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accession-icon GSE13355
Gene expression data of skin from psoriatic patients and normal controls
  • organism-icon Homo sapiens
  • sample-icon 115 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Gene expression has been proposed as an intermediate phenotype that can increase power in complex trait gene-mapping studies. Psoriasis, an immune-mediated, inflammatory and hyperproliferative disease of the skin and joints, provides an ideal model system to evaluate this paradigm, as conclusive evidence demonstrates that psoriasis has a genetic basis and the disease tissue is readily accessible.

Publication Title

Genome-wide scan reveals association of psoriasis with IL-23 and NF-kappaB pathways.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE57671
Human XCR1+ Dendritic Cells Derived In Vitro from CD34+ Progenitors Closely Resemble Blood Dendritic Cells, Including Their Adjuvant Responsiveness, Contrary to Monocyte-Derived Dendritic Cells
  • organism-icon Homo sapiens
  • sample-icon 74 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Functional characterization of human dendritic cell subsets is limited due to the very low frequency of these cells in vivo. We developed an in vitro culture system for the simultaneous generation of XCR1+ DCs and MoDCs from cord blood CD34+ cells. Their global gene expression profiles at steady state and under activation, phenotypes, morphologies and responses to different TLR ligands where characterized and compared with those of their in vivo counterparts. The study demonstrated that the XCR1+ DCs generated in vitro from cord blood CD34+ cells are equivalent to blood XCR1+ DCs and also allowed a rigorous comparison of this DC subset with MoDC which are often considered as the reference model for DCs. Altogether, our results showed that in vitro generated XCR1+ DCs are a better model for the study of blood DC than the conventionally used MoDCs.

Publication Title

Human XCR1+ dendritic cells derived in vitro from CD34+ progenitors closely resemble blood dendritic cells, including their adjuvant responsiveness, contrary to monocyte-derived dendritic cells.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon GSE144708
Distinct signature, origin and dynamics of macrophages in the peripheral and central nervous system
  • organism-icon Mus musculus
  • sample-icon 25 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Profiling peripheral nerve macrophages reveals two macrophage subsets with distinct localization, transcriptome and response to injury.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE144702
Distinct signature, origin and dynamics of macrophages in the peripheral and central nervous system (microarray)
  • organism-icon Mus musculus
  • sample-icon 25 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

We performed ontogenic, transcriptomic and spatial characterization of sciatic nerve Macs (snMacs). Using multiple fate-mapping systems, we show that snMacs do not derive from the early embryonic precursors colonizing the CNS, but originate primarily from late embryonic precursors and get replaced by bone marrow-derived Macs over time. Using single-cell profiling, we identified a tissue-specific core signature of snMacs and found two spatially-separated snMacs: Relmα + Mgl1 + snMacs in the epineurium and Relmα Mgl1 snMacs in the endoneurium. Globally, snMacs lack most core signature genes of microglia, with only the endoneurial subset expressing a restricted number of these genes. Single-cell transcriptomics revealed that in response to injury both snMacs respond differently and that the PNS, in contrast to the CNS, is permissive to prolonged engraftment of monocyte-derived Macs recruited upon injury.

Publication Title

Profiling peripheral nerve macrophages reveals two macrophage subsets with distinct localization, transcriptome and response to injury.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP049140
Identifying synaptically enriched mRNA by using next generation sequencing
  • organism-icon Mus musculus
  • sample-icon 2 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Preparation of Synaptosomes by density gradient and compare synaptically enriched mRNA to total homogenate transcriptome Overall design: In brief, mouse brains were homogenized in 5 ml homogenization buffer (0.32 M sucrose, 1 mM EDTA pH 7.4, 1 mM dithiothreitol, phenylmethanesulfonyl fluoride solution (Sigma, 93482-50ML-F), complete mini-protease inhibitor (Roche Diagnostics) for 10 sec using a polytron. The homogenate was centrifuged at 1,000g for 10 min at 4 °C yielding the nuclear fraction (Nuc) and the supernatant (Sup). The supernatant was centrifuged at 31,000g for 5 min at 4°C using a discontinuous Percoll gradient. The layer between 3% and 10% of Percoll were collected, washed in 30 ml of homogenization buffer and further centrifuged at 22,000 × g for 15 min at 4°CT. The pellet was resuspended in in EBC buffer (50 mM Tris-HCl pH 8.0, 120 mM NaCl and 0.5% NP-40) containing complete mini-protease inhibitor (Roche Diagnostics) and phosphatase inhibitor cocktail 1 and 2 (Sigma–Aldrich)) for Western blot analysis or lysis buffer for RNA extraction (GenElute Mammalian Total RNA Miniprep Kit, Sigma).

Publication Title

Mutations in NONO lead to syndromic intellectual disability and inhibitory synaptic defects.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon SRP094482
Transciptiome of human primary resting CD4 T lymphocytes infected with HIV-1
  • organism-icon Homo sapiens
  • sample-icon 16 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Assessing the impact of HIV-1 infection on trancriptional program of quiescent CD4 T lymphocytes. Such cells were made susceptible to HIV-1 by dowmodulating SAMHD1 restriction factor using VLP-Vpx without any activation signal.

