Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

SHIP1 modulation and proteome characterization of microglia

ABSTRACT: Understanding microglial states in the aging brain has become crucial, especially with the discovery of numerous Alzheimer’s disease (AD) risk and protective variants in genes such as INPP5D and TREM2, which are essential to microglia function in AD. Here we present a thorough examination of microglia-like cells and primary mouse microglia at the proteome and transcriptome levels to illuminate the roles these genes and the proteins they encode play in various cell states. First, we compared the proteome profiles of wildtype and INPP5D (SHIP1) knockout primary microglia. Our findings revealed significant proteome alterations only in the homozygous SHIP1 knockout, revealing its impact on the microglial proteome. Additionally, we compared the proteome and transcriptome profiles of commonly used in vitro microglia BV2 and HMC3 cells with primary mouse microglia. Our results demonstrated a substantial similarity between the proteome of BV2 and mouse primary cells, while notable differences were observed between BV2 and human HMC3. Lastly, we conducted targeted lipidomic analysis to quantify different phosphatidylinositols (PIs) species, which are direct SHIP1 targets, in the HMC3 and BV2 cells. This in-depth omics analysis of both mouse and human microglia enhances our systematic understanding of these microglia models.

ORGANISM(S): Mus Musculus (mouse)

SUBMITTER: Timothy Richardson

PROVIDER: PXD052147 | JPOST Repository | Fri May 10 00:00:00 BST 2024

REPOSITORIES: jPOST

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	05Feb2023_B6_hetKO1_cytoskeleton_GH6_1.raw	Raw
	05Feb2023_B6_hetKO1_cytosol_GD2_1.raw	Raw
	05Feb2023_B6_hetKO1_membrane_GE3_1.raw	Raw
	05Feb2023_B6_hetKO1_nuclear-mem_GF5_1.raw	Raw
	05Feb2023_B6_hetKO1_nuclear-sol_GF4_1.raw	Raw

Items per page:

1 - 5 of 20

Similar Datasets

Tau accumulation induces microglial state alterations in Alzheimer’s disease model mice (snRNA-seq, part 2)

Project description:Unique microglial states have been identified in Alzheimer’s disease (AD) model mice and postmortem AD brains. Although it has been well documented that amyloid-β accumulation induces the alteration of microglial states, the relationship between tau pathology and microglial states remains incompletely understood because of a lack of suitable AD models. In the present study, we generated a novel AD model mouse by the intracerebral administration of tau purified from human brains with primary age-related tauopathy into AppNL-G-F/MAPT double knock-in (dKI) mice.

2024-12-16 | GSE270386 | GEO

Tau accumulation induces microglial state alterations in Alzheimer’s disease model mice (snRNA-seq, part 1)

2024-12-16 | GSE270385 | GEO

Tau accumulation induces microglial state alterations in Alzheimer’s disease model mice (Spatial Transcriptomics)

2024-12-16 | GSE270382 | GEO

Exploration and clinical validation of molecular typing of early colorectal cancer

Project description:Interventions: Case series:None Primary outcome(s): exon genes;transcriptional expression;proteome;protein phosphorylation group Study Design: Sequential

| 2739647 | ecrin-mdr-crc

Systemic transcriptome alternation under mtDNA depletion in 143B TK- osteosarcoma cells

Project description:The mitochondrial protein repertoire varies depending on cellular states, tissue type, species, and disease state. However, little is known about how this repertoire changes under different cellular or disease states. To gain a better understanding of dynamic mitochondrial proteomic changes, we compared alterations of mitochondrial proteome with transcriptome under mitochondrial DNA depletion. Total RNA obtained from 143B TK- osteosarcoma ?+ cells or 143B TK- osteosarcoma ?° cells

