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Nono deficiency impedes the proliferation and adhesion of H9c2 cardiomyocytes through Pi3k/Akt signaling pathway

ABSTRACT: Nono deficiency impedes the proliferation and adhesion of H9c2 cardiomyocytes through Pi3k/Akt signaling pathway

PROVIDER: PRJNA870105 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR21091912.fastq.gz	Fastqsanger.gz
	SRR21091913.fastq.gz	Fastqsanger.gz
	SRR21091914.fastq.gz	Fastqsanger.gz
	SRR21091915.fastq.gz	Fastqsanger.gz
	SRR21091916.fastq.gz	Fastqsanger.gz

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Similar Datasets

Nono deficiency impedes the proliferation and adhesion of H9c2 cardiomyocytes through Pi3k/Akt signaling pathway [RNA-seq

Project description:Nono deficiency impedes the proliferation and adhesion of H9c2 cardiomyocytes through Pi3k/Akt signaling pathway [RNA-seq

| PRJNA870107 | ENA

Nono deficiency impedes the proliferation and adhesion of H9c2 cardiomyocytes through Pi3k/Akt signaling pathway [ATAC-seq]

Project description:Nono deficiency impedes the proliferation and adhesion of H9c2 cardiomyocytes through Pi3k/Akt signaling pathway [ATAC-seq]

| PRJNA870109 | ENA

Nono deficiency impedes the proliferation and adhesion of H9c2 cardiomyocytes through Pi3k/Akt signaling pathway [ATAC-seq]

Project description:Purpose: Congenital heart disease (CHD) is the most common type of birth defect and the main noninfectious cause of death during the neonatal stage. Currently, hemizygous loss-of-function variants in NONO(The non-POU domain containing, octamer-binding) gene have been described as the cause of congenital heart defects in males. However, the effects of NONO on cardiac development have not been fully elucidated.

2023-05-01 | GSE211403 | GEO

Nono deficiency impedes the proliferation and adhesion of H9c2 cardiomyocytes through Pi3k/Akt signaling pathway [RNA-seq

2023-05-01 | GSE211401 | GEO

Nono deficiency impedes the proliferation and adhesion of H9c2 cardiomyocytes through Pi3k/Akt signaling pathway.

Project description:Congenital heart disease (CHD) is the most common type of birth defect and the main noninfectious cause of death during the neonatal stage. The non-POU domain containing, octamer-binding gene, NONO, performs a variety of roles involved in DNA repair, RNA synthesis, transcriptional and post-transcriptional regulation. Currently, hemizygous loss-of-function mutation of NONO have been described as the genetic origin of CHD. However, essential effects of NONO during cardiac development have not been fully elucidated. In this study, we aim to understand role of Nono in cardiomyocytes during development by utilizing the CRISPR/Cas9 gene editing system to deplete Nono in the rat cardiomyocytes H9c2. Functional comparison of H9c2 control and knockout cells showed that Nono deficiency suppressed cell proliferation and adhesion. Furthermore, Nono depletion significantly affected the mitochondrial oxidative phosphorylation (OXPHOS) and glycolysis, resulting in H9c2 overall metabolic deficits. Mechanistically we demonstrated that the Nono knockout impeded the cardiomyocyte function by attenuating phosphatidyl inositol 3 kinase-serine/threonine kinase (Pi3k/Akt) signaling via the assay for transposase-accessible chromatin using sequencing in combination with RNA sequencing. From these results we propose a novel molecular mechanism of Nono to influence cardiomyocytes differentiation and proliferation during the development of embryonic heart. We conclude that NONO may represent an emerging possible biomarkers and targets for the diagnosis and treatment of human cardiac development defects.

| S-EPMC10154399 | biostudies-literature

Nono deficiency impedes the proliferation and adhesion of H9c2 cardiomyocytes through Pi3k/Akt signaling pathway

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

2023-05-01 | GSE211404 | 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

NONO knockdown RNA-seq and neuroblastoma PARCLIP analysis of NONO

Project description:siRNA knockdown of NONO mRNA followed by RNA-seq was carried out in the KELLY neuroblasotma cell line. In order to determine potential regulatory targets of NONO protein, we performed differential expression analysis. To identify the RNA targets of NONO in neuroblastoma, we carried out PAR-CLIP (Photoactivatable Ribonucleoside-Enhanced Crosslinking and Immunoprecipitation) using an antibody recognising NONO protein.

2023-01-28 | GSE114376 | GEO

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