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Genome-wide map of long non-coding RNA steroid receptor RNA activator (SRA) in human erythroleukemic K562 cell line

ABSTRACT: Genome-wide map of long non-coding RNA steroid receptor RNA activator (SRA) in human erythroleukemic K562 cell line

PROVIDER: PRJNA641150 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12070822.fastq.gz	Fastqsanger.gz
	SRR12070823.fastq.gz	Fastqsanger.gz
	SRR12070824.fastq.gz	Fastqsanger.gz
	SRR12070825.fastq.gz	Fastqsanger.gz
	SRR12070826.fastq.gz	Fastqsanger.gz

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Expression Profiling Reveals Unexpected Targets and Functions of the Human Steroid Receptor RNA Activator (SRA) Gene

2010-02-01 | GSE20081 | GEO

Multiple Roles for Steroid Receptor RNA Activator (SRA) in Regulation of Adipogenesis and Insulin Sensitivity

Project description:PPARγ is a master transcriptional regulator of adipogenesis. Hence, the identification of PPARγ coactivators should help reveal mechanisms controlling gene expression in adipose tissue development and physiology. We show that the non-coding RNA Steroid receptor RNA Activator, SRA, associates with PPARγ and coactivates PPARγ-dependent reporter gene expression. Overexpression of SRA in ST2 adipocyte precursor cells promotes their differentiation into adipocytes. Conversely, knockdown of endogenous SRA inhibits 3T3-L1 preadipocyte differentiation. Microarray analysis reveals hundreds of SRA-responsive genes in adipocytes, including genes in cell cycle, insulin and TNFα signaling pathways. Some functions of SRA may involve mechanisms other than coactivation of PPARγ. SRA increases insulin-stimulated glucose uptake in adipocytes. SRA promotes S-phase entry during mitotic clonal expansion, decreases expression of cyclin-dependent kinase inhibiters p21Cip1 and p27Kip1, and increases phosphorylation of Cdk1/Cdc2. SRA also inhibits the TNFα-induced phosphorylation of c-Jun NH2-terminal kinase. In conclusion, SRA enhances adipogenesis and adipocyte function through multiple pathways.

2013-05-07 | GSE21594 | GEO

Genome-wide map of long non-coding RNA steroid receptor RNA activator (SRA) in human erythroleukemic K562 cell line

Project description:We performed Chromatin Isolation by RNA Purification (ChIRP) of SRA by high-throughput sequencing in K562 cell line. We find that SRA occupied genome-wide including alpha- and beta-globin loci.

2020-07-04 | GSE153004 | GEO

Multiple Roles for Steroid Receptor RNA Activator (SRA) in Regulation of Adipogenesis and Insulin Sensitivity

Project description:PPARM-NM-3 is a master transcriptional regulator of adipogenesis. Hence, the identification of PPARM-NM-3 coactivators should help reveal mechanisms controlling gene expression in adipose tissue development and physiology. We show that the non-coding RNA Steroid receptor RNA Activator, SRA, associates with PPARM-NM-3 and coactivates PPARM-NM-3-dependent reporter gene expression. Overexpression of SRA in ST2 adipocyte precursor cells promotes their differentiation into adipocytes. Conversely, knockdown of endogenous SRA inhibits 3T3-L1 preadipocyte differentiation. Microarray analysis reveals hundreds of SRA-responsive genes in adipocytes, including genes in cell cycle, insulin and TNFM-NM-1 signaling pathways. Some functions of SRA may involve mechanisms other than coactivation of PPARM-NM-3. SRA increases insulin-stimulated glucose uptake in adipocytes. SRA promotes S-phase entry during mitotic clonal expansion, decreases expression of cyclin-dependent kinase inhibiters p21Cip1 and p27Kip1, and increases phosphorylation of Cdk1/Cdc2. SRA also inhibits the TNFM-NM-1-induced phosphorylation of c-Jun NH2-terminal kinase. In conclusion, SRA enhances adipogenesis and adipocyte function through multiple pathways. Total RNA was isolated from fully differentiated (MDIT day 4) SRA overexpressing (pMSCV-SRA) and control (pMSCV empty vector) ST2 adipocytes, or fully differentiated (MDIT day 8) shSRA knockdown (pSuperior-shSRA) or shControl (pSuperior-shcontrol) 3T3-L1 adipocytes. Genome wide gene expression analysis was performed using Affymetrix mouse genome 430 2.0 arrays. Triplicate samples were analyzed.

