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Mus musculus
24 Downloadable Samples
Illumina HiSeq 2500
Description
Aging is a key factor in Alzheimer''s disease, but it''s correlation with the pathology and pathological factors like amyloid-beta remains unclear In our study we aimed to provide an extensive characterisation of age-related changes in the gene expression profile of APP23 mice and controls and correlate these changes to pathological and symptomatic features of the model We found a clear biphasic expression profile with a developmental and aging phase. The second phase, particularly, displays aging features and similarties with the progression of Alzheimer pathology in human patients Processes involved in microglial activation, lysosomal processing, neuronal differantion and cytoskeletal regulation appear key factors in this stage. Interestingly, the changes in the gene expression profile of APP23 mice also seem to occur in control animals, but at a later age. The changes appear accelerated and/or exacerbated in APP23 mice. Overall design: mRNA profiles of APP23 mice and wild-type control littermates aged 1.5, 6, 18 or 24 months. For all the age groups, samples of 3 mice of each genotype were analyzed
Publication Title
Aging, microglia and cytoskeletal regulation are key factors in the pathological evolution of the APP23 mouse model for Alzheimer's disease.
Sample Metadata Fields
Age, Specimen part, Subject
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SRP089875- Danio rerio
- 10 Downloadable Samples
- IlluminaHiSeq2500
Description
Purpose: Identify zebrafish microglia transcriptome in the healthy and neurodegenerative brain. Methods: RNA sequencing was performed on FACS-sorted microglia (3x), other brain cells (3x) and activated microglia (4x). Microglia activation was induced using nitroreductase-mediated cell ablation. 10-20 million reads per sample were obtained. Reads were mapped to zebrafish genome GRC10. Results: We identified the zebrafish microglia transcriptome, which shows overlap with previously identified mouse microglia transcriptomes. Transcriptomes obtained 24h and 48h after treatment appeared highly similar. Therefore, these datasets were pooled. Additionally, we identified an acute proliferative response of microglia to induced neuronal cell death. Overall design: Zebrafish microglia transcriptomes of homeostatic microglia (triplicate), other brain cells (triplicate), activated microglia 24h (duplo), activated microglia 48h (duplo). In data analysis all activated microglia samples were pooled.
Publication Title
Identification of a conserved and acute neurodegeneration-specific microglial transcriptome in the zebrafish.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 89 Downloadable Samples
Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
PBMC from house dust mite (HDM) sensitized atopics were cultured in the presence or absence of HDM extract for 24 hours.
Publication Title
Distinguishing benign from pathologic TH2 immunity in atopic children.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 17 Downloadable Samples
- Illumina HiSeq 2500
Description
Background: Tissue macrophages contribute to development and protection, both requiring appropriately timed and located source(s) of factors controlling growth, cell differentiation and migration. Goal: To understand the role of microglia (tissue macrophages of the central nervous system), in promoting neurodevelopment and controlling neuroinflammation. Summary of findings: We show that microglia fulfill both these roles. In contrast to adult cells, neonatal microglia show a unique neurogenic phenotype with stem cell-like potential. Neonatal microglia are protective against neuroinflammation, and their transplantation ameliorates experimental autoimmune encephalomyelitis. A CD11c+ microglial subset predominates in primary myelinating areas of the developing brain and expresses genes for neuronal and glial survival, migration and differentiation. CD11c+ microglia are also found in clusters of repopulating microglia after experimental ablation and in neuroinflammation in adult mice, but despite some similarities, they do not recapitulate neurogenic neonatal microglia characteristics. Conclusions: We therefore identify a unique phenotype of neonatal microglia that deliver signals necessary for neurogenesis and myelination and suppress neuroinflammation. Overall design: The overall design was to compare transcriptomes of subsets of microglia isolated from neonatal mice, healthy adults, and adult mice with a neuroinflammatory disease (Experimental autoimmune encephalomyelitis, EAE), and to compare anti-inflammatory function of adult and neonatal microglia. Microglia were isolated by cell-sorting based on surface phenotype, and RNAseq data was analyzed using WGCNA, GO and DAVID approaches. Expression of selected genes and pathways was confirmed by histology and flow cytometry. Functional analysis involved transfer of isolated microglia to the central nervous system of animals with EAE and evaluation of outcome. EAE = Experimental autoimmune encephalomyelitis
Publication Title
A novel microglial subset plays a key role in myelinogenesis in developing brain.
