Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Defining key transcriptional regulators of extravillous trophoblast differentiation [ChIP-seq]

ABSTRACT: Defining key transcriptional regulators of extravillous trophoblast differentiation [ChIP-seq]

PROVIDER: PRJNA874728 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR21299511_1.fastq.gz	Fastqsanger.gz
	SRR21299511_2.fastq.gz	Fastqsanger.gz
	SRR21299512_1.fastq.gz	Fastqsanger.gz
	SRR21299512_2.fastq.gz	Fastqsanger.gz
	SRR21299513_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 92

Similar Datasets

Defining key transcriptional regulators of extravillous trophoblast differentiation

Project description:Defining key transcriptional regulators of extravillous trophoblast differentiation

| PRJNA874727 | ENA

Defining key transcriptional regulators of extravillous trophoblast differentiation [RNA-seq]

Project description:Defining key transcriptional regulators of extravillous trophoblast differentiation [RNA-seq]

| PRJNA874733 | ENA

Defining key transcriptional regulators of extravillous trophoblast differentiation [RNA-seq]

Project description:During early human pregnancy, extravillous trophoblasts (EVT) play a central role in placental anchorage and blood vessel remodeling. Despite the essential roles in pregnancy, key factors and mechanisms underlying EVT differentiation remain largely unknown. Here, we defined key transcription factors (TFs) by monitoring the dynamics of transcriptome and enhancer usage during EVT differentiation. We confirmed the requirements of the defined TFs and identified their action mechanisms.

2024-01-16 | GSE212266 | GEO

Defining key transcriptional regulators of extravillous trophoblast differentiation [ChIP-seq]

2024-01-16 | GSE212265 | GEO

Defining key transcriptional regulators of extravillous trophoblast differentiation

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

2024-01-16 | GSE212267 | GEO

Human uterine Natural Killer cells regulate differentiation of extravillous trophoblast early in pregnancy - scRNA-seq data

Project description:We used trophoblast organoids differentiating to extravillous trophoblast (EVT) to study the effects of key cytokines secreted by uterine Natural Killer (uNK) cells on EVT behaviour. Specifically, we exposed the organoids to four uNK-derived cytokines (CSF1, CSF2, XCL1, CCL5) and collected cells at different time points along the EVT differentiation pathway for scRNA-seq. We observe enhanced EVT differentiation in cytokine-treated organoids demonstrated by the increased proportion of late EVT subtypes and regulation of related pathways such as epithelial-mesenchymal transition. Moreover, uNK cytokines affect other processes important during early pregnancy including dampening of inflammatory and adaptive immune responses, regulation of blood flow, and placental access to nutrients.

2024-01-10 | E-MTAB-13382 | biostudies-arrayexpress

RRBS investigation of matched side-population trophoblast, cytotrophoblast and extravillous trophoblast populations from 4 human placentae

Project description:To better understand how DNA methylation influences placentation, DNA from first trimester primary trophoblast populations (side-population trophoblasts, cytotrophoblasts and extravillous trophoblasts) isolated using FACS underwent reduced representation bisulfite sequencing and were compared to publicly available data of blastocyst-derived and somatic cell populations.

2018-12-25 | GSE109682 | GEO

Human uterine Natural Killer cells regulate differentiation of extravillous trophoblast early in pregnancy - bulk RNA-seq data

Project description:An allorecognition system depending on interactions between uterine Natural Killer (uNK) cells and placental extravillous trophoblast (EVT) during early pregnancy influences reproductive outcomes in humans. Our previous immunogenetic studies show that particular combinations of maternal Killer Immunoglobulin-like Receptors (KIR) in uNK cells with fetal HLA-C variants on EVT are associated with disorders of pregnancy, especially pre-eclampsia. To identify responses stimulated in uNK cells specifically when activating KIR (KIR2DS1) binds to C2+HLA-C, a combination protective against pre-eclampsia, we modelled KIR-HLA interactions by co-culturing uNK cells with the 721.221 HLA-null cell line transfected to express either C1+ or C2+HLA-C molecules, followed by transcriptome profiling by RNA sequencing. We detect the secretion of key cytokines by uNK cells under the protective combination between KIR2DS1 and C2+HLA-C.

2024-01-10 | E-MTAB-13379 | biostudies-arrayexpress

NOTUM-MEDIATED WNT SILENCING DRIVES EXTRAVILLOUS TROPHOBLAST CELL LINEAGE DEVELOPMENT

Project description:NOTUM-MEDIATED WNT SILENCING DRIVES EXTRAVILLOUS TROPHOBLAST CELL LINEAGE DEVELOPMENT

| PRJNA848817 | ENA

iPSC-based modeling of preeclampsia identifies defects in extravillous trophoblast differentiation

Project description:Preeclampsia (PE) is a hypertensive pregnancy disorder with increased risk of maternal and fetal morbidity and mortality. Abnormal extravillous trophoblast (EVT) development and function is considered to be the underlying cause of PE, but has not previously been modeled in vitro. We previously derived induced pluripotent stem cells (iPSC) from placentas of PE patients and characterized abnormalities in formation of syncytiotrophoblast and responses to changes in oxygen tension. In this study, we converted these primed iPSC to naïve iPSC, then derived trophoblast stem cells (TSC) and EVT to evaluate molecular mechanisms underlying PE. We found that primed (but not naïve) iPSC-derived PE-EVT have reduced surface HLA-G, blunted invasive capacity, and altered EVT-specific gene expression. These abnormalities correlated with promotor hypermethylation of genes associated with the epithelial-mesenchymal transition pathway, specifically in primed-iPSC derived PE-EVT. Our findings indicate that abnormal epigenetic regulation might play a role in the PE pathogenesis.

2024-03-27 | GSE243579 | 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