Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Cortical single-cell RNA sequencing of the microglia specific TREM2 inducible mouse models in the middle stage of amyloid deposition

ABSTRACT: Cortical single-cell RNA sequencing of the microglia specific TREM2 inducible mouse models in the middle stage of amyloid deposition

PROVIDER: PRJNA675896 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other
	SRR13021348.fastq.gz	Fastqsanger.gz

Items per page:

1 - 2 of 2

Similar Datasets

Cortical single-cell RNA sequencing of the microglia specific TREM2 inducible mouse models in the middle stage of amyloid deposition

Project description:We induced TREM2 expression at 2 months of age in our 5xFAD/TREM2 mouse models and harvested the animals at 5 months of age. The single cells from the cortex were isolated and subjected to the single-cell RNA seq to investigate the effects of TREM2 on microglia transcriptomic profiles in the middle stage of amyloid development. Our data showed that TREM2-WT induced the mTOR/EIF2 signaling pathways and restricted the disease associated microglia (DAM) signature. In contrast TREM2-R47H variant significantly upregulated the MHC class II molecules, enriched the antigen presentation pathway, and exacerbated a signature of antigen presentation contributing to enhanced amyloid pathology.

2020-11-11 | GSE161227 | GEO

Expression data from WT and TREM2 deficient microglia in a mouse model of Alzheimer's disease

Project description:We examined the role of TREM2 on microglia responses to amyloid-beta deposition in a mouse model of Alzheimer's disease Microglia were FACS-purified from 8.5 month old WT, Trem2-/-, 5XFAD, and Trem2-/- 5XFAD mice

2015-03-13 | E-GEOD-65067 | biostudies-arrayexpress

Cortical single-cell RNA sequencing of the microglia specific TREM2 inducible mouse models in the early stage of amyloid deposition

Project description:We induced TREM2 expression at birth in our 5xFAD/TREM2 mouse models and harvested the animals at 3.5 months of age. The single cells from the cortex were isolated and subjected to the single-cell RNA seq to investigate the effects of TREM2 on microglia transcriptomic profiles in the early stage of amyloid development. Our data showed that TREM2-WT, to a lesser extent of TREM2-R47H, restricted the disease associated microglia (DAM) signature at this stage.

2020-11-11 | GSE161224 | GEO

Cortical single-cell RNA sequencing of the microglia specific TREM2 inducible mouse models in the early stage of amyloid deposition

Project description:Cortical single-cell RNA sequencing of the microglia specific TREM2 inducible mouse models in the early stage of amyloid deposition

| PRJNA675894 | ENA

Expression data from WT and TREM2 deficient microglia in a mouse model of Alzheimer's disease

Project description:We examined the role of TREM2 on microglia responses to amyloid-beta deposition in a mouse model of Alzheimer's disease

2015-03-13 | GSE65067 | GEO

TREM2 regulates microglial cell activation in response to demyelination in vivo

Project description:Microglia are phagocytic cells that survey the brain and perform neuroprotective functions in response to tissue damage, but their activating receptors are largely unknown. Triggering receptor expressed on myeloid cells 2 (TREM2) is a microglial immunoreceptor whose loss-of-function mutations in humans cause presenile dementia, while genetic variants are associated with increased risk of neurodegenerative diseases. In myeloid cells, TREM2 has been involved in the regulation of phagocytosis, cell proliferation and inflammatory responses in vitro. However, it is unknown how TREM2 contributes to microglia function in vivo. Here, we identify a critical role for TREM2 in the activation and function of microglia during cuprizone (CPZ)-induced demyelination. TREM2-deficient (TREM2(-/-)) mice had defective clearance of myelin debris and more axonal pathology, resulting in impaired clinical performances compared to wild-type (WT) mice. TREM2(-/-) microglia proliferated less in areas of demyelination and were less activated, displaying a more resting morphology and decreased expression of the activation markers MHC II and inducible nitric oxide synthase as compared to WT. Mechanistically, gene expression and ultrastructural analysis of microglia suggested a defect in myelin degradation and phagosome processing during CPZ intoxication in TREM2(-/-) microglia. These findings place TREM2 as a key regulator of microglia activation in vivo in response to tissue damage. Two STAGE (6weeks 12 weeks),

2015-07-06 | E-GEOD-70475 | biostudies-arrayexpress

Trem2 effects on brain resident myeloid cells in PS2APP model

Project description:Comparing Trem2-KO;PS2APP and Trem2-WT;PS2APP CD11b+ cells reveals the role of Trem2 in microglial gene expression in amyloid-laden brains. The "SAMPLE_ID" sample characteristic is a sample identifier internal to Genentech. The ID of this project in Genentech's ExpressionPlot database is PRJ0014430

2020-02-25 | GSE140744 | GEO

Microglia gravitate toward amyloid plaques surrounded by externalized phosphatidylserine via TREM2

Project description:Microglia gravitate toward amyloid plaques surrounded by externalized phosphatidylserine via TREM2

| PRJNA911174 | ENA

Plasmin activity promotes amyloid deposition in a new transgenic model of human transthyretin amyloidosis.

Project description:We have developed a new mouse model of transthyretin (TTR) amyloidosis using transgenic mice expressing the most fibrillogenic variant of TTR (S52P). Following seeding with amyloid fibrils, TTR amyloid is deposited mainly in the heart and tongue. The fibrils contain both full length and truncated (49-127) TTR. The presence of S52P TTR was confirmed by proteomics. Knockout of alpha2-antiplasmin enhanced amyloid deposition.

2021-12-27 | PXD027747 | Pride

TREM2 supports neuronal protection and microglial reactivity independently of affecting misfolded protein deposition in chronic neurodegenerative prion disease

Project description:TREM2 (triggering receptor expressed on myeloid cells-2) variants have been identified as risk factors for neurodegenerative disease including Alzheimer’s disease. TREM2 is a cell surface receptor on microglia that regulates homeostatic and immunomodulatory functions including phagocytosis of apoptotic debris and the resolution of damage-associated inflammation. It remains unclear how TREM2 may mediate an influence on neurodegenerative disease, particularly in relation to key neuropathological hallmarks such as neuronal loss and proteinopathy. We used the ME7 prion disease model to assess the role of TREM2 in the progression and pathology of neurodegenerative disease. Prion diseases are characterised by the accumulation of misfolded prion protein and provide a highly tractable platform to determine if TREM2 has disease-modifying effects. Trem2-/- and wild type mice were inoculated intracerebrally with mouse-passaged ME7 scrapie prions and effects on CNS disease pathogenesis determined. Although the accumulation of prion disease-specific PrP was similar in the brains of mice from each group, the severity of the neuropathology was increased in Trem2-/- mice. Morphometric analysis of the microglia also indicated blunted disease-induced reactivity in the brains of infected Trem2-/- mice compared to wild type (WT) controls. The expression of genes involved in myelination were reduced in prion-infected Trem2-/- mice compared to infected WT mice. We conclude that during infection of the brain with prions, TREM2 supports microglial reactive changes that are associated with resilience to neuronal loss independently of affecting misfolded PrP deposition. These data imply that TREM2 status may be an important influence on the downstream response to CNS proteinopathy that alters the susceptibility of neurons and brain tissue to proteinopathy-induced degenerative changes.

2025-05-30 | GSE281022 | 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