Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

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

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

PROVIDER: PRJNA789388 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR17244400_1.fastq.gz	Fastqsanger.gz
	SRR17244400_2.fastq.gz	Fastqsanger.gz
	SRR17244401_1.fastq.gz	Fastqsanger.gz
	SRR17244401_2.fastq.gz	Fastqsanger.gz
	SRR17244402_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 12

Similar Datasets

Next Generation Sequencing Quantitative Analysis of Wild Type and NONO Knock Down Glioblastoma Cell Line (GSC P3) 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 | GSE191021 | GEO

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

2022-08-03 | GSE190950 | GEO

Expression data from glioblastoma stem cell clones (GSC)

Project description:Comparison of treatment sensitive GSC clones (TSGC) with treatment resistant GSC clones (TRGC). We used microarrays to identify molecular signatures of TRGC (upregulated genes). We used radiation treatment (RT) or RT plus TMZ to select treatment resistant GSC clones (TRGC)

2013-11-01 | E-GEOD-46531 | biostudies-arrayexpress

Glioblastoma stem cell (GSC) clones survived 500uM Temozolomide (TMZ) treatment

Project description:Comparison of parental GSC (GSC-parental) with treatment resistant GSC clones survived 500uM TMZ treatment (GSC-500uM TMZ) We used microarrays to identify defense profiles of GSC-500uM TMZ

2015-10-01 | GSE68029 | GEO

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

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

| PRJNA789164 | ENA

Expression data from glioblastoma stem cell clones (GSC)

2013-11-01 | GSE46531 | 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

Expression profiles of glioblastoma stem cells (GSC) treated with BMP7

Project description:Comparison of untreated and BMP7 treated GSC We used microarrays to identify gene profiles of GSC modulated by BMP7 treatment

2015-10-01 | GSE68030 | GEO

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

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data