2010-07-17 | E-GEOD-22970 | biostudies-arrayexpress

Transcriptional signature in microglia associated with Aβ plaque phagocytosis

Project description:The role of microglia cells in Alzheimer’s disease (AD) is well recognized, however their molecular and functional diversity remain unclear. Here we isolated amyloid plaque-containing (using labelling with methoxy–XO4, XO4+) and non-containing (XO4-) microglia from an AD mouse model. Transcriptomics analysis identified different transcriptional trajectories in ageing and AD mice. XO4+ microglial transcriptomes demonstrated dysregulated expression of genes associated with late onset AD. We further showed that the transcriptional program associated with XO4+ microglia from mice is present in a subset of human microglia isolated from brains of individuals with AD. XO4- microglia displayed transcriptional signatures associated with accelerated ageing and contained more intracellular post-synaptic material than XO4+ microglia, despite reduced active synaptosome phagocytosis. We identified HIF1α as potentially regulating synaptosome phagocytosis in vitro using primary human microglia, and BV2 mouse microglial cells. Together these findings provide insight into molecular mechanisms underpinning the functional diversity of microglia in AD.

2021-04-12 | PXD024731 | Pride

Effect of the combined loss of tomosyn (STXBP5) and tomosyn-2 (STXBP5L) on the proteome of primary mouse hippocampal neurons

Project description:Tomosyn (STXBP5) is a non-canonical SNARE protein enriched in many secretory cells and implicated in regulation of exocytosis. In neurons, loss of tomosyn affects fusion of synaptic vesicles. Here, we examined the impact of the loss of tomosyn (STXBP5) and its close paralog, tomosyn-2 (STXBP5L), on the proteome of primary mouse hippocampal neurons. To do this, we used a mouse model carrying floxed alleles of Stxbp5 and Stxbp5l genes. Primary hippocampal neurons isolated from these mice were transduced with Cre-recombinase, which expression resulted in a nearly complete loss of the two genes expression. As control, we used neurons from the same culture preparation but expressing Cre-recombinase lacking DNA-binding domain (ΔCre). This dataset provides the comparison of proteome of control ('WT') and Stxbp5/5l double knockout ('DKO') neurons.

2022-12-19 | PXD038442 | Pride

Stem cell derived human microglia transplanted in mouse brain to study human disease

Project description:While genetics highlight the role of microglia in Alzheimer’s disease (AD), one third of putative AD-risk genes lack adequate mouse orthologs. Here, we successfully engraft human microglia derived from embryonic stem cells in the mouse brain. The cells recapitulate transcriptionally human primary microglia ex vivo and show expression of human specific AD-risk genes. Oligomeric Amyloid-β induces a divergent response in human vs. mouse microglia. This model can be used to study the role of microglia in neurological diseases.

2019-10-16 | GSE137444 | GEO

The olfactory molecular snapshot of Tg2576 mice at early stages of amyloid pathology

Project description:Olfaction is often deregulated in Alzheimer's disease (AD) patients, being also impaired in transgenic Tg2576 AD mouse model, which overexpress the Swedish mutated form of human amyloid precursor protein (APP). However, little is known about the molecular mechanisms that accompany the neurodegeneration of olfactory structures in Tg2576 mice. For that, we have applied proteome- and transcriptome-wide approaches to probe molecular disturbances in the olfactory bulb (OB) dissected from Tg2576 mice (2, and 6 months of age) respect to age-matched wild-type (WT) littermates.

2019-07-01 | GSE106643 | GEO

The olfactory molecular snapshot in aged Tg2576 Alzheimer´s disease mouse model

Project description:Olfaction is often deregulated in Alzheimer´s disease (AD) patients, being also impaired in transgenic Tg2576 AD mouse model, which overexpress the Swedish mutated form of human amyloid precursor protein (APP). However, little is known about the molecular mechanisms that accompany the neurodegeneration of olfactory structures in Tg2576 mice. For that, we have applied proteome- and transcriptome-wide approaches to probe molecular disturbances in the olfactory bulb (OB) dissected from aged Tg2576 mice (18 months of age) respect to age matched wild-type (WT) littermates.

2018-02-14 | GSE103835 | 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