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Links from GEO DataSets

Items: 20

1.

Chromatin remodeling mediated by ARID1A is indispensable for normal hematopoiesis in mice (RNA-Seq)

(Submitter supplied) ARID1A is a component of the mammalian SWI/SNF complex involved in chromatin remodeling. A functional SWI/SNF complex is required for diverse physiological processes including hematopoiesis, however, the precise role played by ARID1A in hematopoietic development is unclear. Here we utilize hematopoietic cell-specific deletion of Arid1a in mice to uncover its role during adult hematopoiesis. We demonstrate that ARID1A is essential for maintaining the frequency and function of hematopoietic stem cells and its loss impaired the differentiation of both myeloid and lymphoid lineages. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL21103
22 Samples
Download data: TSV
Series
Accession:
GSE125846
ID:
200125846
2.

Chromatin remodeling mediated by ARID1A is indispensable for normal hematopoiesis in mice (human RNA-Seq)

(Submitter supplied) ARID1A is a component of the mammalian SWI/SNF complex involved in chromatin remodeling. A functional SWI/SNF complex is required for diverse physiological processes including hematopoiesis, however, the precise role played by ARID1A in hematopoietic development is unclear. Here we utilize hematopoietic cell-specific deletion of Arid1a in mice to uncover its role during adult hematopoiesis. We demonstrate that ARID1A is essential for maintaining the frequency and function of hematopoietic stem cells and its loss impaired the differentiation of both myeloid and lymphoid lineages. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL20301
6 Samples
Download data: TSV
3.

Chromatin remodeling mediated by ARID1A is indispensable for normal hematopoiesis in mice (ChIP-Seq)

(Submitter supplied) ARID1A is a component of the mammalian SWI/SNF complex involved in chromatin remodeling. A functional SWI/SNF complex is required for diverse physiological processes including hematopoiesis, however, the precise role played by ARID1A in hematopoietic development is unclear. Here we utilize hematopoietic cell-specific deletion of Arid1a in mice to uncover its role during adult hematopoiesis. We demonstrate that ARID1A is essential for maintaining the frequency and function of hematopoietic stem cells and its loss impaired the differentiation of both myeloid and lymphoid lineages. more...
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL21103
12 Samples
Download data: BW
Series
Accession:
GSE125845
ID:
200125845
4.

Chromatin remodeling mediated by ARID1A is indispensable for normal hematopoiesis in mice (ATAC-Seq)

(Submitter supplied) ARID1A is a component of the mammalian SWI/SNF complex involved in chromatin remodeling. A functional SWI/SNF complex is required for diverse physiological processes including hematopoiesis, however, the precise role played by ARID1A in hematopoietic development is unclear. Here we utilize hematopoietic cell-specific deletion of Arid1a in mice to uncover its role during adult hematopoiesis. We demonstrate that ARID1A is essential for maintaining the frequency and function of hematopoietic stem cells and its loss impaired the differentiation of both myeloid and lymphoid lineages. more...
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL21103
6 Samples
Download data: BW
Series
Accession:
GSE125844
ID:
200125844
5.

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
6.

Mouse tumors: Chaos3 Mammary Tumors (MTs) vs. Controls

(Submitter supplied) CNV profiling of tumors obtained from our Chaos3 mouse model for spontaneous breast cancer. The goal of this experiment was to determine copy number variations that were specific to MTs derived from this mouse model, when comapared to non-MTs.
Organism:
Mus musculus
Type:
Genome variation profiling by genome tiling array
Platform:
GPL10448
15 Samples
Download data: TXT
Series
Accession:
GSE81967
ID:
200081967
7.

Next Generation Sequencing of 23116 MT (low Arid1a expression) vs AB-C1 and AB-C2 (high Arid1a expression) Transcriptomes

(Submitter supplied) The goal of this study was to identify important genetic pathways that are altered in mammary tumor cells upon over-expression of the tumor suppressor gene Arid1a. The results of this experiment revealed that Arid1a helps regulate key cell-cycle checkpoint and growth regulatory pathways, either directly or indirectly. This helped explain in part the significant decrease in cell proliferation and tumor growth phenotypes observed both in vitro and in vivo, when comparing the same samples analyzed here by RNA-seq (untransduced replicates vs. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL17021
4 Samples
Download data: DIFF, TXT
Series
Accession:
GSE81575
ID:
200081575
8.

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
9.

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
10.

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
11.

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
12.

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
13.

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
14.

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
15.

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
16.

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
17.

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
18.

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
19.

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
20.

ARID1A-dependent maintenance of H3.3 is required for repressive CHD4-ZMYND8 chromatin interactions at super-enhancers [12Z_shARID1A_H3.3_H2A.Zac_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, NARROWPEAK, TXT
Series
Accession:
GSE190551
ID:
200190551
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