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accession-icon GSE76679
Motor cortex after C3 lesion
  • organism-icon Rattus norvegicus
  • sample-icon 17 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Genome 230 2.0 Array (rat2302)

Description

Gene expression analysis of motor cortex after spinal C3 lesion

Publication Title

A Systems-Level Analysis of the Peripheral Nerve Intrinsic Axonal Growth Program.

Sample Metadata Fields

Sex, Specimen part, Time

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accession-icon GSE28886
Modulation of gene expression by complement protein C1q in amyloid-beta injured neurons
  • organism-icon Rattus norvegicus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Gene 1.0 ST Array (ragene10st)

Description

Complement protein C1q is induced after injury in the brain and during Alzheimer's disease and has been shown to protect against amyloid-beta induced neuronal death. In this study, we used microarray approach to identify the pathways modulated by C1q that are associated with neuroprotection.

Publication Title

C1q-induced LRP1B and GPR6 proteins expressed early in Alzheimer disease mouse models, are essential for the C1q-mediated protection against amyloid-β neurotoxicity.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon GSE56483
Modeling the clinical phenotype of BTK inhibition in the mature murine immune system
  • organism-icon Mus musculus
  • sample-icon 18 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Using the novel BTK inhibitor PF-303, we model the clinical phenotype of BTK inhibition by systematically examining the impact of PF-303 on the mature immune system in mice autoimmune indications. However, our current knowledge of the role of BTK in immune competence has been gathered in the context of genetic inactivation of btk in both mice and man. Using the novel BTK inhibitor PF-303, we model the clinical phenotype of BTK inhibition by systematically examining the impact of PF-303 on the mature immune system in mice. We implicate BTK in tonic BCR signaling, demonstrate dependence of the T3 B cell subset and IgM surface expression on BTK activity, and find that B1 cells survive and function independently of BTK. While BTK inhibition does not impact humoral memory survival, antigen-driven clonal expansion of memory B cells and antibody secreting cell generation are inhibited. These data define the role of BTK in the mature immune system and mechanistically predict the clinical phenotype of BTK inhibition.

Publication Title

Modeling the clinical phenotype of BTK inhibition in the mature murine immune system.

Sample Metadata Fields

Specimen part

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accession-icon GSE18860
Regulation of neuronal gene and miRNA expression by the complement protein C1q associated with neuroprotection
  • organism-icon Rattus norvegicus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Gene 1.0 ST Array (ragene10st)

Description

Identification of transcriptional profiles stimulated by the complement protein C1q in rat immature neurons associated with the C1q-dependent neuroprotection observed in vitro.

Publication Title

Complement protein C1q-mediated neuroprotection is correlated with regulation of neuronal gene and microRNA expression.

Sample Metadata Fields

Specimen part

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accession-icon GSE67089
Analysis of mRNA profiles distinguishes proneural (PN) glioma stem cells (GSC) from mesenchymal (Mes) GSCs
  • organism-icon Homo sapiens
  • sample-icon 48 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U219 Array (hgu219)

Description

Tumor heterogeneity of high-grade glioma (HGG) is recognized by four clinically relevant subtypes based on core gene signatures. However, molecular signaling in glioma stem cells (GSCs) in individual HGG subtypes is poorly characterized. Here we identified and characterized two mutually exclusive GSC subtypes with distinct dysregulated signaling pathways. Analysis of mRNA profiles distinguished proneural (PN) from mesenchymal (Mes) GSCs and revealed a pronounced correlation with the corresponding PN or Mes HGGs. Mes GSCs displayed more aggressive phenotypes in vitro and as intracranial xenografts in mice. Further, Mes GSCs were markedly resistant to radiation compared with PN GSCs. The glycolytic pathway, comprising aldehyde dehydrogenase (ALDH) family genes and in particular ALDH1A3, were enriched in Mes GSCs. Glycolytic activity and ALDH activity were significantly elevated in Mes GSCs but not in PN GSCs. Expression of ALDH1A3 was also increased in clinical HGG compared with low-grade glioma or normal brain tissue. Moreover, inhibition of ALDH1A3 attenuated the growth of Mes but not PN GSCs. Last, radiation treatment of PN GSCs up-regulated Mes-associated markers and downregulated PN-associated markers, whereas inhibition of ALDH1A3 attenuated an irradiation-induced gain of Mes identity in PN GSCs. Taken together, our data suggest that two subtypes of GSCs, harboring distinct metabolic signaling pathways, represent intertumoral glioma heterogeneity and highlight previously unidentified roles of ALDH1A3-associated signaling that promotes aberrant proliferation of Mes HGGs and GSCs. Inhibition of ALDH1A3- mediated pathways therefore might provide a promising therapeutic approach for a subset of HGGs with the Mes signature.

