Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Esrrb plays an important role in maintaining self-renewal of trophoblast stem cells (TSCs) and reprogramming somatic cells to induced TSCs

ABSTRACT: Esrrb plays an important role in maintaining self-renewal of trophoblast stem cells (TSCs) and reprogramming somatic cells to induced TSCs

PROVIDER: PRJNA413531 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR6145050_1.fastq.gz	Fastqsanger.gz
	SRR6145050_2.fastq.gz	Fastqsanger.gz
	SRR6145051_1.fastq.gz	Fastqsanger.gz
	SRR6145051_2.fastq.gz	Fastqsanger.gz
	SRR6145052_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 26

Similar Datasets

Esrrb plays an important role in maintaining self-renewal of trophoblast stem cells (TSCs) and reprogramming somatic cells to induced TSCs [ChIP-Seq]

Project description:Trophoblast stem cells (TSCs) are derived from the trophoectoderm of a blastocyst and can maintain self-renewal in vitro. Meanwhile, essential insights into the molecular mechanisms controlling placental developmental could be gained by using TSCs that can differentiate into the various placental trophoblast cell types in vitro. Esrrb is a transcription factor with pivotal roles in maintaining TSCs’ self-renewal, but the exact transcriptional networks that Esrrb involved in TSCs are largely unknown. In the present study, we elucidated the function of Esrrb during TSC self-renewal and differentiation. We demonstrate that precise levels of Essrb are critical for TSCs stemness maintenance and normal trophoblast differentiation, as Esrrb depletion results in down-regulation of the key TSC-specific transcription factors, consequently causing TSCs differentiation and forced expression of Esrrb can partially block TSCs differentiation in the absence of FGF4. This function of Esrrb is exerted by directly binding and activating a core set of TSC-specific target genes including Cdx2, Eomes, Sox2, Fgfr4 and BMP4. Furthermore, we investigate the role of Esrrb in reprogramming of mouse embryonic fibroblasts (MEFs) to induced TSCs (iTSCs). We show that Esrrb can facilitate the conversion of iTSCs from MEFs. Moreover, Esrrb can substitute for Eomes during this conversion process. Our findings provide a better understanding of the molecular mechanism of Esrrb in maintaining TSCs self-renewal and iTSCs reprogramming.

2019-10-06 | GSE104695 | GEO

Esrrb plays an important role in maintaining self-renewal of trophoblast stem cells (TSCs) and reprogramming somatic cells to induced TSCs [RNA-Seq]

2019-10-06 | GSE104694 | GEO

Esrrb plays an important role in maintaining self-renewal of trophoblast stem cells (TSCs) and reprogramming somatic cells to induced TSCs [ChIP-Seq]

Project description:Esrrb plays an important role in maintaining self-renewal of trophoblast stem cells (TSCs) and reprogramming somatic cells to induced TSCs [ChIP-Seq]

| PRJNA413533 | ENA

Esrrb plays an important role in maintaining self-renewal of trophoblast stem cells (TSCs) and reprogramming somatic cells to induced TSCs [RNA-Seq]

Project description:Esrrb plays an important role in maintaining self-renewal of trophoblast stem cells (TSCs) and reprogramming somatic cells to induced TSCs [RNA-Seq]

| PRJNA413534 | ENA

Esrrb plays important roles in maintaining self-renewal of trophoblast stem cells (TSCs) and reprogramming somatic cells to induced TSCs.

Project description:Trophoblast stem cells (TSCs), which can be derived from the trophoectoderm of a blastocyst, have the ability to sustain self-renewal and differentiate into various placental trophoblast cell types. Meanwhile, essential insights into the molecular mechanisms controlling the placental development can be gained by using TSCs as the cell model. Esrrb is a transcription factor that has been shown to play pivotal roles in both embryonic stem cell (ESC) and TSC, but the precise mechanism whereby Esrrb regulates TSC-specific transcriptome during differentiation and reprogramming is still largely unknown. In the present study, we elucidate the function of Esrrb in self-renewal and differentiation of TSCs, as well as during the induced TSC (iTSC) reprogramming. We demonstrate that the precise level of Esrrb is critical for stem state maintenance and further trophoblast differentiation of TSCs, as ectopically expressed Esrrb can partially block the rapid differentiation of TSCs in the absence of fibroblast growth factor 4. However, Esrrb depletion results in downregulation of certain key TSC-specific transcription factors, consequently causing a rapid differentiation of TSCs and these Esrrb-deficient TSCs lose the ability of hemorrhagic lesion formation in vivo. This function of Esrrb is exerted by directly binding and activating a core set of TSC-specific target genes including Cdx2, Eomes, Sox2, Fgfr4, and Bmp4. Furthermore, we show that Esrrb overexpression can facilitate the MEF-to-iTSC conversion. Moreover, Esrrb can substitute for Eomes to generate GEsTM-iTSCs. Thus, our findings provide a better understanding of the molecular mechanism of Esrrb in maintaining TSC self-renewal and during iTSC reprogramming.

| S-EPMC6734492 | biostudies-literature

Esrrb plays an important role in maintaining self-renewal of trophoblast stem cells (TSCs) and reprogramming somatic cells to induced TSCs

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

2019-10-06 | GSE104696 | GEO

DNA methylation abnormal accumulation during cloned TSCs maintaining

Project description:DNA methylation abnormal accumulation during cloned TSCs maintaining

| PRJNA685859 | ENA

DNA methylation abnormal accumulation during cloned TSCs maintaining [RRBS]

Project description:DNA methylation abnormal accumulation during cloned TSCs maintaining [RRBS]

| PRJNA685862 | ENA

DNA methylation abnormal accumulation during cloned TSCs maintaining [RNA-seq]

Project description:DNA methylation abnormal accumulation during cloned TSCs maintaining [RNA-seq]

| PRJNA685861 | ENA

ESRRB facilitates the conversion of Trophoblast-like Stem Cells from induced pluripotent stem cells by directly regulating KRT8 and CDX2 [RNA-seq]

Project description:Studies on porcine induced pluripotent stem cells (piPSCs) served as a great reference for human clinical research. However, the pluripotency genes network of piPSCs, especially the core transcription factor ESRRB, was currently poor understand. Here, we constructed an overexpressing ESRRB piPSC line (ESRRB piPSCs) in which ESRRB expression was efficiently enhanced. It was found that ESRRB piPSCs showed scattered and flat colonies, moreover, the ESRRB piPSCs showed higher chimeric capacity into trophectoderm than that of CON piPSCs. We also found that ESRRB could directly regulate the expressions of the trophoblast stem cells (TSCs) markers, such as KRT8, KRT18 and CDX2, through binding in their promoter regions. Functional analysis of the mutant domains of ESRRB proved. that the zinc finger domain was indispensable for ESRRB to regulate TSCs markers. Moreover, the regulated process needed the participation of OCT4. Accordingly, ESRRB cooperating with OCT4 promoted TSCs markers to facilitate the conversion from the pluripotent state to trophoblastic-like state. Our results revealed the unique and crucial role of ESRRB in the determination of piPSCs fate and provided opportunities for studying the barriers underlying embryonic and extra-embryonic lineage segregation.

2021-10-14 | GSE180057 | 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