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Links from GEO DataSets

Items: 20

1.

scRNAseq of FACS-isolated microglia from spinal cords of Optn KO mice

(Submitter supplied) CD11b+ CX3CR1+ CD45-Int microglia were FACSorted from Optn KO mice and single cell RNA sequenced using the SmartSeq2 protocol.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL21626
384 Samples
Download data: MATRIX
Series
Accession:
GSE167331
ID:
200167331
2.

scRNAseq from spinal cords

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL21626
391 Samples
Download data: MTX, TXT
Series
Accession:
GSE167332
ID:
200167332
3.

scRNAseq of CD45 enriched cells from spinal cords of Optn floxed and KO mice

(Submitter supplied) We prepared spinal cords from Optn floxed and KO mice treated with vehicle or the RIPK1 inhibitor Nec-1s, which were enriched for CD45+ cells and single cell RNA sequenced using the inDrop protocol.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL21626
1 Sample
Download data: MTX, TXT
Series
Accession:
GSE167327
ID:
200167327
4.

scRNAseq from spinal cords of SOD1-G93A and WT mice

(Submitter supplied) We prepared spinal cords from SOD1-G93A and WT mice treated with vehicle or the RIPK1 inhibitor Nec-1s, which were single cell RNA sequenced using the DropSeq protocol.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL21626
6 Samples
Download data: TXT
Series
Accession:
GSE167198
ID:
200167198
5.

RIPK1 kinase-dependent gene expression in human astrocytes in vitro

(Submitter supplied) To determine the role of RIPK1 kinase-dependent transcriptional signaling in human fetal-derived astrocytes, we stimulated cells with the RIPK1 kinase-activating stimulus TNF/Smac/zVAD in the presence or absence of the RIPK1 kinase inhibitor Nec-1s. We identified various genes modulated in a RIPK1 kinase-dependent manner in human astrocytes, and the main biological pathways were related to an interferon signaling and anti-viral response.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL28038
12 Samples
Download data: TXT
6.

RIPK1 kinase-dependent gene expression in mouse microglia and astrocytes in vitro

(Submitter supplied) To determine the role of RIPK1 kinase-dependent transcriptional signaling in microglia and astrocytes, we stimulated cells with RIPK1 kinase-activating stimuli TNF/5z-7 and TNF/Smac/zVAD in the presence or absence of the RIPK1 kinase inhibitor Nec-1s. We identified various genes modulated in a RIPK1 kinase-dependent manner with each stimulation in both microglia and astrocytes, and the main biological pathways were related to an inflammatory and immune response. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platforms:
GPL21103 GPL28457
36 Samples
Download data: TXT
Series
Accession:
GSE154230
ID:
200154230
7.

RIPK1 kinase-dependent gene expression in mouse microglia and astrocytes in vivo during EAE

(Submitter supplied) To determine the role of RIPK1 kinase signaling in microglia and astrocytes during EAE (mouse model of MS), we extracted spinal cords of naive, EAE-vehicle and EAE mice treated with RIPK1 kinase inhibitor (GSK’547) for transcript profiling using RNAseq. We identify various genes that are differentially expressed in EAE disease compared to naive mice, and a subset of these are modulated in a RIPK1 kinase-dependent manner in both astrocytes and microglia. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL28457
30 Samples
Download data: TXT
Series
Accession:
GSE154228
ID:
200154228
8.

TBK1 suppresses RIPK1-driven apoptosis and inflammation during development and in aging

(Submitter supplied) Aging is a major risk factor for both genetic and sporadic neurodegenerative disorders. However, it is unclear how aging interacts with genetic predispositions to promote neurodegeneration. Here we investigate how partial loss-of-function of TBK1, a major genetic cause for amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) comorbidity, leads to age-dependent neurodegeneration. We show that TBK1 is an endogenous inhibitor of RIPK1 and the embryonic lethality of Tbk1-/- mice is dependent on RIPK1 kinase activity. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL19057
18 Samples
Download data: TXT
Series
Accession:
GSE116613
ID:
200116613
9.

