Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Transcriptome analysis of Foxj3 or Zbtb18 stable expressed embryonic stem (ES) cell lines

ABSTRACT: To understand the specific mechanism by which Foxj3 and Zbtb18 control RA-induced neural directional differentiation of ESCs, total mRNAs of Foxj3-ES and Zbtb18-ES were extracted and used for RNA seq and transcriptome analyses. Compared with the control, 1331 genes were differentially expressed (P < 0.05) by twofold in Foxj3-ES (557 were underexpressed and 774 were overexpressed), and 1175 genes were differentially expressed (P < 0.05) by twofold in Zbtb18-ESCs (548 were underexpressed and 627 were overexpressed). Through Gene ontology and gene co-expression network analysis, we identified four critical genes in the neural regulatory networks: Olig1, Zic5, Erbb2, and Olig2. Our study shows that Foxj3 and Zbtb18 could trigger the gene regulatory networks of neurodevelopment by mediating the expression of Olig1, Zic5, Erbb2, and Olig2.

ORGANISM(S): Mus musculus

PROVIDER: GSE61748 | GEO | 2017/08/21

SECONDARY ACCESSION(S): PRJNA262016

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

ID4 function antagonizes OLIG1 and OLIG2 to suppressive aggressive glioma

Project description:The basic helix-loop-helix proteins Olig1 and Olig2 are expressed in high grade, aggressive human glioblastoma multiformes (GBMs). Here we investigated genetic mechanisms regulating Olig1/2 function during gliomagenesis. Although Olig2 function is necessary for early-aggressive tumor formation in a genetically relevant model of classic GBMs with intact p53 function, late-onset gliomas do eventually form. Using an unbiased approach, we identified Id4, encoding a negative HLH protein, as a gene target potently repressed by Olig2 in glioma progenitors. Although Id4 is thought to antagonize proneural genes involved in differentiation, we report a paradoxical role for Id4 in glioma. Genetic deletion of Id4 converts Olig2-/- gliomas to the early-aggressive form, and conversely, overexpression of Id4 inhibits intact Olig2 and prevents even late-onset tumors. Olig1 overexpression is sufficient for gliomagenesis in an Id4-dependent manner. Together, these findings indicate that gliomagenic factors Olig1 and Olig2 are opposed by Id4 function, which acts as tumor suppressor in p53-intact gliomas.

2018-01-02 | GSE44151 | GEO

A mouse Embryonic Stem Cell Bank for inducible overexpression of human chromosome 21 genes

2010-12-06 | GSE19836 | GEO

Breast Milk-Associated Oxysterol Reverses Neonatal Brain Injury Through Gli2-Dependent Oligodendrogenesis

Project description:We identified an emerging oligodendrocyte committed subpopulation based on their gene expression that included Pdgfra, Cspg4 also known as Ng2, Olig1, Olig2.

2018-10-20 | GSE121540 | GEO

A mouse Embryonic Stem Cell Bank for inducible overexpression of human chromosome 21 genes

Project description:The HSA21-mES Cell Bank includes, in triplicate clones, thirty-two murine orthologs of HSA21 genes, which can be overexpressed in an inducible manner using the Tet-off system integrated in the Rosa26 locus. The following subset of twenty clones were characterized by microarray analysis: Bach1, Erg, Ets2, Gabpa, ZFP295, Nrip1, Olig1, Olig2, Pknox1, 1810007M14Rik, Runx1, Aire, Sim2, Dscr1, DYRK1A, SNF1LK, Ripk4 , Hunk, Pdxk, Pfkl. Each triplicate clone was transcriptionally profiled by microarray analysis using Affymetrix Mouse 430_2 arrays before and after induction (Affymetrix 430A_2 in case of Runx1), yielding six arrays for each overexpression experiment.