Sample Metadata Fields
Subject
View Samples- Mus musculus, Homo sapiens
- 8 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Analysis of expression profiles of human pDC cell line (CAL1) compared to an immature T cell line (MOLT4)
Publication Title
Transcription factor E2-2 is an essential and specific regulator of plasmacytoid dendritic cell development.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 4 Downloadable Samples
Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Analysis of expression profiles of pDCs from wild type and heterozygous E2-2 mice. Results show the control by E2-2 of the expression of pDC-enriched genes.
Publication Title
Transcription factor E2-2 is an essential and specific regulator of plasmacytoid dendritic cell development.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 144 Downloadable Samples
- Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
PBMC from house dust mite (HDM) sensitized atopics with or without asthma (or nonallergic controls) were cultured in the presence or absence of HDM extract for 24 hours.
Publication Title
Differential gene network analysis for the identification of asthma-associated therapeutic targets in allergen-specific T-helper memory responses.
Sample Metadata Fields
Specimen part, Disease stage, Subject
View Samples- Homo sapiens
- 253 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Many cases of acute myeloid leukemia (AML) are associated with mutational activation of RTKs such as FLT3. However, RTK inhibitors have limited clinical efficacy as single agents, indicating that AML is driven by concomitant activation of different signaling molecules. We used a functional genomic approach to identify RET, encoding an RTK not previously implicated in AML, as essential gene in different AML subtypes, and observed that RET-dependent AML cells show activation of RET signaling via ARTN/GFRA3 and NRTN/GFRA2 ligand/co-receptor complexes.
Publication Title
RET-mediated autophagy suppression as targetable co-dependence in acute myeloid leukemia.
Sample Metadata Fields
Specimen part, Disease
View Samples- Mus musculus
- 115 Downloadable Samples
- Illumina HiSeq 2000, Illumina HiSeq 1500
Description
Roquin proteins are required to preclude spontaneous T cell activation and aberrant T follicular helper (Tfh) or T helper 17 (Th17) differentiation. Here, we show that deletion of Roquin encoding alleles in regulatory T cells (Tregs) also caused the activation of conventional T cells. These Tregs exhibited a follicular Treg phenotype, CD25 downregulation and could not protect from colitis. Mechanistically, Roquin was required for full expression and activity of Pten and Foxo1, two essential signaling molecules in Tregs and effector T cells. Roquin upregulated Pten by interfering with miR-17~92 binding to an overlapping cis-element in the Pten 3' UTR and downregulated the Foxo1-specific E3 ubiquitin ligase Itch. Loss of Roquin enhanced mTOR signaling and global protein synthesis, while inhibition of PI3K or mTOR in Roquin-deficient CD4+ T cells corrected increased Tfh and Th17 differentiation. Thereby, the control of PI3K-mTOR signaling by Roquin prevents autoimmunity through T cell-intrinsic and Treg-mediated regulation. Overall design: Examination of transcriptome and ribosome occupancy in MEF and T cells upon Roquin expression and inhibition. Examination of Roquin binding sites in the mouse transcriptome of MEF cells. Examination of transcriptome in CD25+ and CD25- Treg cells from WT and Roquin DKO mice.
Publication Title
Roquin targets mRNAs in a 3'-UTR-specific manner by different modes of regulation.
Sample Metadata Fields
Specimen part, Cell line, Subject
View Samples- Mus musculus
- 204 Downloadable Samples
- Illumina HiSeq 2000
Description
Cortical GABAergic interneurons constitute a highly diverse population of inhibitory neurons that are key regulators of cortical microcircuit function. An important and heterogeneous group of cortical interneurons specifically expresses the serotonin receptor 3A (5-HT3AR) but how this diversity emerges during development is poorly understood. Here we use single-cell transcriptomics to identify gene expression patterns operating in Htr3a-GFP+ interneurons during early steps of cortical circuit assembly. We identify 3 main molecular types of Htr3a-GFP+ interneurons, each displaying distinct developmental dynamics of gene expression. The transcription factor Meis2 is specifically enriched in a type of Htr3a-GFP+ interneurons spatially confined to the cortical white matter. These MEIS2 expressing interneurons appear to originate from a restricted region located at the embryonic pallial-subpallial boundary. Overall, this study identifies MEIS2 as a subclass-specific marker for 5-HT3AR-containing interstitial interneurons and demonstrates that the transcriptional and anatomical parcellation of cortical interneurons is developmentally coupled. Overall design: Single cell transcriptomics of cortical interneurons FACS sorted according to GFP-Htr3a+. Acquired from mouse brains of 3 different developmental ages: E18, P2, P5
Publication Title
Transcriptomic and anatomic parcellation of 5-HT<sub>3A</sub>R expressing cortical interneuron subtypes revealed by single-cell RNA sequencing.
Sample Metadata Fields
Subject
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