Microglia RAGE exacerbates the progression of neurodegeneration within the SOD1G93A murine model of amyotrophic lateral sclerosis in a sex-dependent manner

(Submitter supplied) Burgeoning evidence highlights seminal roles for microglia in the pathogenesis of neurodegenerative diseases including amyotrophic lateral sclerosis (ALS). The receptor for advanced glycation end products (RAGE) binds ligands relevant to ALS that accumulate in the diseased spinal cord and RAGE has been previously implicated in the progression of ALS pathology. We generated a novel mouse model to temporally delete Ager from microglia in the murine SOD1G93A model of ALS. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24247
8 Samples
Download data: TXT
Series
Accession:
GSE160402
ID:
200160402
10.

Next Generation Sequencing to check the enrichment of RIPK1/BAF on chromatin, RIPK1-dependent chromatin state and RIPK1-dependent transcriptome during inflammatory responses.

(Submitter supplied) RIPK1 is a master regulator of multiple cell death pathways, including apoptosis and necroptosis, and inflammation. Multiple RIPK1 inhibitors have been advanced into human clinical trials as new therapeutics for human inflammatory and neurodegenerative diseases, including ALS and AD. However, while the mechanism of cytosolic RIPK1 in control of cell death has been extensively investigated, how the activation of RIPK1 may promote transcription of proinflammatory cytokines is unclear as a nuclear function of RIPK1 has not been explored, nor is it clear if and how RIPK1 kinase activity may directly mediate inflammation independent of cell death. more...
Organism:
Homo sapiens; Mus musculus
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing; Other
Platforms:
GPL19057 GPL18573
73 Samples
Download data: BED, BW, TXT
Series
Accession:
GSE179018
ID:
200179018
11.

Single-cell RNA-seq analysis of the brainstem of mutant SOD1 mice reveals perturbed cell types and pathways of amyotrophic lateral sclerosis

(Submitter supplied) Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease in which motor neurons throughout the brain and spinal cord progressively degenerate resulting in muscle atrophy, paralysis and death. Recent studies using animal models of ALS implicate multiple cell-types (e.g., astrocytes and microglia) in ALS pathogenesis in the spinal motor systems. To ascertain cellular vulnerability and cell-type specific mechanisms of ALS in the brainstem that orchestrates oral-motor functions, we conducted parallel single cell RNA sequencing (scRNA-seq) analysis using the high-throughput Drop-seq method. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL21103
4 Samples
Download data: TAR
Series
Accession:
GSE178693
ID:
200178693
12.

Interleukin 4 modulates microglia homeostasis and attenuates the early slowly progressive phase of Amyotrophic Lateral Sclerosis

(Submitter supplied) CNS-delivery of Interleukin 4 (IL-4) - via a lentiviral-mediated gene therapy strategy - skews microglia to proliferate, inducing these cells to adopt the phenotype of slowly proliferating cells. Transcriptome analysis revealed that IL-4-treated microglia express a broad number of genes normally encoded by embryonic microglia.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL17021
6 Samples
Download data: XLSX
Series
Accession:
GSE103607
ID:
200103607
13.

The Loss of TBK1 Kinase Activity in Motor Neurons or in All Cell Types Differentially Impacts ALS Disease Progression in SOD1 Mice

(Submitter supplied) DNA sequence variants in the TBK1 gene associate with or cause sporadic or familial amyotrophic lateral sclerosis (ALS). Here we show that mice bearing human ALS-associated TBK1 missense loss-of-function mutations, or mice in which the Tbk1 gene is selectively deleted in motor neurons, do not display a neurodegenerative disease phenotype. However, loss of TBK1 function in motor neurons of the SOD1G93A mouse model of ALS impairs autophagy, increases SOD1 aggregation, and accelerates early disease onset without affecting lifespan. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL21626
12 Samples
Download data: BW
Series
Accession:
GSE146141
ID:
200146141
14.

