ARID1A and ARID1B loss in HCT116 and TOV21G cells

(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; Other
Platforms:
GPL16791 GPL18573
74 Samples
Download data: TXT
Series
Accession:
GSE101975
ID:
200101975
5.

ARID1A and ARID1B loss in TOV21G cells

(Submitter supplied) ARID1A, a subunit of the SWI/SNF chromatin remodeling complex, is frequently mutated in cancer. Deficiency in its homolog ARID1B is synthetically lethal with ARID1A mutation. However, the functional relationship between these homologs has not been explored. Here we use ATAC-seq, genome-wide histone modification mapping, and expression analysis to examine colorectal cancer cells lacking one or both ARID proteins. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing; Other
Platforms:
GPL18573 GPL16791
22 Samples
Download data: TXT
6.

ARID1A and ARID1B loss in HCT116 cells

(Submitter supplied) ARID1A, a subunit of the SWI/SNF chromatin remodeling complex, is frequently mutated in cancer. Deficiency in its homolog ARID1B is synthetically lethal with ARID1A mutation. However, the functional relationship between these homologs has not been explored. Here we use ATAC-seq, genome-wide histone modification mapping, and expression analysis to examine colorectal cancer cells lacking one or both ARID proteins. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing; Other
Platforms:
GPL16791 GPL18573
52 Samples
Download data: TXT
7.

ARID1A-mutated ovarian cancers depend on HDAC6 activity

(Submitter supplied) ARID1A, encoding a subunit of the SWI/SNF chromatin remodeling complex, is the most mutated epigenetic regulator in human cancers. ARID1A and TP53 mutations are typically mutually exclusive. Therapeutic approaches that correlate with ARID1A mutational status remain a challenge. Here, we show that HDAC6 activity is essential in ARID1A-mutated ovarian cancers. Inhibition of HDAC6 activity using a clinically applicable small molecule inhibitor significantly improved the survival of mice bearing ARID1A-mutated ovarian tumors. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL18573
5 Samples
Download data: TXT
8.

Genome-wide nucleosome occupancy and DNA methylation profiling in endometriosis cells

(Submitter supplied) We show that knocking down ARID1A in an immortalized endometriosis cell line leads to phenotypic changes in vitro. Additionally, we find strong increases in the active H3K27ac mark in promoter regions but decrease of H3K27ac at potential enhancers with targeted DNA methylation-independent alterations in nucleosome occupancy.
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing; Methylation profiling by high throughput sequencing
Platform:
GPL11154
2 Samples
Download data: BED, BW
Series
Accession:
GSE97373
ID:
200097373
9.

Genome-wide histone modification profiling in endometriosis cells

(Submitter supplied) We show that knocking down ARID1A in an immortalized endometriosis cell line leads to phenotypic changes in vitro. Additionally, we find strong increases in the active H3K27ac mark in promoter regions but decrease of H3K27ac at potential enhancers.
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL11154 GPL18573
18 Samples
Download data: TXT
Series
Accession:
GSE86810
ID:
200086810
10.

ARID1A loss impairs enhancer-mediated gene regulation and drives colon cancer in mice

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens; Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing; Expression profiling by high throughput sequencing
Platforms:
GPL11154 GPL13112
34 Samples
Download data: WIG
Series
Accession:
GSE71514
ID:
200071514
11.

ARID1A loss impairs enhancer-mediated gene regulation and drives colon cancer in mice [primary cells_RNA-seq]

(Submitter supplied) Genes encoding subunits of SWI/SNF chromatin remodeling complexes are collectively mutated in ~20% of all human cancers. Although ARID1A is the most frequent target of mutations, the mechanism by which its inactivation promotes tumorigenesis is unclear. Here, we demonstrate that Arid1a functions as a tumor suppressor in the mouse colon, but not the small intestine, and that invasive ARID1A-deficient adenocarcinomas resemble human colorectal cancer (CRC). more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL13112
5 Samples
Download data: WIG
Series
Accession:
GSE71513
ID:
200071513
12.

