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ARID1B, a molecular suppressor of erythropoiesis, is essential for the prevention of Monge’s disease

ABSTRACT: ARID1B, a molecular suppressor of erythropoiesis, is essential for the prevention of Monge’s disease

PROVIDER: PRJNA690089 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13370638_1.fastq.gz	Fastqsanger.gz
	SRR13370638_2.fastq.gz	Fastqsanger.gz
	SRR13370639_1.fastq.gz	Fastqsanger.gz
	SRR13370639_2.fastq.gz	Fastqsanger.gz
	SRR13370640_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

ARID1B, a molecular suppressor of erythropoiesis, is essential for the prevention of Monge’s disease

Project description:In this work, we used genomic and molecular functional assays to understand the role of ARID1B in regulating red blood cells under hypoxia using iPS cells derived from non-CMS adapted individuals and comparing the non-CMS wild type cells to non-CMS cells with ARID1B-KD using in-vitro iPSC-derived model system.

2022-06-07 | GSE164351 | GEO

ARID1B, a molecular suppressor of erythropoiesis, is essential for the prevention of Monge's disease.

Project description:At high altitude Andean region, hypoxia-induced excessive erythrocytosis (EE) is the defining feature of Monge's disease or chronic mountain sickness (CMS). At the same altitude, resides a population that has developed adaptive mechanism(s) to constrain this hypoxic response (non-CMS). In this study, we utilized an in vitro induced pluripotent stem cell model system to study both populations using genomic and molecular approaches. Our whole genome analysis of the two groups identified differential SNPs between the CMS and non-CMS subjects in the ARID1B region. Under hypoxia, the expression levels of ARID1B significantly increased in the non-CMS cells but decreased in the CMS cells. At the molecular level, ARID1B knockdown (KD) in non-CMS cells increased the levels of the transcriptional regulator GATA1 by 3-fold and RBC levels by 100-fold under hypoxia. ARID1B KD in non-CMS cells led to increased proliferation and EPO sensitivity by lowering p53 levels and decreasing apoptosis through GATA1 mediation. Interestingly, under hypoxia ARID1B showed an epigenetic role, altering the chromatin states of erythroid genes. Indeed, combined Real-time PCR and ATAC-Seq results showed that ARID1B modulates the expression of GATA1 and p53 and chromatin accessibility at GATA1/p53 target genes. We conclude that ARID1B is a novel erythroid regulator under hypoxia that controls various aspects of erythropoiesis in high-altitude dwellers.

| S-EPMC9256584 | biostudies-literature

Downregulation of ARID1B, a tumor-suppressor in the WNT subgroup medulloblastoma, activates multiple oncogenic signaling pathways

Project description:About 85% of WNT subgroup medulloblastomas exhibit the loss of one copy of chromosome 6. Loss of function mutations were identified in the ARID1B gene located on chromosome 6 in WNT subgroup tumors suggesting tumor suppressor role for ARID1B in WNT medulloblastomas. The expression of ARID1B was downregulated in the medulloblastoma cell line Daoy using two independent shRNA sequences in a doxycycline-inducible lentiviral vector tet-pLKO-puro and the effect of its downregulation on the gene expression profile was studied by the RNA-seq analysis

2021-08-26 | GSE163810 | GEO

ARID1B

Project description:ARID1B

| PRJEB30505 | ENA

Inability to switch from ARID1A-BAF to ARID1B-BAF impairs exit from pluripotency and commitment towards neural crest formation in ARID1B-related neurodevelopmental disorders

