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RNA-seq analysis of the gene expression profile regulated by CHIR and Spautin-1 in mouse ESCs

ABSTRACT: RNA-seq analysis of the gene expression profile regulated by CHIR and Spautin-1 in mouse ESCs

PROVIDER: PRJNA723353 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14289124.fastq.gz	Fastqsanger.gz
	SRR14289125.fastq.gz	Fastqsanger.gz
	SRR14289127.fastq.gz	Fastqsanger.gz
	SRR14289128.fastq.gz	Fastqsanger.gz

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RNA-seq analysis of the gene expression profile regulated by CHIR and Spautin-1 in mouse ESCs

Project description:Purpose:The goals of this study is to analyze the gene expession pattern in mouse embryonic stem cells (ESCs) treated with CHIR99021(CHIR) in the presence or absence of Spautin-1 for 24 h.

2021-04-21 | GSE172469 | GEO

Next generation sequencing facilitates lineage identity of RA-induced and RA/CHIR-induced ESCs

Project description:To uncover the mechanism that Wnt signaling modulates RA-induced ESC differentiation, we conducted time course RNA-seq analysis during the differentiation. Transcriptome profiles of RA-induced and RA/CHIR-induced ESC differentiation were generated by deep sequencing, in triplicate, using Illumina HiSeq 2000. The RNA-seq data revealed a significant decrease in mesoderm (one of the major source of vascular SMCs) markers and increase in PrE markers in CHIR treated samples, while other lineage markers showed no significant expression, implying a diverging to PrE fate by Wnt activation. Subsequent hierarchical clustering analysis also showed that the gene expression profiles of cells derived from RA induction alone clustered with adult SMCs, while cells derived from RA/CHIR induction gradually clustered to XEN cells with differentiation and was very close to XEN cells at day 16, suggesting that RA/CHIR-induced ESCs differentiated into PrE lineage. This study provided new insights into the importance of RA/Wnt crosstalk in the lineage differentiation of ESCs.

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Global gene expression profile of mouse ESC-2i, EpiSC-CHIR/XAV and EpiSC-FGF2/activin

Project description:The requirements for self-renewal differ between EpiSCs and ES cells and the underlying mechanism is largely unknown. Here we show that mouse EpiSCs can be efficiently derived and robustly propagated even from single cells, using two small-molecule inhibitors: CHIR99021 and XAV939. The whole-genome microarray analyses is performed to confirm the identity of EpiSC maintained in CHIR/XAV by comparing the expression profile in EpiSC-CHIR/XAV to those in ESC maintained in 2i and EpiSC maintained in FGF2/activin. Total RNA from ESC-2i, EpiSC-CHIR/XAV, and EpiSC-FGF2/activin were extracted for microarray analisys

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Global gene expression profile of mouse ESC-2i, EpiSC-CHIR/XAV and EpiSC-FGF2/activin

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Next generation sequencing facilitates lineage identity of RA-induced and RA/CHIR-induced ESCs

Project description:Next generation sequencing facilitates lineage identity of RA-induced and RA/CHIR-induced ESCs

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Microarray expression data of HT-29 cells treated with spautin-1 or buformin under 2DG- or tunicamycin-stressed conditions

Project description:Spautin-1 as well as buformin showed preferential cytotoxicity under 2-deoxy-D-glucose (2DG)-stressed, but not tunicamycin-stressed conditions in HT-29 cells. By a microarray-based transcription analyses, we previously identified an unfolded protein response (UPR) expression signature, consisting of 246 probes up- or down-regulated in glucose starvation- and 2DG-stressed HT-29 and other cancer cell lines. Thus, we compared the effects of spautin-1 and buformin on the UPR transcriptional program. The two UPR inhibitors partly canceled 2DG-induced, but not TM-induced changes in UPR expression signature, indicating that spautin-1 can indeed suppress the UPR transcriptional program under 2DG-stressed conditions.

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RNA-seq analysis of the gene expression profile regulated by Prdm14 in mouse ESCs

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RNA-seq analysis of the gene expression profile regulated by Gadd45g in mouse ESCs

Project description:RNA-seq analysis of the gene expression profile regulated by Gadd45g in mouse ESCs

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E. coli gene expression following CHIR-090 treatment

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