Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Genome-wide analysis of the transcriptional profile of IL1b/TNFa-treated and EAE astrocytes in B6 mice.

ABSTRACT: Genome-wide analysis of the transcriptional profile of IL1b/TNFa-treated and EAE astrocytes in B6 mice.

PROVIDER: PRJNA565156 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR10103174.fastq.gz	Fastqsanger.gz
	SRR10103175.fastq.gz	Fastqsanger.gz
	SRR10103176.fastq.gz	Fastqsanger.gz
	SRR10103177.fastq.gz	Fastqsanger.gz
	SRR10103178.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 6

Similar Datasets

Genome-wide analysis of the transcriptional profile of IL1b/TNFa-treated and EAE astrocytes in B6 mice.

Project description:We identify pathways regulated by IL1b/TNFa ICV injection and EAE in astrocytes

2020-02-12 | GSE137314 | GEO

Signatures of IL1b, IL6 and TNFa in immune cell-types

Project description:A complete profiling of inflammatory cytokines (IL1b, IL6 and TNFa) in 14 immune cell-types

2025-01-14 | GSE239946 | GEO

Genome-wide analysis of the transcriptional profile of WT and Mafg KD astrocytes during EAE in B6 mice.

Project description:We identify pathways regulated by Mafg in astrocytes during EAE

2020-02-12 | GSE135571 | GEO

Genome-wide analysis of the transcriptional profile of WT and Lamp1 KD astrocytes during EAE in B6 mice

Project description:We identify pathways regulated by Lamp1 in astrocytes during EAE.

2021-01-09 | GSE144855 | GEO

Signatures of IL1b, IL6 and TNFa in immune cell-types

Project description:Signatures of IL1b, IL6 and TNFa in immune cell-types

| PRJNA1001800 | ENA

Genome-wide analysis of the transcriptional profile of WT and Nfe2l2 KD astrocytes during EAE in B6 mice [Nrf2 RNA-seq]

Project description:We identify pathways regulated by Nfe2l2 in astrocytes during EAE Multiple sclerosis (MS) is an autoimmune neurologic disease leading to demyelination and neurologic dysfunction controlled by both genetic and environmental factors. In addition to CNS-infiltrating immune cells, CNS-resident cells, such as astrocytes, are thought to play an important role in MS pathogenesis. However, a comprehensive understanding of the extent to which gene expression is disrupted in astrocytes is not known. Here, we implement single-cell RNA sequencing, in vivo genetic perturbations, cell-specific RNA profiling by Ribotag, as well as single-cell RNA sequencing of human MS patient samples to identify a transcriptional regulatory network in astrocytes that controls the pathogenesis of EAE and potentially, MS. We defined an astrocyte subpopulation characterized by expression of the small Maf protein, MAFG, which represses NRF2-driven antioxidant mechanisms and promotes EAE pathogenesis. Mechanistically, MAFG suppresses NRF2-dependent antioxidant genetic programs by cooperating with its cofactor, MAT2a, to promote DNA methylation in the context of CNS inflammation, which in turn increases pathogenic signaling processes in astrocytes. MAFG/MAT2a astrocytes are controlled by GM-CSF signaling, which drives EAE pathogenesis and MAFG expression. MAFG is activated in astrocytes derived from MS patients, which are characterized by DNA methylation programs, pro-inflammatory signaling processes including GM-CSF signaling, and repressed NRF2 activation. Together, these data create a transcriptional and epigenetic framework to analyze CNS inflammation in MS and may provide new therapeutic targets.

2020-02-12 | GSE129774 | GEO

Genome-wide analysis of the transcriptional profile of the CNS during EAE in B6 mice by scRNA-seq [scRNA-seq]

Project description:We identify cellular heterogeneity during EAE in B6 mice. Multiple sclerosis (MS) is an autoimmune neurologic disease leading to demyelination and neurologic dysfunction controlled by both genetic and environmental factors. In addition to CNS-infiltrating immune cells, CNS-resident cells, such as astrocytes, are thought to play an important role in MS pathogenesis. However, a comprehensive understanding of the extent to which gene expression is disrupted in astrocytes is not known. Here, we implement single-cell RNA sequencing, in vivo genetic perturbations, cell-specific RNA profiling by Ribotag, as well as single-cell RNA sequencing of human MS patient samples to identify a transcriptional regulatory network in astrocytes that controls the pathogenesis of EAE and potentially, MS. We defined an astrocyte subpopulation characterized by expression of the small Maf protein, MAFG, which represses NRF2-driven antioxidant mechanisms and promotes EAE pathogenesis. Mechanistically, MAFG suppresses NRF2-dependent antioxidant genetic programs by cooperating with its cofactor, MAT2a, to promote DNA methylation in the context of CNS inflammation, which in turn increases pathogenic signaling processes in astrocytes. MAFG/MAT2a astrocytes are controlled by GM-CSF signaling, which drives EAE pathogenesis and MAFG expression. MAFG is activated in astrocytes derived from MS patients, which are characterized by DNA methylation programs, pro-inflammatory signaling processes including GM-CSF signaling, and repressed NRF2 activation. Together, these data create a transcriptional and epigenetic framework to analyze CNS inflammation in MS and may provide new therapeutic targets.

2020-02-12 | GSE129609 | GEO

Disease-associated astrocyte epigenetic memory promotes CNS pathology [RNA-Seq of p300 KD, ACLY KD and scramble NOD-EAE mice]

Project description:Gene profiling of scramble, ACLY, and p300 KD astrocytes during NOD-EAE in B6 mice.

2024-03-21 | GSE252498 | GEO

Pharmacologic inhibition of EphB3 receptor kinase ameliorates EAE

Project description:To evaluate the potential of EphB3 as a therapeutic target during CNS inflammation, we induced EAE in B6 WT mice and starting at the peak of the disease we initiated treatment with A38 administered. A38 administration ameliorated EAE, and the transcriptional analysis of the astrocytes and microglia revealed the decreased expression of genes associated to inflammation and neurodegeneration.

2022-02-25 | GSE149135 | GEO

RIPK1 kinase-dependent gene expression in mouse microglia and astrocytes in vivo during EAE

Project description:To determine the role of RIPK1 kinase signaling in microglia and astrocytes during EAE (mouse model of MS), we extracted spinal cords of naive, EAE-vehicle and EAE mice treated with RIPK1 kinase inhibitor (GSK’547) for transcript profiling using RNAseq. We identify various genes that are differentially expressed in EAE disease compared to naive mice, and a subset of these are modulated in a RIPK1 kinase-dependent manner in both astrocytes and microglia. The top RIPK1 kinase-dependent gene pathways include oxidative phosphorylation and mitochondrial dysfunction in microglia and EIF2 signaling and cholesterol biosynthesis in astrocytes. This study demonstractes critical and distinct roles for RIPK1 kinase signaling in both microglia and astrocytes during EAE

2021-08-12 | GSE154228 | 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