Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

GSK3 acts as a switch for transcriptional programs in a model of low-grade gliomagenesis

ABSTRACT: GSK3 acts as a switch for transcriptional programs in a model of low-grade gliomagenesis

PROVIDER: PRJNA1253969 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR33245400_1.fastq.gz	Fastqsanger.gz
	SRR33245400_2.fastq.gz	Fastqsanger.gz
	SRR33245401_1.fastq.gz	Fastqsanger.gz
	SRR33245401_2.fastq.gz	Fastqsanger.gz
	SRR33245402_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 60

Similar Datasets

GSK3 acts as a switch for transcriptional programs in a model of low-grade gliomagenesis

Project description:Mutations in isocitrate dehydrogenase (IDH)-1/2 are defining drivers of low-grade gliomagenesis. However, mutant IDH alone is not sufficient for malignant transformation, and additional events are required for the development of low-grade glioma. While specific genetic lesions have been identified to contribute to low-grade gliomagenesis, less is known about the signaling pathways involved in acquiring malignancy. To identify prerequisites of IDH mutant tumorigenesis, we modulated pathways previously implicated in glioma initiation using a tractable in vitro model system for early IDH1R132H-dependent gliomagenesis. Through the use of chemical compounds, we targeted WNT/GSK3, TGF-β and NOTCH-signaling, assessing their functional, transcriptional, and translational impacts. Expression of LGG-related marker L1CAM was affected by perturbation of all pathways, though only modulation of WNT/GSK3-signaling resulted in profound molecular transformation, including glioma-associated genes and programs regulating cellular architecture and cell replication. This was accompanied by altered cell morphology, migration capacity, and enhanced proliferation. Transcription factor RUNX2 was identified as a potential downstream effector, whose inhibition abrogated cell proliferation. Disrupted WNT/GSK3 signaling in a model system of early low-grade gliomagenesis fundamentally impacted cell fate, as demonstrated by a reshaped transcriptional landscape, aberrant transcription factor activity, ECM restructuring, and altered proliferation capacity. Our data suggests that GSK3 may play a central role during low-grade gliomagenesis, warranting further investigation.

2025-04-25 | GSE295254 | GEO

Vemurafenib acts as molecular switch in Langerhans Cell Histiocytosis

Project description:Vemurafenib acts as molecular switch in Langerhans Cell Histiocytosis

| PRJNA732460 | ENA

Von Hippel-Lindau Acts as a Metabolic Switch Controlling Nephron Progenitor Differentiation

Project description:Von Hippel-Lindau Acts as a Metabolic Switch Controlling Nephron Progenitor Differentiation

| PRJNA506841 | ENA

The RelA hydrolase domain acts as a molecular switch for (p)ppGpp synthesis

Project description:The RelA hydrolase domain acts as a molecular switch for (p)ppGpp synthesis

| PRJNA632006 | ENA

Lysine Crotonylation Acts as an Epigenetic Switch for Glutamate Neurotransmission and Spatial Memory

Project description:Lysine Crotonylation Acts as an Epigenetic Switch for Glutamate Neurotransmission and Spatial Memory

| PRJNA1181824 | ENA

DksA acts as a transcriptional switch in stress and virulence in Acinetobacter baumannii

Project description:DksA acts as a transcriptional switch in stress and virulence in Acinetobacter baumannii

| PRJNA715173 | ENA

Polyubiquitination analysis upon GSK3 inhibition in HeLa cell extracts

Project description:HeLa cell extracts with or without GSK3 enzyme inhibition were assayed using protein microarrays in order to detect GSK3-dependent changes in protein polyubiquitination.

2014-05-15 | GSE50629 | GEO

Regulatory phosphorylation of eIF6 by GSK3

Project description:The overall goal of this project is to determine the key sites in the C-terminus of eIF6 that are recognized and phosphorylated by GSK3. Analysis of kinase reactions using the site-specific mutants as well as the C-terminus deletion mutants of eIF6 indicated that there are GSK3-specific motifs in the C-terminus that are phosphorylated by GSK3. The purpose of the Mass Spectrometry studies is to use MS as a targeted and secondary approach to validate and identify GSK3-specific sites of phosphorylation in the C-terminus of eIF6.

2020-06-16 | MSV000085596 | MassIVE

Differential gene expression by A2B5-defined Human glioma-initiating progenitor cells at all stages of gliomagenesis

Project description:Glial progenitor cells (GPCs) of the adult human white matter, which express gangliosides recognized by monoclonal antibody A2B5, are a potential source of glial tumors of the brain. We used A2B5-based sorting to extract progenitor-like cells from a range of human glial tumors, that included low-grade glioma, oligodendroglioma, oligo-astrocytomas, anaplastic astrocytoma, and glioblastoma multiforme. The A2B5+ tumor cells proved tumorigenic upon orthotopic xenograft, and the tumors generated reflected the phenotypes of those from which they derived. Expression profiling revealed that A2B5+ tumor progenitors expressed a cohort of genes by which they could be distinguished from A2B5+ GPCs isolated from normal adult white matter. Most of the genes differentially expressed by glioma-derived A2B5+ cells varied as a function of tumor stage; however, a small number were invariably expressed at all stages of gliomagenesis. These glioma progenitor-associated genes included CD24, SIX1 and EYA1, which were up-regulated at all stages of gliomagenesis, and MTUS1 and SPOCK3, which were down-regulated at all stages of tumor progression. qPCR and immunolabeling confirmed the differential expression of these genes in primary gliomas, while pathway analysis permitted their segregation into differentially active signaling pathways. By comparing the expression patterns of glial tumor progenitors to their identically-isolated normal homologues, we have identified a discrete set of oncogenic pathways by which glial tumorigenesis may be both better understood, and more efficiently targeted. Samples originating from patients with matched disease and/or pathology were considered as replicates either on the basis of exact tumor phenotype, tumor grade, or tumor vs. normal tissue samples.

2013-05-16 | E-GEOD-29796 | biostudies-arrayexpress

Polycomb dysregulation in gliomagenesis targets a Zfp423-dependent differentiation network [ChIP-Seq]

Project description:Malignant gliomas constitute one of the most significant areas of unmet medical need, due to the invariable failure of surgical eradication and their marked molecular heterogeneity. Accumulating evidence has revealed a critical contribution by the Polycomb axis of epigenetic repression. However, a coherent understanding of the regulatory networks affected by Polycomb during gliomagenesis is still lacking. Here we integrate transcriptomic and epigenomic analyses to define Polycomb-dependent networks that promote gliomagenesis, validating them both in two independent mouse models and in a large cohort of human samples. We found that Polycomb dysregulation in gliomagenesis affects transcriptional networks associated to invasiveness and de-differentiation. The dissection of these networks uncovers Zfp423 as a crtitical Polycomb-dependent transcription factor whose silencing negatively impacts survival. The anti-gliomagenic activity of Zfp423 requires interaction with the SMAD proteins within the BMP signaling pathway, pointing to a novel synergic circuit through which Polycomb inhibits BMP signaling. Analysis of H3K27me3 distribition in two different stages of gliomagenesis

2016-03-02 | E-GEOD-76289 | biostudies-arrayexpress

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