2010-12-06 | E-GEOD-19836 | biostudies-arrayexpress

Transit-amplifying lineage states convey the susceptibility of PTEN and P53 loss to gliomagenesis [ATAC-seq]

Project description:To investigate the glioma mouse model by knocking out Pten and Trp53 in embryonal Olig2 and Olig1 positive cells in glioma pathogenesis. ATAC-seq

2023-01-03 | GSE200890 | GEO

Transit-amplifying lineage states convey the susceptibility of PTEN and P53 loss to gliomagenesis [PPO1_and PPO1_Cells_RNA-seq]

Project description:To investigate the glioma mouse model by knocking out Pten and Trp53 in embryonal Olig2 and Olig1 positive cells in glioma pathogenesis. We then performed gene expression profiling analysis using data obtained from RNA-seq of 4 PPO2, 4 PPO1 and 2 OPN cell lines.

2023-01-03 | GSE200889 | GEO

Effect of ZBTB18 on gene expression and chromatin organization [RNA-seq]

Project description:This study set out to delineate gene expression programs that are differentially modulated in metastatic breast cancer cells with high versus low ability to further metastasize. To this end, the gene expression profiles of E0771GFP cells, M11GFP and M12GFP cells were determined. Analysis of these data sets identified ZBTB18 as a transcriptional repressor with lower activity in tumor cells that retain a high metastatic potential. To determine how ZBTB18 affects gene expression and chromatin organization, ZBTB18 was overexpressed in E0771GFP breast cancer cells. Gene expression profiles and differentially accessible DNA regions analyses were performed and identified Tgfbr2 as one of the genes most significantly repressed by ZBTB18. To determine the contribution of the TGFb1 -TGFBR2 signaling axis towards ZBTB18-mediated effects, E0771GFP cells overexpressing ZBTB18 were transduced with a doxycycline-inducible Tgfbr2 construct. These cells were then treated with doxycycline and recombinant TGFb1 or vehicle control and gene expression profiles were determined. These studies revealed that inhibition of ZBTB18 activity in tumor cells promotes metastasis by increasing chromatin accessibility and by enabling pro-metastatic TGFb1-TGFBR2-driven changes.

2022-12-22 | GSE195942 | GEO

Effect of ZBTB18 on gene expression and chromatin organization [ATAC-seq]

2022-12-22 | GSE195941 | GEO

Transit-amplifying lineage states convey the susceptibility of PTEN and P53 loss to gliomagenesis [CUT&RUN]

Project description:To investigate the glioma mouse model by knocking out Pten and Trp53 in embryonal Olig2 and Olig1 positive cells in glioma pathogenesis. Chromatin immunoprecipitation DNA-sequencing (ChIP-seq) for H3K27Ac in PPO1 and PPO2 mouse glioma cell lines and compare the active enhancers with oligodendrocyte progenitor cells.

2023-01-03 | GSE200891 | GEO

Genome-wide mapping of Olig2 targets in primary oligodendrocytes

Project description:Myelination by oligodendrocytes in the central nervous system (CNS) is essential for proper brain function, yet the molecular determinants that control this process remain poorly understood. The basic helix-loop-helix transcription factors Olig1 and Olig2 promote myelination, whereas bone morphogenetic protein (BMP) and Wnt/?-catenin signaling inhibit myelination. Here we show that these opposing regulators of myelination are functionally linked by the Olig1/2 common target Smad-interacting protein-1 (Sip1). We demonstrate that Sip1 is an essential modulator of CNS myelination. Sip1 represses differentiation inhibitory signals by antagonizing BMP receptor-activated Smad activity while activating crucial oligodendrocyte-promoting factors. Importantly, a key Sip1-activated target, Smad7, is required for oligodendrocyte differentiation and partially rescues differentiation defects caused by Sip1 loss. Smad7 promotes myelination by blocking the BMP- and ?-catenin-negative regulatory pathways. Thus, our findings reveal that Sip1-mediated antagonism of inhibitory signaling is critical for promoting CNS myelination and point to new mediators for myelin repair. ChIP-seq was performed to identify Olig2 direct target genes in oligodendrocytes during oligodendrocyte differentiation.

2012-08-31 | E-GEOD-40506 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

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