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

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

PROVIDER: PRJNA633080 | ENA |

REPOSITORIES: ENA

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Dataset's files

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			Action	DRS
	SRR11795000.fastq.gz	Fastqsanger.gz
	SRR11795100.fastq.gz	Fastqsanger.gz
	SRR11795001.fastq.gz	Fastqsanger.gz
	SRR11795101.fastq.gz	Fastqsanger.gz
	SRR11795002.fastq.gz	Fastqsanger.gz

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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.

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

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

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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.

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