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NONO preferentially binds to exon-intron boundary and regulates alternative splicing in Rat Cardiac Fibroblasts

ABSTRACT: NONO preferentially binds to exon-intron boundary and regulates alternative splicing in Rat Cardiac Fibroblasts

PROVIDER: PRJNA844354 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19379111_1.fastq.gz	Fastqsanger.gz
	SRR19379111_2.fastq.gz	Fastqsanger.gz
	SRR19379112_1.fastq.gz	Fastqsanger.gz
	SRR19379112_2.fastq.gz	Fastqsanger.gz
	SRR19379113_1.fastq.gz	Fastqsanger.gz

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NONO preferentially binds to exon-intron boundary and regulates alternative splicing in Rat Cardiac Fibroblasts [RIP-seq]

Project description:NONO preferentially binds to exon-intron boundary and regulates alternative splicing in Rat Cardiac Fibroblasts [RIP-seq]

| PRJNA841993 | ENA

NONO preferentially binds to exon-intron boundary and regulates alternative splicing in Rat Cardiac Fibroblasts [RNA-seq]

Project description:NONO preferentially binds to exon-intron boundary and regulates alternative splicing in Rat Cardiac Fibroblasts [RNA-seq]

| PRJNA844346 | ENA

NONO preferentially binds to exon-intron boundary and regulates alternative splicing in Rat Cardiac Fibroblasts [RNA-seq]

Project description:Myocardial fibrosis occurs in a variety of cardiac diseases. As one of the markers of cardiac activated-myofibroblast protein, NONO may be involved in this process while the underlying mechanisms have not been explored. NONO, assumed to hold a role in the regulation of global transcriptome profile in cardiac fibrotic, was silenced in rat cardiomyocytes. RNA-seq and improved RNA immunoprecipitation and sequencing (iRIP-seq) were used to analyze the dysregulated transcriptome by NONO, as well as the NONO-bound RNAs in the control and siNONO group. Quantitative PCR and western blotting were applied to determine NONO-regulated mRNA and protein expression levels in rat cardiomyocytes. RNA-seq and iRIP-seq were successfully performed, and NONO-bound RNAs were characterized.

2025-05-12 | GSE205302 | GEO

NONO preferentially binds to exon-intron boundary and regulates alternative splicing in Rat Cardiac Fibroblasts [RIP-seq]

2025-05-12 | GSE203077 | GEO

NONO preferentially binds to exon-intron boundary and regulates alternative splicing in Rat Cardiac Fibroblasts

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

2025-05-12 | GSE205304 | GEO

Next Generation Sequencing Quantitative Analysis of Wild Type and NONO Knock Down Glioblastoma Cell Line(U251) Transcriptomes

Project description:We identified non-POU domain-containing octamer-binding protein (NONO), a Drosophila behavior human splicing (DBHS) protein, among the most upregulated mRNA splicing factors in glioblastoma multiforme (GBM). NONO was associated with poor prognosis in GBM patients, and overexpression of NONO promoted GBM cell proliferation, invasion and tumorigenesis in a GBM orthotopic xenograft model. Through RNA sequencing based transcriptomic profiling, we found that knockdown of NONO resulted in global changes in alternative splicing-intron retention, and identified GPX1 and CCN1 as two pre-mRNAs targeted by NONO. NONO directly bound to the intron of GPX1 pre-mRNA through the RNA-recognition motifs 2 (RRM2) domain and required interaction with another DBHS protein family member, PSPC1. Knockdown of NONO interfered with redox homeostasis in cells, at least partially, through abnormal splicing of GPX1. Finally, Auranofin, a small-molecule inhibitor targeting NONO, inhibited GBM growth in an orthotopic xenograft model in mice. Taken together, our data revealed that NONO was a key regulator of mRNA splicing in GBM, and that targeting NONO represents a novel and effective therapeutic strategy for the treatment of GBM.

2022-08-03 | GSE190950 | GEO

Next Generation Sequencing Quantitative Analysis of Wild Type and NONO Knock Down Glioblastoma Cell Line (GSC P3) Transcriptomes

2022-08-03 | GSE191021 | GEO

NONO mutations cause syndromic intellectual disability and inhibitory synaptic defects

Project description:Identifying causes of sporadic intellectual disability remains a considerable medical challenge. Here, we demonstrate that null mutations in the NONO gene, a member of the Drosophila Behavior Human Splicing (DBHS) protein family, are a novel cause of X-linked syndromic intellectual disability. Comparing humans to Nono-deficient mice revealed related behavioral and craniofacial anomalies, as well as global transcriptional dysregulation. Nono-deficient mice also showed deregulation of a large number of synaptic transcripts, causing a disorganization of inhibitory synapses, with impaired postsynaptic scaffolding of gephyrin. Alteration of gephyrin clustering could be rescued by over-expression of Gabra2 in NONO-compromised neurons. These findings link NONO to intellectual disability and first highlight the key role of DBHS proteins in functional organization of GABAergic synapses.

2015-09-02 | E-MTAB-2895 | biostudies-arrayexpress

NONO mutations cause syndromic intellectual disability and inhibitory synaptic defects

2015-09-02 | E-MTAB-2894 | biostudies-arrayexpress

RNA binding properties of NONO and NONO-delta-ER in testis;

Project description:To investigate the RNA binding proterties of NONO and NONO-delta-ER in testis; we collected adult NONO and NONO-delta-ER mice testis We then performed eCLIP-seq respectively and convey subsequent bioinformatic analysis.

2024-08-08 | GSE263329 | GEO

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