Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

EOFAD-causing mutations in psen1 orchestrate dedifferentiation through remodeling of the chromatin landscape in hiPSC-derived neurons

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE123998 | GEO | 2020/11/13

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

EOFAD-causing mutations in psen1 orchestrate dedifferentiation through remodeling of the chromatin landscape in hiPSC-derived neurons [ChIP-Seq]

Project description:In this work, we used an integrative, multi-omics approach and systems-level analysis to generate a mechanistic disease model for EOFAD in an hiPSC-derived neuron model system.

2020-11-13 | GSE123884 | GEO

EOFAD-causing mutations in psen1 orchestrate dedifferentiation through remodeling of the chromatin landscape in hiPSC-derived neurons [ATAC-Seq]

2020-11-13 | GSE123997 | GEO

EOFAD-causing mutations in psen1 orchestrate dedifferentiation through remodeling of the chromatin landscape in hiPSC-derived neurons [RNA-Seq]

2020-11-13 | GSE123891 | GEO

EOFAD-causing mutations in psen1 orchestrate dedifferentiation through remodeling of the chromatin landscape in hiPSC-derived neurons

Project description:EOFAD-causing mutations in psen1 orchestrate dedifferentiation through remodeling of the chromatin landscape in hiPSC-derived neurons

| PRJNA510451 | ENA

EOFAD-causing mutations in psen1 orchestrate dedifferentiation through remodeling of the chromatin landscape in hiPSC-derived neurons [ATAC-Seq]

Project description:EOFAD-causing mutations in psen1 orchestrate dedifferentiation through remodeling of the chromatin landscape in hiPSC-derived neurons [ATAC-Seq]

| PRJNA510453 | ENA

EOFAD-causing mutations in psen1 orchestrate dedifferentiation through remodeling of the chromatin landscape in hiPSC-derived neurons [ChIP-Seq]

Project description:EOFAD-causing mutations in psen1 orchestrate dedifferentiation through remodeling of the chromatin landscape in hiPSC-derived neurons [ChIP-Seq]

| PRJNA510452 | ENA

EOFAD-causing mutations in psen1 orchestrate dedifferentiation through remodeling of the chromatin landscape in hiPSC-derived neurons [RNA-Seq]

Project description:EOFAD-causing mutations in psen1 orchestrate dedifferentiation through remodeling of the chromatin landscape in hiPSC-derived neurons [RNA-Seq]

| PRJNA510454 | ENA

Familial Alzheimer's disease-associated PSEN1 mutations affect neurodevelopment through increased Notch signaling.

Project description:Alzheimer's disease (AD) is the most common neurodegenerative disorder, but its root cause may lie in neurodevelopment. PSEN1 mutations cause the majority of familial AD, potentially by disrupting proper Notch signaling, causing early unnoticed cellular changes that affect later AD progression. While rodent models are useful for modeling later stages of AD, human induced pluripotent stem cell-derived cortical spheroids (hCSs) allow access to studying the human cortex at the cellular level over the course of development. Here, we show that the PSEN1 L435F heterozygous mutation affects hCS development, increasing size, increasing progenitors, and decreasing post-mitotic neurons as a result of increased Notch target gene expression during early hCS development. We also show altered Aβ expression and neuronal activity at later hCS stages. These results contrast previous findings, showing how individual PSEN1 mutations may differentially affect neurodevelopment and may give insight into fAD progression to provide earlier time points for more effective treatments.

| S-EPMC10362499 | biostudies-literature

PGC7 promotes tumor oncogenic dedifferentiation through remodeling DNA methylation pattern for key developmental transcription factors.

Project description:Poorly differentiated tumors usually exhibit phenotypes similar to that of their developmental precursor cells. Tumor cells that acquire the lineage progenitor cells feature usually exploit developmental signaling to potentiate cancer progression. However, the underlying molecular events remain elusive. In this study, based on analysis of an in vitro hepatocyte differentiation model, the maternal factor PGC7 (also known as DPPA3, STELLA) was found closely associated with liver development and tumor differentiation in hepatocellular carcinoma (HCC). Expression of PGC7 decreased during hepatocyte maturation and increased progressively from well-differentiated HCCs to poorly differentiated HCCs. Whole-genome methylation sequencing found that PGC7 could induce promoter demethylation of genes related to development. Pathway-based network analysis indicated that downstream targets of PGC7 might form networks associated with developmental transcription factor activation. Overexpression of PGC7 conferred progenitor-like features of HCC cells both in vitro and in vivo. Mechanism studies revealed that PGC7 could impede nuclear translocation of UHRF1, and thus facilitate promoter demethylation of GLI1 and MYCN, both of which are important regulators of HCC self-renewal and differentiation. Depletion or inhibition of GLI1 effectively downregulated MYCN, abolished the effect of PGC7, and sensitized HCC cells to sorafenib treatment. In addition, we found a significant correlation of PGC7 with GLI1/MYCN and lineage differentiation markers in clinical HCC patients. PGC7 expression might drive HCC toward a "dedifferentiated" progenitor lineage through facilitating promoter demethylation of key developmental transcription factors; further inhibition of PGC7/GLI1/MYCN might reverse poorly differentiated HCCs and provide novel therapeutic strategies.

| S-EPMC8185079 | biostudies-literature

The transcriptomic landscape of glutamatergic cortical neurons carrying Alzheimer’s disease PSEN1 mutations reveals alterations in structural components, signalling, and ncRNA regulation

Project description:To investigate gene expression changes related to two fAD mutations (A79V and L150P) in the Presenilin-1 gene (PSEN1) we compared the transcriptomes (polyA and total) of glutamatergic cortical neurons derived from fAD-mutant human induced pluripotent stem cells and their individual isogenic controls generated via precision CRISPR/Cas9 genome editing.

2023-01-24 | GSE211993 | 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