Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Oncogene-induced maladaptive activation of Trained Immunity in the pathogenesis of human inflammatory myeloid neoplasm [ECD]

ABSTRACT: Trained immunity (TI) is a pro-inflammatory program induced in monocyte/macrophages upon sensing of specific pathogens and characterized by immunometabolic and epigenetic changes enhancing cytokine production. Maladaptive activation of TI (i.e., in the absence of infection) might result in detrimental inflammation and disease development; however, the exact role and extent of inappropriate activation of TI in the pathogenesis of human diseases is undetermined.

ORGANISM(S): Homo sapiens

PROVIDER: GSE173828 | GEO | 2021/05/05

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Oncogene-induced maladaptive activation of Trained Immunity in the pathogenesis of human inflammatory myeloid neoplasm [BRAF]

Project description:Trained immunity (TI) is a pro-inflammatory program induced in monocyte/macrophages upon sensing of specific pathogens and characterized by immunometabolic and epigenetic changes enhancing cytokine production. Maladaptive activation of TI (i.e., in the absence of infection) might result in detrimental inflammation and disease development; however, the exact role and extent of inappropriate activation of TI in the pathogenesis of human diseases is undetermined.

2021-05-05 | GSE173829 | GEO

Oncogene-induced maladaptive activation of Trained Immunity in the pathogenesis of human inflammatory myeloid neoplasm [ECD]

Project description:Oncogene-induced maladaptive activation of Trained Immunity in the pathogenesis of human inflammatory myeloid neoplasm [ECD]

| PRJNA727237 | ENA

Oncogene-induced maladaptive activation of Trained Immunity in the pathogenesis of human inflammatory myeloid neoplasm

Project description:Oncogene-induced maladaptive activation of Trained Immunity in the pathogenesis of human inflammatory myeloid neoplasm

| PRJNA727232 | ENA

Oncogene-induced maladaptive activation of Trained Immunity in the pathogenesis of human inflammatory myeloid neoplasm

Project description:This SuperSeries is composed of the SubSeries listed below.

2021-05-05 | GSE173830 | GEO

Oncogene-induced maladaptive activation of Trained Immunity in the pathogenesis of human inflammatory myeloid neoplasm [BRAF]

Project description:Oncogene-induced maladaptive activation of Trained Immunity in the pathogenesis of human inflammatory myeloid neoplasm [BRAF]

| PRJNA727240 | ENA

APOE4 drives transcriptional heterogeneity and maladaptive immunometabolic responses of astrocytes

Project description:APOE4 drives transcriptional heterogeneity and maladaptive immunometabolic responses of astrocytes

| PRJNA890284 | ENA

APOE4 drives transcriptional heterogeneity and maladaptive immunometabolic responses of astrocytes (Spatial)

Project description:APOE4 drives transcriptional heterogeneity and maladaptive immunometabolic responses of astrocytes (Spatial)

| PRJNA890289 | ENA

APOE4 drives transcriptional heterogeneity and maladaptive immunometabolic responses of astrocytes (Spatial)

Project description:Apolipoprotein 4 (APOE4), is the strongest genetic risk allele associated with the development of late onset Alzheimer’s disease (AD). Across the CNS, astrocytes are the predominant expressor of Apoe while also being critical mediators of neuroinflammation and cerebral metabolism. APOE4 has been consistently linked with dysfunctional neuro-immunometabolism, however insights into the molecular constituents driving these responses remain unclear. Utilizing complimentary approaches across humanized ApoE expressing mice and isogenic IPS astrocytes, we demonstrate that harboring ApoE4 alters astrocyte immunometabolic response to pro-inflammatory stimuli. Our findings demonstrate that ApoE4-expressing astrocytes acquire distinct transcriptional repertoires at the single-cell and spatially-resolved domains, which driven, in-part, by preferential utilization of the cRel transcription factor. Further, inhibiting cRel translocation abrogated inflammatory-induced glycolytic shift and ultimately resulted in significantly dampened glycolysis-associated metabolites in tandem with mitigating production of multiple pro-inflammatory cytokines. Altogether, our findings elucidate novel cellular underpinnings by which ApoE4 drives maladaptive immunometabolic responses of astrocytes.

2022-10-20 | GSE215445 | GEO

APOE4 drives transcriptional heterogeneity and maladaptive immunometabolic responses of astrocytes (scRNA-Seq)

2022-10-20 | GSE215444 | GEO

APOE4 drives transcriptional heterogeneity and maladaptive immunometabolic responses of astrocytes (scRNA-Seq)

Project description:APOE4 drives transcriptional heterogeneity and maladaptive immunometabolic responses of astrocytes (scRNA-Seq)

| PRJNA890285 | ENA