Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Analysis of astrocyte interferon gamma signaling during EAE.

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

ORGANISM(S): Mus musculus

PROVIDER: GSE144872 | GEO | 2021/01/09

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Analysis of astrocyte interferon gamma signaling during EAE.

Project description:Analysis of astrocyte interferon gamma signaling during EAE.

| PRJNA605188 | ENA

Analysis of microglia responses following astrocyte knockdown of interferon gamma signaling during EAE.

Project description:We identify pathways in microglia regulated by astrocyte interferon gamma signaling during EAE

2021-01-09 | GSE154389 | GEO

Analysis of microglia responses following astrocyte knockdown of interferon gamma signaling during EAE.

Project description:Analysis of microglia responses following astrocyte knockdown of interferon gamma signaling during EAE.

| PRJNA646122 | ENA

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

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

2019-01-18 | GSE122113 | GEO

Conserved interferon-gamma signaling and decreased immune exclusion programs in responses to immune checkpoint blockade therapy

Project description:We analyzed baseline and on-therapy tumor biopsies from 101 patients with advanced melanoma treated with nivolumab (anti-PD-1) alone or combined with ipilimumab (anti-CTLA-4). Analysis of whole transcriptome data showed that T cell infiltration and interferon-gamma signaling signatures corresponded most highly with clinical response to therapy, with a reciprocal decrease in cell cycle and WNT signaling pathways in responding biopsies. Clinical outcome differences were likely not due to differential melanoma cell responses to interferon-gamma, as 57 human melanoma cell lines exposed in vitro to this cytokine showed a conserved interferon-gamma transcriptome response unless they had mutations that precluded signaling from the interferon-gamma receptor. Therefore, the magnitude of the antitumor T cell response and the corresponding downstream interferon-gamma signaling are the main drivers of clinical response or resistance to immune checkpoint blockade therapy.

| EGAS00001004545 | EGA

Interferon-gamma signaling promotes melanoma progression and metastasis

Project description:To investigate the effect of Interferon-gamma signaling on gene expression in melanoma cells We performed gene expression analysis of mouse melanoma cell lines that have been treated with Interferon-gamma cytokine as compared with mock-treated controls.

2022-10-08 | GSE214873 | GEO

Force expression LNK suppresses interferon Gamma signaling

Project description:Force expression LNK suppresses interferon Gamma signaling

| PRJNA525355 | ENA

Astrocyte-specific and region-specific transcriptomes in control and EAE mice

Project description:Changes in gene expression that occur across the entire central nervous system (CNS) during disease do not take into account variability from one CNS region to another and can be confounded by alterations in cellular composition during disease. Multiple sclerosis (MS) is characterized by cell proliferation, migration and damage in various cell types in different CNS regions and causes disabilities related to distinct neurological pathways, such as walking, vision and cognition. Here, a cell-specific and region-specific transcriptomic approach was used to determine changes in gene expression in astrocytes derived from spinal cord, cerebellum, cerebral cortex, and hippocampus in the preclinical MS model, chronic experimental autoimmune encephalomyelitis (EAE). RNA sequencing and bioinformatics analysis showed that changes in gene expression pathways in astrocytes differed between neuroanatomic regions. Further, while astrocytes from spinal cord showed increased expression of immune pathway genes during EAE, cholesterol biosynthesis pathway genes were decreased. Translating these findings from the preclinical model to humans, optic nerve from EAE and optic chiasm from MS each showed a significant decrease in cholesterol biosynthesis pathways. Finally, a treatment targeting cholesterol homeostasis in astrocytes was protective in EAE, suggesting a novel neuroprotective strategy for MS. Using a cell-specific and region-specific gene expression approach can provide therapeutically relevant insights into mechanisms underlying specific disabilities in complex multifocal neurological diseases.

2017-12-23 | GSE100329 | 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

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