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Links from GEO DataSets

Items: 20

1.

Assay for Transposase Accessible Chromatin with high-throughput sequencing (ATAC-seq) revealed genomic chromatin accessibilities change induced by loss of ARID1A in differentiated (day 4) H9 hESCs

(Submitter supplied) We reported loss of ARID1A promoted neurogenesis and inhibited cardiogenesis. Under microscopy, we observed that spontaneously differentiated cells were induced in ARID1A KO H9 hESCs cultured in mTesR medium. We did not know what cells types were. Here ATAC-seq were used to investigate chromatin accessibilities change in differentiated (day 4) WT H9 hESCs and ARID1A KO hESC cells.
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL24676
2 Samples
Download data: BW
2.

Genome-wide maps of ARID1A binding genes in H9 human embryonic stem cells

(Submitter supplied) We reported loss of ARID1A promoted neurogenesis and inhibited cardiogenesis. Here we used specific ARID1A antibody to pull down ARID1A binding genomic DNA in human embryonic stem cells, which let us know the potential genes regulated by ARID1A during neurogenesis and inhibited cardiogenesis. IgG was used as the control.
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL20301 GPL18573
2 Samples
Download data: BW, NARROWPEAK
Series
Accession:
GSE152324
ID:
200152324
3.

Essential and Opposite Roles of ARID1A in Coordinating Human Cardiogenesis and Neurogenesis from Pluripotent Stem Cells

(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:
GPL18573 GPL24676
8 Samples
Download data: BW, NARROWPEAK, TAR
Series
Accession:
GSE139343
ID:
200139343
4.

Single cell RNA-seq revealed different cell types induced by loss of ARID1A in undifferentiated and differentiation (day 10) H9 hESCs.

(Submitter supplied) We reported loss of ARID1A promoted neurogenesis and inhibited cardiogenesis. Under microscopy, we observed that spontaneously differentiated cells were induced in ARID1A KO H9 hESCs cultured in mTesR medium. After cardiac differentiation for 10 days, we also observed the cell types were totally different between WT and ARID1A KO cells. We did not know what cells types were. Here scRNA-seq were used to identify the cell types in WT H9 hESCs and ARID1A KO H9 hESCs.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platforms:
GPL18573 GPL24676
4 Samples
Download data: TAR
Series
Accession:
GSE139342
ID:
200139342
5.

Genome-wide maps of ARID1A binding genes in H9 human embryonic stem cells.

(Submitter supplied) We reported loss of ARID1A promoted neurogenesis and inhibited cardiogenesis. Here we used specific ARID1A antibody to pull down ARID1A binding genomic DNA in human embryonic stem cells, which let us know the potential genes regulated by ARID1A during neurogenesis and inhibited cardiogenesis. 1% Input sample was collected from the same sample after chromatin shearing.
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL18573
2 Samples
Download data: BW, NARROWPEAK
Series
Accession:
GSE139260
ID:
200139260
6.

Identification of the dedifferentiation trajectory of the cells without Arid1a using single cell RNA-seq

(Submitter supplied) The primary mouse hepatocytes were isolated from the liver tissue Arid1af/f mouse. To immortalize mouse primary hepatocytes, the isolated cells were first infected with lentivirus expressing simian virus 40 large-T protein (SV40LT), and then cultured until proliferated cell colonies appear. Cells were further transformed with lentivirus expressing HrasV12D to generate a cell line called AB17, which were cultured in DMEM supplemented with 10% FBS and 100 µg/ml penicillin-streptomycin in a humidified incubator at 37℃ with 5% CO2.To get insight into trajectory of dedifferentiation induced by Arid1a loss, we performed single-cell RNA sequencing (scRNA-seq) on FACS-sorted GFP+ AB17 cells using Fluidigm C1 platform, and obtained the scRNA-seq data from 76 cells with Arid1a knockout induced by Ad-Cre and 73 cells infected with Ad-GFP as control. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL21273
149 Samples
Download data: TXT
Series
Accession:
GSE140924
ID:
200140924
7.

Genome-wide transcriptomic analysis and chromatin accessibility profiling of cardiomyocyte differentiation from human embryonic stem cells and iPS cells

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing; Other
Platform:
GPL11154
64 Samples
Download data: BED
Series
Accession:
GSE85332
ID:
200085332
8.

Genome-wide transcriptomic analysis of cardiomyocyte differentiation from human embryonic stem cells and iPS cells (RNA-seq)

(Submitter supplied) In this study, time-course transcriptome profiling of caidiomyocyte differentiation derived from human hESCs and hiPSCs was investigated. Two hiPSC lines (C15 and C20) and two hESC lines (H1 and H9) were differentiated to caidiomyocytes. The cells were collected for RNA-seq analysis at day0(undifferentiated cells) day2 (mesoderm), day4 (cardiac mesoderm) and day30 (cardiomyocytes) using Illumina HiSeq 2000 sequencer.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL11154
32 Samples
Download data: TXT
9.

Genome-wide chromatin accessibility profiling of cardiomyocyte differentiation from human embryonic stem cells and iPS cells (ATAC-seq)

(Submitter supplied) In this study, time-course genome-wide chromatin accessibility of caidiomyocyte differentiation derived from human hESCs and hiPSCs was profiled. Two hiPSC lines (C15 and C20) and two hESC lines (H1 and H9) were differentiated to caidiomyocytes by ATAC-seq. The cells were collected for ATAC-seq at day 0(undifferentiated cells) day 2 (mesoderm), day 4 (cardiac mesoderm) and day 30 (cardiomyocytes).
Organism:
Homo sapiens
Type:
Other
Platform:
GPL11154
32 Samples
Download data: BED
Series
Accession:
GSE85330
ID:
200085330
10.

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
11.

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
12.

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
13.

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
14.

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
15.

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
16.

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
17.

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
18.

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
19.

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
20.

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
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