Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Transcriptional profilling of hESC with and without 17q gain upon induction of replicative stress through HU treatment [targeted exome sequencing]

ABSTRACT: Transcriptional profilling of hESC with and without 17q gain upon induction of replicative stress through HU treatment [targeted exome sequencing]

PROVIDER: PRJNA648929 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR12331450_1.fastq.gz	Fastqsanger.gz
	SRR12331450_2.fastq.gz	Fastqsanger.gz
	SRR12331451_1.fastq.gz	Fastqsanger.gz
	SRR12331451_2.fastq.gz	Fastqsanger.gz
	SRR12331452_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 8

Similar Datasets

Transcriptional profilling of hESC with and without 17q gain upon induction of replicative stress through HU treatment [sWGS]

Project description:Human embryonic stem cells (hESC) and cancer cells rapidly divide with a short G1/S-phase causing increased replicative stress (RS). Since both in vitro cultured hESCs and most high-risk neuroblastomas have large chromosome 17q gains (17q+), we hypothesize that this may provide a "RS-resistance phenotype". We co-cultured parental cells and a derived hESC line with 17q+ under normal growth conditions and under RS. We could show a proliferative ad-vantage of hESC with 13q+17q+ over wild type by measurement of the cumulative growth and molecular analysis for chromosomal copy number analysis. To monitor effects of 17q+ on RS-resistance, cell cycle and transcriptome analysis were performed. In conclusion, we show that extra chromosomal aberrations, such as 17q+, provide proliferative advantage to hESC under RS and suggest that this phenomenon explains the high incidence of 17q+ in in vitro cultured hESC lines.

2021-05-11 | GSE150645 | GEO

Transcriptional profilling of hESC with and without 17q gain upon induction of replicative stress through HU treatment [RNA-Seq]

2021-05-11 | GSE150639 | GEO

Transcriptional profilling of hESC with and without 17q gain upon induction of replicative stress through HU treatment [targeted exome sequencing]

2021-05-11 | GSE155181 | GEO

Transcriptional profilling of hESC with and without 17q gain upon induction of replicative stress through HU treatment

Project description:Transcriptional profilling of hESC with and without 17q gain upon induction of replicative stress through HU treatment

| PRJNA633092 | ENA

Transcriptional profilling of hESC with and without 17q gain upon induction of replicative stress through HU treatment [sWGS]

Project description:Transcriptional profilling of hESC with and without 17q gain upon induction of replicative stress through HU treatment [sWGS]

| PRJNA633094 | ENA

Transcriptional profilling of hESC with and without 17q gain upon induction of replicative stress through HU treatment [RNA-Seq]

Project description:Transcriptional profilling of hESC with and without 17q gain upon induction of replicative stress through HU treatment [RNA-Seq]

| PRJNA633080 | ENA

Transcriptional profilling of hESC with and without 17q gain upon induction of replicative stress through HU treatment

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

2021-05-11 | GSE150647 | GEO

Synergistic Inhibition of CHK1 and MUS81 to target replicative stress in high-risk neuroblastoma

Project description:Neuroblastoma (NB) is a pediatric tumor marked by genetic heterogeneity and frequent chromosomal alterations, including MYCN amplification and 17q gain, both linked to poor prognosis. These alterations affect key genes involved in transcriptional regulation and DNA damage response (DDR). NB cells experience high replicative stress (RS), making them particularly sensitive to DDR inhibition. Through integrative bioinformatics, genes such as EME1, RAD51C, and FANCJ on 17q were identified as critical in RS regulation. Targeting the downstream endonuclease MUS81, especially in combination with CHK1 inhibition, produced synergistic anti-tumor effects. This combination offers a promising strategy to exploit RS vulnerability in high-risk NB.

2025-11-20 | GSE294750 | GEO

Human Placenta profilling LTQ-OrbiTrap

Project description:Profilling normal human placantal proteomes using LTQ-OrbiTrap

2015-05-26 | PXD000754 | Pride

HU treatment of Sulfolobus solfataricus P2

Project description:Hydroxyurea (HU) is toxic to Sulfolobus cells. To address the basis of the HU toxicity, we performed transcriptome analyses on untreated cells and cells following exposure to 5 mM HU for 4 hours.

2016-10-05 | GSE87612 | 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