Defining the microglia transcriptome during disease progression in ALS transgenic mice

(Submitter supplied) Purpose: We purified spinal cord microglia utilizing percoll gradients and magnetic beads, followed by transcriptome profiling (RNA-seq) to define microglia expression profiles against other neural, immune cell-types. We next observed how the microglai transcriptomes change during activation in the SOD1-G93A mouse model of motor neuron degeneration at 3 timepoints. We also compared these profiles with that induced by LPS injection. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL13112
42 Samples
Download data: TXT
Series
Accession:
GSE43366
ID:
200043366
15.

Microglia-specific microarray analysis at early symptomatic age in a mouse model of amyotrophic lateral sclerosis

(Submitter supplied) Microarray analysis of microglia in a mouse model of amyotrophic lateral sclerosis identified the dysregulation of Brca1.
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL1261
6 Samples
Download data: CEL
Series
Accession:
GSE96047
ID:
200096047
16.

Amyotrophic lateral sclerosis

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens
Type:
Expression profiling by array; Non-coding RNA profiling by array
Platforms:
GPL15846 GPL15847
48 Samples
Download data: TXT
Series
Accession:
GSE39644
ID:
200039644
17.

NanoString miRNA profiling of peripheral blood sorted CD14+CD16- monocytes from amyotrophic lateral sclerosis, multiple sclerosis and healthy control subjects

(Submitter supplied) We investigated the innate immune system in the SOD1 ALS model. We found that splenic Ly6CHi monocytes were activated and their progressive recruitment to the spinal cord, but not brain, correlated with neuronal loss. We found a decrease in resident microglia in the spinal cord with disease progression. Two months prior to disease onset, splenic Ly6CHi monocytes had an M1 signature which included increased CCR2. more...
Organism:
Homo sapiens
Type:
Non-coding RNA profiling by array
Platform:
GPL15847
24 Samples
Download data: TXT
Series
Accession:
GSE39643
ID:
200039643
18.

NanoString nCounter immune-related gene expression in blood sorted CD14+CD16- monocytes from sALS, fALS and HC subjects

(Submitter supplied) We investigated the innate immune system in the SOD1 ALS model. We found that splenic Ly6CHi monocytes were activated and their progressive recruitment to the spinal cord, but not brain, correlated with neuronal loss. We found a decrease in resident microglia in the spinal cord with disease progression. Two months prior to disease onset, splenic Ly6CHi monocytes had an M1 signature which included increased CCR2. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL15846
24 Samples
Download data: TXT
Series
Accession:
GSE39642
ID:
200039642
19.

Microglial gene signature reveals loss of homeostatic microglia associated with neurodegeneration of Alzheimer's disease

(Submitter supplied) Microglia-mediated neuroinflammation has been implicated in the pathogenesis of Alzheimer's disease (AD). Although microglia in aging and neurodegenerative disease model mice show a loss of homeostatic phenotype and activation of disease-associated microglia (DAM), a correlation between those phenotypes and the degree of neuronal cell loss has not been clarified. In this study, we performed RNA sequencing of microglia isolated from three representative neurodegenerative mouse models, AppNL-G-F/NL-G-F with amyloid pathology, rTg4510 with tauopathy, and SOD1G93A with motor neuron disease by magnetic activated cell sorting. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platforms:
GPL24247 GPL21273
22 Samples
Download data: XLSX
Series
Accession:
GSE236268
ID:
200236268
20.

Genetic background variation impacts microglial heterogeneity and disease progression in amyotrophic lateral sclerosis model mice

(Submitter supplied) Recent single-cell analyses have revealed the complexity of microglial heterogeneity in brain development, aging, and neurodegenerative diseases such as amyotrophic lateral sclerosis (ALS). Disease-associated microglia (DAMs) have been identified in ALS mice model, but their role in ALS pathology remains unclear. The effect of genetic background variations on microglial heterogeneity and functions remains unknown. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL21273
16 Samples
Download data: XLSX
Series
Accession:
GSE252050
ID:
200252050
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