ARID1A loss impairs enhancer-mediated gene regulation and drives colon cancer in mice [primary cells_ChIP-seq]

(Submitter supplied) Genes encoding subunits of SWI/SNF chromatin remodeling complexes are collectively mutated in ~20% of all human cancers. Although ARID1A is the most frequent target of mutations, the mechanism by which its inactivation promotes tumorigenesis is unclear. Here, we demonstrate that Arid1a functions as a tumor suppressor in the mouse colon, but not the small intestine, and that invasive ARID1A-deficient adenocarcinomas resemble human colorectal cancer (CRC). more...
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL13112
5 Samples
Download data: WIG
Series
Accession:
GSE71512
ID:
200071512
13.

ARID1A loss impairs enhancer-mediated gene regulation and drives colon cancer in mice [HCT116_RNA-seq]

(Submitter supplied) Genes encoding subunits of SWI/SNF chromatin remodeling complexes are collectively mutated in ~20% of all human cancers. Although ARID1A is the most frequent target of mutations, the mechanism by which its inactivation promotes tumorigenesis is unclear. Here, we demonstrate that Arid1a functions as a tumor suppressor in the mouse colon, but not the small intestine, and that invasive ARID1A-deficient adenocarcinomas resemble human colorectal cancer (CRC). more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL11154
6 Samples
Download data: WIG
14.

ARID1A loss impairs enhancer-mediated gene regulation and drives colon cancer in mice [HCT116_ChIP-seq]

(Submitter supplied) Genes encoding subunits of SWI/SNF chromatin remodeling complexes are collectively mutated in ~20% of all human cancers. Although ARID1A is the most frequent target of mutations, the mechanism by which its inactivation promotes tumorigenesis is unclear. Here, we demonstrate that Arid1a functions as a tumor suppressor in the mouse colon, but not the small intestine, and that invasive ARID1A-deficient adenocarcinomas resemble human colorectal cancer (CRC). more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL11154
18 Samples
Download data: WIG
Series
Accession:
GSE71510
ID:
200071510
15.

Loss of HDAC-mediated repression and gain of NF-kB activation underlies cytokine induction in ARID1A and PIK3CA mutation-driven ovarian cancer

(Submitter supplied) ARID1A is frequently mutated in ovarian clear-cell carcinoma (OCCC) and often co-exists with activating mutations of PIK3CA. Although induction of pro-inflammatory cytokines has been observed in this cancer, the mechanism by which the two mutations synergistically activate cytokine genes remains elusive. Here we established an in vitro model of OCCC by introducing ARID1A knock-down and mutant PIK3CA in a normal human ovarian epithelial cell line, which resulted in cell transformation and cytokine gene induction. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL16791
12 Samples
Download data: XLSX
Series
Accession:
GSE86004
ID:
200086004
16.

Genome-Wide Transcriptional Regulation Mediated By Biochemically Distinct Forms of SWI/SNF

(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:
GPL11154
28 Samples
Download data
Series
Accession:
GSE69568
ID:
200069568
17.

Combinatorial Regulation Mediated by Biochemically Distinct Forms of SWI/SNF [RNA-Seq]

(Submitter supplied) The precise makeup of chromatin remodeling complexes is important for determining cell type and cell function. The SWI/SNF chromatin remodeling complex is made up of multiple subunits that can be filled by mutually exclusive proteins. Inclusion or exclusion of these proteins has profound functional consequences, yet we currently understand little about the direct functional relationship between these biochemically distinct forms of remodeling complexes. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL11154
19 Samples
Download data: CSV
18.

Combinatorial Regulation Mediated by Biochemically Distinct Forms of SWI/SNF [ChIP-Seq]

(Submitter supplied) The precise makeup of chromatin remodeling complexes is important for determining cell type and cell function. The SWI/SNF chromatin remodeling complex is made up of multiple subunits that can be filled by mutually exclusive proteins. Inclusion or exclusion of these proteins has profound functional consequences, yet we currently understand little about the direct functional relationship between these biochemically distinct forms of remodeling complexes. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL11154
9 Samples
Download data: BED, BW, CSV
Series
Accession:
GSE69566
ID:
200069566
19.

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
20.

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
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