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accession-icon SRP173201
Transcriptome of Dp1Tyb and wild-type mouse embryonic fibroblasts [ERCC spike-ins]
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 4000

Description

Purpose: to identify the effects of the Dp1Tyb mutation on the transcriptome of mouse embryonic fibroblasts Overall design: RNAseq libraries were prepared from RNA isolated from mouse embryonic fibroblasts. Libraries were prepared from total RNA using the TruSeq Stranded mRNA Sample Prep Kit (Illumina) by the Advanced Sequencing Facility, The Francis Crick Institute. Libraries were sequenced (100 bases paired end) on the Illumina Hiseq 4000 Please note that this dataset contains ERCC spike ins to normalise the data

Publication Title

Gene expression dysregulation domains are not a specific feature of Down syndrome.

Sample Metadata Fields

Specimen part, Subject

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accession-icon GSE38205
Expression data for inbred mouse brains
  • organism-icon Mus musculus
  • sample-icon 25 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Prion diseases are fatal neurodegenerative disorders that include bovine spongiform encephalopathy (BSE) and scrapie in animals and Creutzfeldt-Jakob disease (CJD) in humans. They are characterized by long incubation periods, variation in which is determined by many factors including genetic background. In some cases it is possible that incubation time may be directly correlated to the level of gene expression. In order to test this hypothesis we combined incubation time data from five different inbred lines of mice with quantitative gene expression profiling in normal brains and identified five genes with expression levels that correlate with incubation time. One of these genes, Hspa13 (Stch), is a member of the Hsp70 family of ATPase heat shock proteins which have been previously implicated in prion propagation. To test whether Hspa13 plays a causal role in determining the incubation period we tested two over-expressing mouse models. The Tc1 human chromosome 21 (Hsa21) transchromosomic mouse model of Down syndrome is trisomic for many Hsa21 genes including Hspa13 and following Chandler/RML prion inoculation shows a 4% reduction in incubation time. Furthermore, a transgenic model with eight fold over-expression of mouse Hspa13 exhibited highly significant reductions in incubation time of 16%, 15% and 7% following infection with Chandler/RML, ME7 and MRC2 prion strains respectively. These data further implicate Hsp70-like molecular chaperones in protein misfolding disorders such as prion disease.

Publication Title

Overexpression of the Hspa13 (Stch) gene reduces prion disease incubation time in mice.

Sample Metadata Fields

Specimen part

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accession-icon SRP077255
Vav proteins are key regulators of Card9 signaling for innate antifungal immunity
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Fungal infections are major causes of morbidity and mortality, especially in immunocompromised individuals. The innate immune system senses fungal pathogens through a family of Syk-coupled C-type lectin receptors (CLRs), which signal through the conserved immune adapter Card9. Although Card9 complexes are essential for antifungal defense in humans and mice, the mechanisms that couple CLR-proximal events to Card9 control are not well defined. Here, using a proteomic approach, we identified Vav proteins as key activators of the Card9 pathway. Vav1, Vav2 and Vav3 cooperate downstream of Dectin-1, Dectin-2 and Mincle to selectively engage Card9 for NF-?B control and proinflammatory gene transcription but are not involved in MAPK activation. Although Vav family members show functional redundancy, Vav1/2/3 triple-deficient cells are severely impaired for NF-?B and cytokine responses upon stimulation with CLR agonists or hyphae, and Vav1/2/3-/- mice phenocopy Card9-/- animals with extreme susceptibility to fungi and rapid mortality upon Candida albicans infection. In this context, Vav3 is the single most important Vav in mice, and a polymorphism in human VAV3 is associated with susceptibility to candidemia in patients. Our results reveal a molecular mechanism for CLR-mediated Card9 regulation that controls innate immunity to fungal infections. Overall design: RNA profiles of unstimulated or Curdlan-stimulated bone marrow-derived dendritic cells (BMDCs) from wild type (WT) and Vav1/2/3-/- (VAV KO) mice were generated by deep sequencing, in triplicate, using Illumina HiSeq 2000.

Publication Title

Vav Proteins Are Key Regulators of Card9 Signaling for Innate Antifungal Immunity.

Sample Metadata Fields

Specimen part, Cell line, Subject

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accession-icon SRP076238
alphaT-catenin in restricted brain cell types and its potential connection to autism
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

RNA-seq analysis was performed between WT and alphaT-cat KO mouse cerebella aiming to discover gene transcripts altered by the loss of alphaT-cat These altered gene transcripts could be associated with several neurologic disease-relevant pathways Overall design: Total RNA extracted of cerebellar tissue (n=3) from the brains of WT ad alphaT-cat KO mice

Publication Title

αT-catenin in restricted brain cell types and its potential connection to autism.

Sample Metadata Fields

Specimen part, Subject

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refine.bio is a repository of uniformly processed and normalized, ready-to-use transcriptome data from publicly available sources. refine.bio is a project of the Childhood Cancer Data Lab (CCDL)

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Cite refine.bio

Casey S. Greene, Dongbo Hu, Richard W. W. Jones, Stephanie Liu, David S. Mejia, Rob Patro, Stephen R. Piccolo, Ariel Rodriguez Romero, Hirak Sarkar, Candace L. Savonen, Jaclyn N. Taroni, William E. Vauclain, Deepashree Venkatesh Prasad, Kurt G. Wheeler. refine.bio: a resource of uniformly processed publicly available gene expression datasets.
URL: https://www.refine.bio

Note that the contributor list is in alphabetical order as we prepare a manuscript for submission.

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