Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Single cell RNA-seq data of microglia cells from normal mouse brain at three ages (embryonic, 3 weeks and 16 weeks)

ABSTRACT: Single cell RNA-seq data of microglia cells from normal mouse brain at three ages (embryonic, 3 weeks and 16 weeks)

PROVIDER: PRJNA494468 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR7949900.fastq.gz	Fastqsanger.gz
	SRR7949910.fastq.gz	Fastqsanger.gz
	SRR7949920.fastq.gz	Fastqsanger.gz
	SRR7949930.fastq.gz	Fastqsanger.gz
	SRR7949940.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 2688

Similar Datasets

Single cell RNA-seq data of microglia cells from normal mouse brain at three ages (embryonic, 3 weeks and 16 weeks)

Project description:Single cell RNA-seq data was obtained from FACS sorted microglia from different brain regions of normal embryonic, 3 weeks and 16 weeks old CD1 mice in order to elucidate microglia heterogeneity in a regional and time specific manner.

2019-02-13 | GSE120745 | GEO

Bulk RNA-seq of microglia at different ages

Project description:Bulk RNA-seq of microglia at different ages

| PRJNA859785 | ENA

Rescuing over-activated microglia by acetaminophen treatment restores cognitive performance in the Dp(16) mouse model of Down Syndrome.

Project description:Microglia are the resident immune cells of the brain and have been implicated in mechanisms essential for cognitive functions. Down syndrome (DS), the most frequent cause of genetic intellectual disability, is caused by the presence of a supernumerary chromosome 21, which contains genes essential for the function of the immune system. Here, we investigated the presence of microglial alterations and their implication for cognitive impairment in the Dp(16) mouse model of DS. In the hippocampus of Dp(16) mice and individuals with DS, we found microglial morphology indicative of an activated state. Accordingly, we found increased levels of pro-inflammatory cytokines and altered interferon signaling in Dp(16) mice. In addition, Dp(16) mice showed decreased dendritic spine density and cognitive deficits. Remarkably, depletion of defective microglia by PLX3397 treatment or rescue of the microglia activated state by the commonly used anti-inflammatory drug acetaminophen fully rescued dendritic-spine density and cognitive deficits in Dp(16) mice. Our data suggest an involvement of microglia in the cognitive impairment of DS animals and identify a new therapeutic approach for the potential rescue of cognitive disabilities in individuals with DS.

2020-09-22 | PXD015148 | Pride

Rescuing over-activated microglia by acetaminophen treatment restores cognitive performance in the Dp(16) mouse model of Down Syndrome.

2020-09-22 | PXD015113 | Pride

Single cell RNA-seq data of microglia cells from normal mouse brain as well as in the context of neurodegenerative inhury models

Project description:Single cell RNA-seq data was obtained from FACS sorted microglia from different brain regions of normal 16 weeks old CD1 mice as well as from mice undergoing facial nerve axotomy or cuprizone treatment in order to elucidate microglia heterogeneity in a regional and disease model specific manner.

2019-02-13 | GSE120744 | GEO

Bulk RNA-seq of microglia at different ages

Project description:Microglia are important immune cells in the brain. Microglia undergo a series of alterations during aging and increase the susceptibility to brain dysfunctions. However, the characteristics of microglia during the aging process are not fully understood. In this study, we mapped transcriptional and epigenetic profiles of microglia from 3- to 24-month-old mice. We observed unexpected gender divergences and identified age-dependent microglia (ADEM) genes in the aging process. We then compared characteristics between microglial aging and activation. To dissect the function of aged microglia excluding the influence from other aged brain cells, we established an accelerated microglial turnover model without directly affecting other brain cells. By this model, we achieved aged microglia in non-aged brains and confirmed that aged microglia per se contribute to cognitive decline. Collectively, we provide a comprehensive resource to decode the aging process of microglia, shedding light on how microglia maintain brain functions.

2023-07-25 | GSE208386 | GEO

Effect of Diaph1 knockout on gene expression of mouse livers on western diet for 16 weeks

Project description:Diaph1 was knocked out in Ldlr-/- mice on western diet for 16 weeks and the effect of gene expression in liver was measured.

2023-03-14 | GSE156403 | GEO

Rescuing over-activated microglia by acetaminophen treatment restores cognitive performance in the Dp(16) mouse model of Down syndrome.

Project description:Microglia are the resident immune cells of the brain and have been implicated in mechanisms essential for cognitive functions. Down syndrome (DS), the most frequent cause of genetic intellectual disability, is caused by the presence of a supernumerary chromosome 21, which contains genes essential for the function of the immune system. Here, we investigated the presence of microglial alterations and their implication for cognitive impairment in the Dp(16) mouse model of DS. In the hippocampus of Dp(16) mice and individuals with DS, we found microglial morphology indicative of an activated state. Accordingly, we found an electrophysiological profile typical of activated microglia, increased levels of pro-inflammatory cytokines, and altered interferon signaling in Dp(16) mice. In addition, DS mice showed decreased neuronal spine density and neuronal activity, as well as cognitive behavioral deficits. Remarkably, depletion of defective microglia by PLX3397 treatment or rescue of the microglia activated state by the commonly used anti-inflammatory drug acetaminophen rescued the neuronal deficits and cognitive impairment in Dp(16) mice. Our data suggest an involvement of microglia in the cognitive impairment of DS animals and identify a new therapeutic approach for the potential rescue of cognitive disabilities in individuals with DS.

2020-09-22 | GSE137939 | GEO

Endoglin study 4, 20, 40 weeks 0 vs.16 Gy

Project description:Endoglin study 4, 20, 40 weeks 0 vs.16 Gy

2013-06-15 | E-MTAB-1488 | biostudies-arrayexpress

Liver-specific deletion of Pten and atypical E2Fs in 16-weeks old mice.

Project description:RNA-sequencing analysis of liver gene expression after combinatorial liver-specific deletion of tumor suppressor genes in a mouse fatty liver disease and liver cancer model. Gene expression was determined at 16 weeks of age, before onset of liver tumor formation. Aim was to study how loss of atypical E2F transcription repressors affected gene expression in Pten-mutant livers.

2022-05-12 | GSE202546 | 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