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accession-icon GSE47900
Differential gene expression analysis in motor and sensory cortex as a result of experimental autoimmune encephalomyelitis (EAE), a neuroinflammatory model for Multiple sclerosis.
  • organism-icon Mus musculus
  • sample-icon 20 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

We performed micrarrays to investigate neuronal gene expression changes during acute inflammatory CNS axon injury using the murine myelin oligodendrocyte glycoprotein 35-55 (MOG35-55)-induced experimental autoimmune encephalomyelitis (EAE) model. The present study was assigned to assess the direct and indirect endogenous neuronal response to spinal axonal injury in the motor and sensory cortex.

Publication Title

Axonally derived matrilin-2 induces proinflammatory responses that exacerbate autoimmune neuroinflammation.

Sample Metadata Fields

Sex, Specimen part, Treatment

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accession-icon GSE98823
Knockout of HDAC1 and HDAC2 in Microglia
  • organism-icon Mus musculus
  • sample-icon 9 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000, Affymetrix Mouse Gene 2.0 ST Array (mogene20st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Histone Deacetylases 1 and 2 Regulate Microglia Function during Development, Homeostasis, and Neurodegeneration in a Context-Dependent Manner.

Sample Metadata Fields

Sex, Age, Specimen part, Treatment

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accession-icon SRP106889
Constitutive and Tamoxifen inducible knockout of HDAC1 and HDAC2 in Microglia
  • organism-icon Mus musculus
  • sample-icon 44 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 1000

Description

Hdac1 and 2 are important regulators of developmental processes. In this study we created microglia specific compound Hdac1 and Hdac2 knock out mice. Pre-natal ablation of both Hdac1 and 2 from microglia leads to reduced cell number and altered cell morphology. To investigate how Hdac1 and 2 knock out in microglia alters cellular gene expression profile we carried out RNA-seq analysis at different time points. Overall design: We used FACS sorted microglia cells from control and Hdac1/2fl/flCx3cr1Cre (constituitive knockout) or Hdac1/2fl/flCx3cr1CreERT2 (inducible) mice at different time points viz. Embryonic day 16 (E16 - inducible knockout only), Post natal day 0 (P0), 2 and 6 weeks after birth

Publication Title

Histone Deacetylases 1 and 2 Regulate Microglia Function during Development, Homeostasis, and Neurodegeneration in a Context-Dependent Manner.

Sample Metadata Fields

Age, Treatment, Subject

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accession-icon GSE96622
Expression data from Hdac1 and 2 knock out microglia in 5X familial Alzheimer's disease (FAD) background
  • organism-icon Mus musculus
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 2.0 ST Array (mogene20st)

Description

Epigenetic alterations has been implicated in the pathology of several neurodegenerative diseases. To investigate the role of microglial Hdac1 and 2 in the pathogenesis of Alzheimer's disease (AD), we created microglia specific compound Hdac1 and Hdac2 knock out mice in 5X FAD background. Genetic ablation of Hdac1 and 2 from microglia reduced amyloid plaque burden and improved spatial learning and memory function.

Publication Title

Histone Deacetylases 1 and 2 Regulate Microglia Function during Development, Homeostasis, and Neurodegeneration in a Context-Dependent Manner.

Sample Metadata Fields

Sex, Specimen part

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accession-icon GSE25067
Gene expression in response to genetic and chemical perturbations of chromatin structure
  • organism-icon Arabidopsis thaliana
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)

Description

Microarray expression profiling was used to identify genes expressed misexpressed in wild-type Arabidopsis seedlings treated with 5-aza-2 deoxyctidine (5AC) or trichostatin A (TSA), and in decrease in dna methylation1 (ddm1) mutant seedlings.

Publication Title

Changes in global gene expression in response to chemical and genetic perturbation of chromatin structure.

Sample Metadata Fields

Specimen part

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accession-icon GSE23310
Uncovering Genes and Regulatory Pathways Related to Urinary Albumin Excretion in Mice
  • organism-icon Mus musculus
  • sample-icon 173 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Identifying the genes underlying quantitative trait loci (QTL) for disease has proven difficult, mainly due to the low resolution of the approach and the complex genetics involved. However, recent advances in bioinformatics and the availability of genetic resources now make it possible to narrow the genetic intervals and test candidate genes. In addition to identifying the causative genes, defining the pathways that are affected by these QTL is of major importance as it can give us insight into the disease process and provide evidence to support candidate genes. In this study we mapped three significant and one suggestive QTL on Chromosomes (Chrs) 1, 4, 15, and 17, respectively, for increased albumin excretion (measured as albumin-to-creatinine ratio) in a cross between the MRL/MpJ and SM/J mouse inbred strains. By combining data from several sources and by utilizing gene expression data, we identified Tlr12 as a likely candidate for the Chr 4 QTL. Through the mapping of 33,881 transcripts measured by microarray on kidney RNA from each of the 173 male F2 animals, we identified several downstream pathways associated with these QTL. Among these were the glycan degradation, leukocyte migration, and antigen presenting pathways. We demonstrate that by combining data from multiple sources, we can identify not only genes that are likely to be causal candidates for QTL, but also the pathways through which these genes act to alter phenotypes. This combined approach provides valuable insights into the causes and consequences of renal disease.

Publication Title

Uncovering genes and regulatory pathways related to urinary albumin excretion.