Publication Title

Mesenchymal glioma stem cells are maintained by activated glycolytic metabolism involving aldehyde dehydrogenase 1A3.

Sample Metadata Fields

Specimen part

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accession-icon GSE92938
The Impact of Influenza Infection on the Lung Transcriptome During Repair
  • organism-icon Mus musculus
  • sample-icon 32 Downloadable Samples
  • Technology Badge IconIllumina MouseWG-6 v2.0 expression beadchip

Description

Seasonal and pandemic influenza is a cause of morbidity and mortality worldwide. Most people infected with influenza virus display mild to moderate disease phenotypes and recover within a few weeks.

Publication Title

Epigenetic and Transcriptomic Regulation of Lung Repair during Recovery from Influenza Infection.

Sample Metadata Fields

Specimen part

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accession-icon GSE42276
Gene expression profile of conventional T cells (Tconv) and regulatory T cells (Treg) stimulated with anti-costimulatory molecule antibodies
  • organism-icon Mus musculus
  • sample-icon 85 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Co-stimulatory molecules of the CD28 family on T lymphocytes integrate cues from innate immune system sensors, and modulate activation responses in conventional CD4+ T cells (Tconv) and their FoxP3+ regulatory counterparts (Treg). To better understand how costimulatory and co-inhibitory signals might be integrated, we profiled the changes in gene expression elicited in the hours and days after engagement of Treg and Tconv by anti-CD3 and either anti-CD28, -CTLA4, -ICOS, -PD1, -BTLA or -CD80.

Publication Title

Convergent and divergent effects of costimulatory molecules in conventional and regulatory CD4+ T cells.

Sample Metadata Fields

Sex, Age, Specimen part

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accession-icon GSE110308
Treg cells limit IFN-g production to control macrophage accrual and phenotype during skeletal muscle regeneration
  • organism-icon Mus musculus
  • sample-icon 13 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

We report transcriptional characterization of skeletal muscle macrophage subsets in normal and injured muscle after intramuscular injection with cardiotoxin. We profiled transcriptional differences in macrophage subsets from mice depleted of Treg cells using Foxp3-DTR mice. We uncovered an IFN-g-centered regulatory loop, in which Treg cells inhibit NK and T cells to control macrophage accumulation and phenotype during muscle regeneration.

Publication Title

T<sub>reg</sub> cells limit IFN-γ production to control macrophage accrual and phenotype during skeletal muscle regeneration.

Sample Metadata Fields

Sex, Age, Specimen part

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accession-icon GSE1085
Profiling of aggressive vs benign pancreatic infiltrates in the BDC2.5 Tg model of Type I diabetes
  • organism-icon Mus musculus
  • sample-icon 24 Downloadable Samples
  • Technology Badge Icon Affymetrix Murine Genome U74A Version 2 Array (mgu74av2)

Description

This study was performed to understand what controls the aggressivity of the pancreatic infiltrate during type-I diabetes development. We used the BDC2.5 transgenic mouse model. Samples were obtained at the age of onset of insultis. Depending on their genetic background, mice transgenic for the BDC2.5 T cell receptor present very different forms of insulitis. The NOD genetic background leads to a benign insulitis whereas the C57Bl/6-H2g7/g7 leads to an aggressive insulitis. We first studied how antigen-specific T cells are affected by these differences by obtaining the transcriptional profiles of BDC2.5 T cells from pancreas and pancreatic lymph nodes. We also compared the gene expression profiles of the entire leukocyte population present in the pancreatic lesion.

Publication Title

Natural killer cells distinguish innocuous and destructive forms of pancreatic islet autoimmunity.

Sample Metadata Fields

Age, Specimen part

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accession-icon GSE3039
Innate vs. adaptive lymphocyte gene expression
  • organism-icon Mus musculus
  • sample-icon 16 Downloadable Samples
  • Technology Badge Icon Affymetrix Murine Genome U74A Version 2 Array (mgu74av2)

Description

Three innate (B1-B, NKT, CD8aaT cells) and adaptive (B2-B, CD4T, CD8abT cells) cell-types were sorted by FACS. Three biological replicates for NKT, CD4T, CD8aaT, CD8abT cells and two biological replicates for B1 and B2 cells were generated and the expression profiles were determined using Affymetrix Mu74Av2 chip. Comparisons between the sample groups allow the identification of genes differentially expressed between the innate and adaptive cell-types.

Publication Title

A shared gene-expression signature in innate-like lymphocytes.

Sample Metadata Fields

No sample metadata fields

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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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