2013-05-07 | E-GEOD-21594 | biostudies-arrayexpress

Expression Profiling Reveals Unexpected Targets and Functions of the Human Steroid Receptor RNA Activator (SRA) Gene

Project description:The human steroid receptor RNA activator (SRA) gene encodes both non-coding RNAs (ncRNAs) and protein-generating isoforms. However, the breadth of endogenous target genes that might be regulated by SRA RNAs remains largely unknown. To address this, we depleted SRA RNA in two human cancer cell lines (HeLa and MCF-7) with small interfering RNAs, then assayed for changes in gene expression by microarray analyses using Affymetrix HGU133+2 arrays. We also tested if SRA depletion affects estradiol-regulated genes in MCF-7 breast cancer cells. We transiently transfected HeLa or MCF-7 human cancer cell lines with with non-targeting (NT) or SRA-targeting siRNAs. Six total HeLa RNA samples were analyzed on an Affymetrix HGU133+2 array, representing three biological triplicates. Likewise, 12 total MCF-7 RNA samples were analyzed on Affymetrix HGU133+2 arrays, representing biological trilplicates for both NT and siSRA transfected cells and with/without 10 nM estradiol (E2) for 6 hours.

2010-02-21 | E-GEOD-20081 | biostudies-arrayexpress

Mediation of CTCF transcriptional insulation by DEAD-box RNA-binding protein p68 and steroid receptor RNA activator SRA

Project description:CCCTC-binding factor (CTCF) is a DNA-binding protein that plays important roles in chromatin organization, though the mechanism by which CTCF carries out these functions is not fully understood. Recent studies show that CTCF recruits the cohesin complex to insulator sites and that cohesin is required for insulator activity. Here we have shown that the DEAD box RNA helicase p68 (DDX5) and its associated noncoding RNA, steroid receptor RNA activator (SRA), form a complex with CTCF that is essential for insulator function. p68 was detected at CTCF sites in the IGF2/H19 imprinted control region (ICR) as well as other genomic CTCF sites. In vivo depletion of SRA or p68 reduced CTCF-mediated insulator activity at the IGF2/H19 ICR, increased levels of IGF2 expression, and increased interactions between the endodermal enhancer and IGF2 promoter. p68/SRA also interacts with members of the cohesin complex. Depletion of either p68 or SRA does not affect CTCF binding to its genomic sites, but it does reduce cohesin binding. The results suggest that p68/SRA stabilizes the interaction of cohesin with CTCF, by binding to both, and is required for proper insulator function.

2010-11-16 | GSE24126 | GEO

Mediation of CTCF transcriptional insulation by DEAD-box RNA-binding protein p68 and steroid receptor RNA activator SRA

2010-11-16 | E-GEOD-24126 | biostudies-arrayexpress

Next Generation Sequencing Quantitative Analysis of steroid receptor RNA activator (SRA1) Transcriptomes

Project description:The steroid receptor RNA activator gene (SRA1) produces both a functional RNA (SRA) and a protein (SRAP), whose exact roles remain unknown. To identify cellular processes regulated by this unusual bi-faceted system, we characterized the transcriptome of two differenct cell lines upon depletion of these molecules.

2015-11-05 | GSE74461 | GEO

Targeting steroid receptor RNA activator as a novel therapeutic strategy for myocardial hypertrophy

Project description:Myocardial hypertrophy develops when the heart is subjected to biomechanical stress, neurohormonal or hemodynamic stimuli. Isoprenaline-induced myocardial hypertrophy in mice exhibited abnormally elevated steroid receptor RNA activator (SRA) level in hypertrophic myocardium, suggesting SRA’s potential functions in hypertrophic pathogenesis. SRA knockout or cardiac-specific knockdown attenuated cardiac remodeling without impairing baseline cardiac function. RNA sequencing and mechanistic studies identified SRA as a transcriptional coactivator that enhances GR-mediated upregulation of HSP70, which in turn activates pro-hypertrophic Akt signaling. Adenoviral SRA overexpression in H9C2 cardiomyocytes amplified isoprenaline-triggered hypertrophic gene expression via this GR-HSP70-Akt axis. Those findings establish SRA as a stress-responsive regulator of maladaptive cardiac growth and propose SRA inhibition as a targeted therapeutic strategy for hypertrophy-related cardiomyopathy. This work bridges noncoding RNA biology with metabolic signaling in heart disease, offering both mechanistic insights and translational potential.

2025-06-30 | GSE300259 | GEO

Next Generation Sequencing Quantitative Analysis of steroid receptor RNA activator (SRA1) Transcriptomes

2015-11-05 | E-GEOD-74461 | biostudies-arrayexpress