Sample Metadata Fields

Sex, Age

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accession-icon GSE15822
High-fat diet leads to tissue-specific changes reflecting risk factors for diseases in DBA/2J mice
  • organism-icon Mus musculus
  • sample-icon 96 Downloadable Samples
  • Technology Badge IconIllumina mouse-6 v1.1 expression beadchip

Description

Analysis of tissues of DBA/2 mice fed a standard breeding diet (SBD) and high fat diet (HFD) revealed tissue specific roles in inflammation and disease, and altered communication between tissues. The tissues surveyed incuded adipose tissues (brown, inguinal, mesenteric, retro-peritoneal, subcutaneious and gonadal), muscle and liver.

Publication Title

High-fat diet leads to tissue-specific changes reflecting risk factors for diseases in DBA/2J mice.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon GSE73125
Transcriptome-based profiling reveals a macrophage pedigree and identifies Irf8 as pivotal for macrophage homeostasis and function
  • organism-icon Mus musculus
  • sample-icon 81 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 2.1 ST Array (mogene21st)

Description

Recent studies have shown that tissue macrophages (MF) arise from embryonic progenitors of the yolk sac (YS) and fetal liver and colonize the tissues before birth. Further studies have proposed that developmentally distinct tissue MF can be identified based on the differential expression of F4/80 and CD11b, but whether a characteristic transcriptional profile exists is largely unknown. Here, we established an inducible fate mapping system that facilitated the identification of A2 progenitors of the YS as source of F4/80hi but not CD11bhi MF. Large-scale transcriptional profiling of MF precursors from the YS until adulthood allowed the description of a complex MF pedigree. We further identified a distinct molecular signature of F4/80hi and CD11bhi MF and found that Irf8 was vital for MF maturation and the innate immune response. Our data provide new cellular and molecular insights into the origin and developmental pathways of tissue MF.

Publication Title

Transcriptome-based profiling of yolk sac-derived macrophages reveals a role for Irf8 in macrophage maturation.

Sample Metadata Fields

Specimen part

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accession-icon SRP158633
Single-cell profiling of the myeloid landscape identifies cell subsets with distinct fates during neuroinflammation
  • organism-icon Mus musculus
  • sample-icon 55 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 3000

Description

The innate immune cell compartment is highly diverse in the healthy central nervous system (CNS) including parenchymal and non-parenchymal macrophages. However, this complexity is increased in inflammatory settings by the recruitment of circulating myeloid cells. It is unclear which disease-specific myeloid subsets exist and what their transcriptional profiles and dynamics during CNS pathology are. By combining deep single-cell transcriptome analysis, fate mapping, in vivo imaging, clonal analysis, and transgenic lines, we comprehensively characterized unappreciated myeloid subsets in several CNS compartments during neuroinflammation. During inflammation, CNS macrophage subsets undergo self-renewal, and random proliferation shifted towards clonal expansion. Finally, functional studies demonstrated that endogenous CNS tissue macrophages are redundant for antigen presentation. Our results highlight myeloid cell diversity and provide insights into the brain's innate immune system. Overall design: CD45+ cells isolated from different CNS compartments (including leptomeninges, perivascular space and parenchyma, and choroid plexus) and Ly6Chigh and Ly6Clow monocytes from blood were FACS-sorted in 384-well plates and used for scRNAseq. All myeloid cells were sorted from C57BL/6N mice with 8-10 weeks of age at naive stage or at different stages of Experimental Autoimmune Encephalomyelitis (preclinical, onset and peak of the disease). Data are representative of 16-18 mice from three independent experiments. mCEL-Seq2 protocol was used for single cell sequencing (Hashimshony et al. 2016, Herman et al. 2018).

Publication Title

Single-cell profiling identifies myeloid cell subsets with distinct fates during neuroinflammation.

Sample Metadata Fields

Age, Specimen part, Disease, Disease stage, Cell line, Subject

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accession-icon SRP149193
A subset of skin macrophages modulates surveillance and regeneration of local nerves
  • organism-icon Mus musculus
  • sample-icon 16 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500, Illumina HiSeq 3000

Description

Host-environment interfaces such as the dermis comprise tissue macrophages as the most abundant resident immune cell type. Diverse tasks, i.e. to resist against invading pathogens, to attract bypassing immune cells from penetrating vessels and to aid tissue development and repair require a dynamic postnatal coordination of tissue macrophages specification. Here, we delineated the postnatal development of dermal macrophages and their differentiation into distinct subsets by adapting single cell transcriptomics, fate-mapping and tissue imaging. We thereby identified a small phenotypically and transcriptionally distinct subset of embryo-derived skin macrophages that was maintained and largely excluded from the overall postnatal exchange by monocytes. These macrophages specifically interacted with dermal sensory nerves, surveilled and trimmed the myelin sheets and regulated axon sprouting after mechanical injury. In summary, our data show long-lasting functional specification of macrophages in the dermis that is driven by step-wise adaptation to guiding structures and ensures codevelopment of ontogenetically distinct cells within the same compartment. Overall design: Single Cell Sequencing was performed on CD45+CD11b+CD64+Lin-(lineage B220, CD3, NK1.1, Siglec-F, Ly6G) CX3CR1 (low, mid, high) macrophage subsets from mouse dermis after enzymatic digestion

Publication Title

A Subset of Skin Macrophages Contributes to the Surveillance and Regeneration of Local Nerves.

Sample Metadata Fields

Age, Specimen part, Cell line, 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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