Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

RNA-Seq of U251 glioblastoma cell line with and without (-)-SDS-1-021.

ABSTRACT: RNA-Seq of U251 glioblastoma cell line with and without (-)-SDS-1-021.

PROVIDER: PRJNA823377 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR18609774_1.fastq.gz	Fastqsanger.gz
	SRR18609774_2.fastq.gz	Fastqsanger.gz
	SRR18609775_1.fastq.gz	Fastqsanger.gz
	SRR18609775_2.fastq.gz	Fastqsanger.gz
	SRR18609776_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 12

Similar Datasets

RNA-Seq of U251 glioblastoma cell line with and without (-)-SDS-1-021.

Project description:RNA-Seq analyses polysome-bound mRNAs of glioblastoma cell line NSC11 after 10nM (-)-SDS-1-021 treatement to evaluate drug-induced changes in mRNA translation

2022-04-11 | GSE200162 | GEO

Low cytosolic folate cycling is a hallmark of U251 glioblastoma cells reprogramming towards pluripotency [RNA-seq]

Project description:we report that U251 glioblastoma tumor spheres exhibit low cytosolic folate cycle and a reprogrammmed mitochondrial folate cycle that is presumably oriented towards oxidizing the formyl group to CO2 with the production of TetraHydroFolate and release of NADPH instead of synthesizing formate

2019-07-01 | GSE117543 | GEO

Transcriptome analysis of microglia isolated from the mPFC or NAc without or with repeated social defeat stress (R-SDS)

Project description:To identify R-SDS-induced changes in gene expression profiles in medial prefrontal cortex (mPFC) and nucleus accumbens (NAc) microglia, we performed transcriptome analysis in mPFC and NAc microglia without or with R-SDS. Based on our observation that TLR2/TLR4 mediate R-SDS-induced activation of mPFC microglia, we performed the analysis in wild-type (WT) mice and TLR2/TLR4-double knockout (TLR-DKO) mice.

2018-08-09 | GSE115995 | GEO

Modulation of gene expression in U251 glioblastoma cells by binding of mutant p53 to intronic and intergenic sequences

Project description:Missense point mutations in the TP53 gene are frequent genetic alterations in human tumor tissue and cell lines derived thereof. Mutant p53 (mutp53) proteins have lost sequence-specific DNA binding, but have retained the ability to interact in a structure-selective manner with non-B DNA and to act as regulators of transcription. To identify functional binding sites of mutp53, we established a small library of genomic sequences bound by p53R273H in U251 human glioblastoma cells using chromatin immunoprecipitation (ChIP). Mutp53 binding to isolated DNA fragments confirmed the specificity of the ChIP. The mutp53 bound DNA sequences are rich in repetitive DNA elements, which are dispersed over non-coding DNA regions. Stable down-regulation of mutp53 expression strongly suggested that mutp53 binding to genomic DNA is functional. We identified the PPARGC1A and FRMD5 genes as p53R273H targets regulated by binding to intronic and intra-genic sequences. We propose a model that attributes the oncogenic functions of mutp53 to its ability to interact with intronic and intergenic non-B DNA sequences and modulate gene transcription via re-organization of chromatin. For the study of the consequences of mutant p53 (R273H) knockdown on gene expression, total RNA from parental U251 glioblastoma cells and UsiA12 clone was prepared from two independent cell culture experiments (biological replicates) and processed for microarray-based profiling of gene expression. UsiA12 clone was derived from the U251 cells transfected with the pSuper-p53 and pCI-neo vectors.

2010-06-24 | E-GEOD-13991 | biostudies-arrayexpress

Transcriptomic sequencing analysis of glioblastoma cell lines DBTRG and U251.

Project description:We showed that DBTRG is more invasive than U251 cell lines by novel brain-stiffness-mimicking matrix gel invasion platform and transwell invasion assay. To understand the molecular mechanisms of DBTRG being more invasive than U251, we performed transcriptomic sequencing analysis of DBTRG and U251 cell lines.

2022-04-18 | GSE200574 | GEO

PD-L1 (CD274) overexpression effect on glioblastoma cell line U251

Project description:PD-L1 (CD274) overexpression effect on glioblastoma cell line U251

| PRJNA420727 | ENA

Transcriptomic sequencing analysis of glioblastoma cell lines DBTRG and U251.

Project description:Transcriptomic sequencing analysis of glioblastoma cell lines DBTRG and U251.

| PRJNA825410 | ENA

Expression data of progesterone regulated miRNAs in U251 cells, derived from human glioblastoma

Project description:Glioblastoma multiforme (GBM), a grade IV astrocytoma, is the most common and aggressive brain tumor in adults, characterized by being highly infiltrative, angiogenic, and resistant to chemotherapy and radiotherapy. In previous works, has been determined that progesterone P4 increases proliferation, migration and invasion of cells derived from human GBMs through the interaction with its intracellular receptor (PR). In breast cancer, there exist evidence that P4 regulates the expression of miRNAs with tumor suppressor or oncogenic action, via the classical PR. The signature of miRNAs affected by P4 treatment in cells derived from human GBMs has not been determined. Therefore, we studied the effect of P4 on miRNAs expression pattern in U251 cells derived from a human GBM.

2020-01-25 | GSE144204 | GEO

Expression data from U251-shCtrl and U251-shCPVL cells

Project description:we performed microarray expression profiling to analyze the differentially expressed genes between U251-shCtrl and U251-shCPVL cells.

2024-11-01 | GSE188414 | GEO

Repeated social defeat stress (R-SDS)-induced changes in gene expression profiles in the medial prefrontal cortex (mPFC)

Project description:To identify R-SDS-induced changes in gene expression profiles in the mPFC, we performed transcriptome analysis in the mPFC without or with R-SDS. We separately analyzed the data from susceptible mice, which showed social avoidance after R-SDS, and resilient mice, which did not, in addition to those from naïve mice.

2018-08-09 | GSE115994 | 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