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 astrocyte XBP1 activation and regulation of transcriptional programs in CNS cells during EAE.

ABSTRACT: We report XBP1 activation and regulation of pro-inflammatory signaling in astrocytes, microglia, and CNS-recruited pro-inflammatory monocytes during EAE.

ORGANISM(S): Mus musculus

PROVIDER: GSE122113 | GEO | 2019/01/18

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Genome-wide analysis of XBP1 binding in astrocytes during EAE

Project description:We report XBP1 activation and analysis of XBP1 binding to pro-inflammatory genes in astrocytes during EAE compared to naïve mice

2019-01-18 | GSE121935 | GEO

Genome-wide analysis of chromatin profile in astrocytes isolated from EAE mice transduced with astrocyte-specific Xbp1-targeting or non-targeting lentiviruses.

Project description:We report XBP1 activation and regulation of pro-inflammatory gene expression in astrocytes during EAE.

2019-01-18 | GSE121923 | GEO

Genome-wide analysis of XBP1 binding in astrocytes during EAE

Project description:Genome-wide analysis of XBP1 binding in astrocytes during EAE

| PRJNA499097 | ENA

Genome-wide analysis of astrocyte XBP1 activation and regulation of transcriptional programs in CNS cells during EAE.

Project description:Genome-wide analysis of astrocyte XBP1 activation and regulation of transcriptional programs in CNS cells during EAE.

| PRJNA503623 | ENA

Analysis of astrocyte interferon gamma signaling during EAE.

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

2021-01-09 | GSE144872 | 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

Microglial Semaphorin4D and astrocyte PlexinB1-B2 knockdown in EAE

Project description:Identification of pathways regulated by semaphorin 4D-PlexinB1/B2 signaling in astrocytes during EAE

2021-04-22 | GSE156757 | 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

Genome-wide analysis of the transcriptional profile of WT and CSF2RB astrocyte conditional KO during EAE in B6 mice [Csf2rb RNA-seq]

Project description:We identify pathways regulated by Csf2rb 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 | GSE129773 | GEO

Genome-wide analysis of chromatin profile in astrocytes isolated from EAE mice transduced with astrocyte-specific Mafg-targeting or non-targeting lentiviruses [ATAC-seq]

Project description: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. We report MAFG regulation of pathogenic activities in astrocytes during EAE.

2020-02-12 | GSE129608 | 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