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

ABSTRACT: 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(S): Homo sapiens

PROVIDER: GSE152324 | GEO | 2023/06/11

REPOSITORIES: GEO

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

Project description: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.

2020-06-19 | GSE139260 | GEO

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

Project description: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.

2020-06-19 | GSE139329 | GEO

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

Project description: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.

2020-06-19 | GSE139342 | GEO

Genome-wide maps of JARID2 binding genes in WT and HBL1 KO human pluripotent stem cells (hPSCs).

Project description:We reported loss of HBL1 lnRNA promoted cardiogenesis and the interaction of HBL1-JARID2 in hPSCs. Here we used specific JARID2 antibody to pull down their binding genomic DNAs in hPSCs, respectively, which let us know the potential genes regulated by HBL1-JARID2 during cardiogenesis. 1% Input samples were collected from the same samples after chromatin shearing.

2021-06-10 | GSE149288 | GEO

Genome-wide maps of EED and H3K27me3 binding genes in WT and HBL1 KO human induced pluripotent stem cells (hiPSCs).

Project description:We reported loss of HBL1 lnRNA promoted cardiogenesis and the interaction of HBL1-EED in hiPSCs. Here we used specific EED and H3K27me3 antibodies to pull down their binding genomic DNAs in hiPSCs, respectively, which let us know the potential genes regulated by HBL1-EED-H3K27me3 during cardiogenesis. 1% Input samples were collected from the same samples after chromatin shearing.

2021-06-10 | GSE149323 | GEO

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

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

| PRJNA579345 | ENA

mRNA-seq for HCT116 Parental and ARID1A knockdown cells, mRNA-seq for DLD1 Parental, ARID1A knockdown and ARID1A knockout cells, mRNA-seq for COLO320DM Parental and ARID1A knockdown and ARID1A knockout cells

Project description:The study identifies genes that are regulated by the loss of the chromatin remodeller subunit ARID1A in colorectal cancer cell lines. This gene is frequently mutated in colorectal cancer.

2019-06-11 | E-MTAB-7791 | biostudies-arrayexpress

ChIP-seq analysis of Arid1a and C/ebpÎ± in the mouse livers

Project description:Arid1a is the subunit of SWI/SNF complex, which was reported to guide SWI/SNF to DNA. Here, we found that loss of Arid1a in the liver and other adult tissues results in improved organ regeneration. Within SWI/SNF complexes, Arid1a physically interacts with C/ebpÎ±, a hepatocyte transcription factor that drives maturation and limits proliferation. Genome-wide analysis showed that loss of Arid1a reduces the recruitment and activity of C/ebpÎ± on target promoters, resulting in expression programs that favor regeneration and cellular fitness during injury. Arid1a binding is enriched in promoters near transcriptional start sites (TSSs), and C/ebpÎ± binds at precisely the same positions, indicating that Arid1a facilitates C/ebpÎ± binding across the genome. Perfuse and isolate primary hepatocytes from mice livers, analysis of genomic occupancy of C/ebpÎ± and H3K4me2 in hepatocytes from Arid1a WT and Arid1a liver specific KO mice by ChIP-seq. Analysis of genomic occupancy of Arid1a in the hepatocytes from V5-Arid1a transgenic mouse by ChIP-seq.

2016-03-30 | E-GEOD-65167 | biostudies-arrayexpress

Targeting EZH2 methyltransferase activity in ARID1A mutated cells as a synthetic lethal therapeutic strategy

Project description:ARID1A, an epigentic modifier, is often mutated in ovarian clear cell carcinoma (OCCC). In addition, EZH2 is frequently upregulated in OCCC. Inhibtion of EZH2 with an inhibitor (GSK126) selectively inhibits ARID1A-mutated cells. This study was designed to understand changes in gene expression profiles following EZH2 inhibition or ARID1A restoration. Chromatin remodelers such as ARID1A are frequently mutated in a broad array of cancers. However, targeted cancer therapy based on ARID1A mutation status has not been described. Intriguingly, ARID1A mutated cancers typically lack genomic instability, suggesting significant involvement of epigenetic mechanisms. Here we show that inhibition of the EZH2 methyltransferase acts in a synthetic lethal manner in ARID1A mutated cells. Remarkably, ARID1A mutation status correlated with response to EZH2 inhibitor. Genome-wide profiling revealed antagonistic roles of ARID1A and EZH2 in gene regulation. Further, we identified PIK3IP1 as a direct ARID1A/EZH2 target gene whose upregulation contributes to the observed synthetic lethality in the EZH2 inhibitor treated ARID1A mutated cells. Significantly, EZH2 inhibitor caused the regression of established ARID1A mutated tumors in vivo. Together, this data demonstrate a synthetic lethality between ARID1A mutation and EZH2 inhibition. They indicate that pharmacological inhibition of EZH2 represents a novel treatment strategy for ARID1A mutated cancers.

2015-01-20 | E-GEOD-54979 | biostudies-arrayexpress

Gene expression data ARID1A knockdown OE33 cells versus mock OE33 cells

Project description:A nonsense mutation in ARID1A was identified by next generation sequencing in non-dysplastic Barrett's esophagus [BE] tissue and esophageal adenocarcinoma [EAC] tissue of a patient diagnosed with EAC. Immunohistochemistry performed on an independent archival cohort demonstrated ARID1A protein loss in 0% (0/76), 4.9% (2/40), 14.3% (4/28), 16.0% (8/50), and 12.2% (12/98) of normal squamous epithelium, BE, low-, high-grade dysplasia, and EAC tissues, respectively. Enhanced cell growth, proliferation and invasion were observed upon ARID1A knockdown in EAC cells. ARID1A was knocked down in OE33 cells (Sample MS_1 and MS_3) using on-TARGET smartpool ARID1A siRNA. At the same time, OE33 cells were transfected with a non-targeting siRNA, and these experiments (Samples MS_2 and MS_4) functioned as mock controls. Cells were harvested after 48 hours and total RNA was extracted using the Rneasy kit (Qiagen) Aim Affymetrix Human PrimeView Gene Expression Array : to determine the downstream effectors of ARID1A that are likely to contribute to the oncogenic phenotype caused by ARID1A down-regulation. Two biological replicates of each condition (2x ARID1A knockdown, and 2x Mock) were used for the microarray experiment.

2012-05-31 | E-GEOD-38380 | biostudies-arrayexpress

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