Project description:The BAF complex modulates chromatin accessibility. Specific BAF configurations have functional consequences, and subunit switches are essential for cell differentiation. ARID1B and its paralog ARID1A encode for mutually exclusive BAF subunits. De novo ARID1B haploinsufficient mutations cause a neurodevelopmental disorder spectrum, including Coffin-Siris syndrome, which is characterized by neurological and craniofacial features. Here, we reprogrammed ARID1B+/- Coffin-Siris patient-derived skin fibroblasts into iPSCs, and modeled cranial neural crest cell (CNCC) formation. We discovered that ARID1B is active only during the first stage of this process, coinciding with neuroectoderm specification, where it is part of a lineage-specific BAF configuration (ARID1B-BAF), including SMARCA4, and nine additional subunits. ARID1B-BAF acts as a gate-keeper, ensuring exit from pluripotency and lineage commitment, by attenuating NANOG, SOX2 and the thousands of enhancers directly regulated by these two pluripotency factors at the iPSC stage. In iPSCs, these enhancers are maintained active by an ARID1A-containing BAF. At the onset of differentiation, cells transition from ARID1A-BAF to ARID1B-BAF, eliciting attenuation of the NANOG/SOX2 networks, and triggering pluripotency exit. Coffin-Siris patient cells fail to perform the ARID1A/ARID1B switch, and maintain ARID1A-BAF at pluripotency enhancers throughout all stages of CNCC formation. This leads to a persistent and aberrant SOX2 and NANOG activity, which impairs CNCC formation. In fact, despite showing the typical neural crest signature (TFAP2A+, SOX9+), the ARID1B-haploinsufficient CNCCs are also NANOG-positive, in stark contrast with the ARID1B-wt CNCCs, which are NANOG-negative. These findings suggest a connection between ARID1B mutations, neuroectoderm formation, and a pathogenic mechanism for Coffin-Siris syndrome.

2021-10-12 | PXD028557 | Pride

Arid1b ChIP-seq

Project description:Arid1b ChIP-seq

2022-12-25 | GSE214879 | GEO

Arid1b ChIP-seq

Project description:Arid1b ChIP-seq

| PRJNA887457 | ENA

RNA-seq analysis upon ARID1B overexpression

Project description:We transduced either an empty vector or ARID1B cDNA in IMR90 cells. Cells were selected with puromycin and 6 days after the infection we collected the RNA. ARID1B is a member of the SWI/SNF chromatin-remodeling complex. Our previous experiments showed that knockdown of ARID1B allows cells to bypass cellular senescence. By performing RNA-seq we have shown that ARID1B expression can induce a set of genes involved in the senescence response.

2016-11-12 | GSE75291 | GEO

RNA-seq analysis of primarily cultured neurospheres from ARID1B haploinsufficient and control mice

Project description:To identify ARID1B associated genes in development of neural progenitor , we carried out RNA-seq gene expression profiling analysis in primarily cultured neurospheres from ARID1B haploinsufficient and control mice. 3 biological independent sample from ARID1B hi (hGAFPCre+;ARID1B flox/+) mice were compared with 2 independent litermate control (hGAFPCre+; ARID1B +/+) samples.

2021-01-07 | GSE143171 | GEO

Antibacterial Effect of Epidemic Prevention Sachets Essential Oil against Staphylococcus Aureus

Project description:Staphylococcus aureus (S. aureus) is one of the most dominant human pathogen, responsible for a variety of chronic and severe infections. As a classic traditional Chinese medicine (TCM) formula, Epidemic Prevention Sachets have been used clinically for centuries to treat infectious diseases. The antimicrobial activity of the essential oil (EO) from Epidemic Prevention Sachets against the S. aureus has not been investigated. In this study, the EO was tested for its antimicrobial activity against S. aureus. We identified that the EOs has high activity against S. aureus. It showed higher activity than the known antibacterial drug combination of Penicillin streptomycin. The same results were demonstrated by transmission electron microscopy. The impact of the EO on transcription of genes from S. aureus was analyzed. SAOUHSC_01002, SAOUHSC_02444, SAOUHSC_00282 and SAOUHSC_00325, which are involved in cation transport (GO:0006812), were significantly affected by the essential oil as defined in the Gene Ontology Biological Process (GO BP), whereas SAOUHSC_00114 and SAOUHSC_03000, which are involved in the protein tyrosine kinase modulator pathway (K19420), were significantly enriched in the Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway. Analysis of clusters of orthologous groups (COG) found that there are differences in multiple metabolic pathways, mainly including secondary biosynthesis metabolism, biofilm related genes and energy metabolism. Our study indicates that the essential oil from Epidemic Prevention Sachets is an effective herbal formula against S. aureus.

2025-05-17 | GSE296946 | GEO

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