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Next Generation Sequencing Facilitates Quantitative Analysis of Transcriptomes of Osteochondroma Explants Nontreated or Treated with Selective Agonist of Retionic acid Nuclear Receptor Gamma (RARg)

ABSTRACT: Next Generation Sequencing Facilitates Quantitative Analysis of Transcriptomes of Osteochondroma Explants Nontreated or Treated with Selective Agonist of Retionic acid Nuclear Receptor Gamma (RARg)

PROVIDER: PRJNA750773 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15298964_1.fastq.gz	Fastqsanger.gz
	SRR15298964_2.fastq.gz	Fastqsanger.gz
	SRR15298965_1.fastq.gz	Fastqsanger.gz
	SRR15298965_2.fastq.gz	Fastqsanger.gz
	SRR15298966_1.fastq.gz	Fastqsanger.gz

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Next Generation Sequencing Facilitates Quantitative Analysis of Transcriptomes of Osteochondroma Explants Nontreated or Treated with Selective Agonist of Retionic acid Nuclear Receptor Gamma (RARg) II

Project description:Purpose: Next-generation sequencing (NGS) has used to detect alterations in cellular pathways by various drugs. The goal of this study is to identify alteration of gene expression in human osteochondromas in response to identify nontreated or RARg agonist-treated osteochondorma transcriptome profiling (RNA-seq) and to evaluate the actions of RARg agonists on osteochondromas. Methods: Osteochondroma mRNA profiles of untreated or RARg agonist treated (4 days) osteochondroma explants were generated by deep sequencing, in triplicate, using Illumina HiSeq 4000. The sequence reads that passed quality filters were analyzed at the transcript isoform level with two methods: Burrows–Wheeler Aligner (BWA) followed by ANOVA (ANOVA) and TopHat followed by Cufflinks. Results and Conclusions: Our study represents the detailed analysis of human osteochondromas, with biologic replicates, generated by RNA-seq technology. We conclude that RNA-seq based transcriptome revealed that RARg agonists acts on human osteochondromas and altered various types of biological functions.

2021-07-30 | GSE181129 | GEO

Next Generation Sequencing Facilitates Quantitative Analysis of Transcriptomes of Osteochondroma Explants Nontreated or Treated with Selective Agonist of Retionic acid Nuclear Receptor Gamma (RARg) I

2021-07-26 | GSE180764 | GEO

Project description:Next Generation Sequencing Facilitates Quantitative Analysis of Transcriptomes of Osteochondroma Explants Nontreated or Treated with Selective Agonist of Retionic acid Nuclear Receptor Gamma (RARg) II

| PRJNA750772 | ENA

Next Generation Sequencing Facilitates Quantitative Analysis of Transcriptomes of Osteochondroma Explants Nontreated or Treated with Selective Agonist of Retionic acid Nuclear Receptor Gamma (RARg) I

| PRJNA749453 | ENA

Next Generation Sequencing Facilitates Quantitative Analysis of Transcriptomes of Osteochondroma Explants Nontreated or Treated with Selective Agonist of Retionic acid Nuclear Receptor Gamma (RARg)

Project description:This SuperSeries is composed of the SubSeries listed below.

2021-07-30 | GSE181133 | GEO

Identifying RARG fusions or PML-RARA binding genes or analysis the epigenetic changes (H3K27ac, H3K4me1, and H3K4me3) in hCD34+ cells overexpressing CPSF6::RARG and NUP98::RARG.

Project description:To understand how RARG fusion proteins regulate their target genes in the hematopoietic system, we overexpressed fusions or PML-RARA in hCD34+ cells and identified target genes that are regulated by RARG fusions. We found that RARG fusions selectively upregulated BCL2 and ATF3 in HSPCs, driving uncontrolled proliferation and disrupting the differentiation of RARG-AML cells.To investigate the mechanism how RARG fusions mediate activation of their downstream targets such as BCL2 and ATF3, we dected the epigenetic changes (H3K27ac, H3K4me1, and H3K4me3) associated with RARG fusions binding in hCD34+ cells overexpressing CPSF6::RARG and NUP98::RARG.

2024-10-16 | GSE275303 | GEO

RARG fusion genes

Project description:RARG fusion genes

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Analysis of the chromatin accessibility in CPSF6-RARG or NUP98-RARG overexpressing hCD34+ cells compared to control hCD34+ cells using ATAC-seq.

Project description:We found that RARG fusions selectively upregulated BCL2 and ATF3 in HSPCs, driving uncontrolled proliferation and disrupting the differentiation of RARG-AML cells.To investigate the mechanism how RARG fusions mediate activation of their downstream targets such as BCL2 and ATF3, we defined the chromatin accessibility using ATAC-seq assay in human CD34+ (hCD34+) cells with or without CPSF6::RARG or NUP98::RARG overexpression.

2024-10-16 | GSE275304 | GEO

The gene expression profiles of leukemia cells isolated from spleens of CreMx-1;CPSF6-RARG mice and Wt1F/+CreMx-1;CPSF6-RARG mice

Project description:We found that CPSF6-RARG fusion gene drives the aberrant expansion of HSCs and progenitor cells, which may lead to a preleukemic phenotype. Moreover, wt1 haploinsufficiency cooperates with RARG fusions to induce AML. To investigate the mechanism by which Wt1 haploinsufficiency cooperates with RARG fusion overexpression to induce AML in vivo, we analyzed the gene expression profiles of leukemia cells isolated from CreMx-1;CPSF6-RARG mice and Wt1F/+CreMx-1;CPSF6-RARG mice through RNA-seq.

2024-10-15 | GSE243415 | GEO

Gene expression profiles of MCF7 with with the following NR ligands: estradiol/E2 (ERÎ± agonist), AM580 (RARA agonist), CD437 (RARG agonist), ATRA (RARA/RARG agonist), GW0742 (PPARD agonist), R5020 (PGR agonist), and dexamethasone (GR/NR3C1 agonist).

Project description:Altered gene expression patterns in human diseases reflect perturbations in the transcriptional networks that regulate cellular state. In breast cancer, Nuclear Receptors (NRs) play a prominent role in governing gene expression. NRs have prognostic utility and are therapeutically important targets. In order to understand the function of nuclear receptors in breast cancer, we treated MCF7 cells with 6 nuclear receptor agonist, and performed expression arrrays with three biological replicates each. MCF-7 cells were cultured for 48 hours in medium with 10% charcoal-stripped FBS, and then were treated with 6 diffferent NR ligand (E2, AM580, CD437, ATRA, R5020, DEX) separately for 24h before collection and processing for microarrays. Three biological replicates were collected and processed for both control and treatment. with the 100nM GW0742 (PPARD specific ligand) and 100nM ATRA (RARs ligand), then collected after 24h for microarray processing. Controls were non-treated MCF7 cells. Both treatments and controls have three biological replicates.

2013-01-01 | E-GEOD-42619 | biostudies-arrayexpress

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