Publication Title

CD32a is a marker of a CD4 T-cell HIV reservoir harbouring replication-competent proviruses.

Sample Metadata Fields

Sex, Specimen part

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accession-icon GSE54043
Global gene expression profile of gastric antrum tissue of patients with eosinophilic gastritis
  • organism-icon Homo sapiens
  • sample-icon 10 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Significant recent progress has been made with understanding eosinophilic gastrointestinal disorders (EGIDs) yet most studies have focused on eosinophilic esophagitis (EoE). Herein, we aimed to provide fundamental information about the molecular characteristics of eosinophilic gastritis (EG).

Publication Title

Histologic eosinophilic gastritis is a systemic disorder associated with blood and extragastric eosinophilia, TH2 immunity, and a unique gastric transcriptome.

Sample Metadata Fields

Specimen part, Disease, Disease stage

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accession-icon SRP079357
Artemisinins target GABA receptor signaling to induce alpha to beta cell transdifferentiation
  • organism-icon Homo sapiens
  • sample-icon 36 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000, Illumina HiSeq 3000

Description

Type 1 diabetes is characterized by the destruction of pancreatic beta cells, and generating new insulin-producing cells from other cell types is a major aim of regenerative medicine. One promising approach is transdifferentiation of developmentally related pancreatic cell types including glucagon-producing alpha cells. In a genetic model, overexpression of the master regulatory transcription factor Pax4 or loss of its counterplayer Arx are sufficient to induce the conversion of alpha cells to functional beta-like cells. Here we identify artemisinins as small molecules that functionally repress Arx and induce beta-cell characteristics in alpha cells. We show that the protein gephyrin is the mammalian target of these antimalaria drugs. Finally, we demonstrate that gephyrin-mediated enhancement of GABAA receptor signaling is the mechanism of action of these molecules in pancreatic transdifferentiation. Our results indicate that gephyrin is a novel druggable target for the regeneration of pancreatic beta cell mass from alpha cells. Overall design: Transcriptional dissection of Artemether treated, human pancreatic islets of one donor using single-cell RNA-seq

Publication Title

Artemisinins Target GABA<sub>A</sub> Receptor Signaling and Impair α Cell Identity.

Sample Metadata Fields

Subject

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accession-icon SRP078950
Artemisinins target GABAA receptor signaling and impair alpha cell identity
  • organism-icon Mus musculus
  • sample-icon 13 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Type 1 diabetes is characterized by the destruction of pancrea tic beta cells, and generating new insulin-producing cells from other cell types is a major aim of regenerative medicine. One promising approach is transdifferentiation of developmentally related pancreatic cell types including glucagon-producing alpha cells. In a genetic model, loss of the master regulatory transcription factor Arx is sufficient to induce the conversion of alpha cells to functional beta-like cells. Here we identify artemisinins as small molecules that functionally repress Arx by causing its translocation to the cytoplasm. We show that the protein gephyrin is the mammalian target of these antimalaria drugs, and that enhancement of GABAA receptor signaling contributes to the mechanism of action of these molecules in pancreatic transdifferentiation. Our results in zebrafish, rodents and primary human pancreatic islets indicate that gephyrin is a novel druggable target for the regeneration of pancreatic beta cell mass from alpha cells. Overall design: There are two parts in the transcriptional study on mouse cell lines in this project. One part is on Min6-ARX inducible cells with different induction time of Dox. This is done in three different clones. The other part is on alpha-TC1 cells. This is done in one concentration of Artemether, one time point and two biological repeats.

Publication Title

Artemisinins Target GABA<sub>A</sub> Receptor Signaling and Impair α Cell Identity.

Sample Metadata Fields

Specimen part, Cell line, Subject

View Samples
accession-icon SRP064857
Rapid conversion of fibroblasts into functional forebrain GABAergic interneurons by direct genetic reprogramming
  • organism-icon Mus musculus
  • sample-icon 18 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Transplantation of GABAergic interneurons (INs) can sustain long-standing benefits in animal models of epilepsy and other neurological disorders. In a therapeutic perspective, a renewable source of functional GABAergic INs is needed. Here, we identified five factors (Foxg1, Sox2, Ascl1, Dlx5 and Lhx6) able to convert fibroblasts directly into induced GABAergic INs (iGABA-INs), displaying the molecular signature of telencephalic INs. The selected factors recapitulate in fibroblasts the activation of transcriptional networks required for the specification of GABAergic fate during telencephalon development. iGABA-INs exhibited progressively maturing firing patterns comparable to those of cortical INs, had synaptic currents and released GABA. Importantly, upon grafting in the hippocampus, iGABA-INs survived, matured and their optogenetic stimulation triggered GABAergic transmission and inhibited the activity of connected granule cells. The five factors also converted human cells into functional GABAergic neurons. These properties define iGABA-INs as a promising tool for disease modeling and cell-based therapeutic approaches. Overall design: Comparison of iGABA-INs transcriptional profile with those of starting fibroblasts and GAD67-GFP+ cortical interneurons.

Publication Title

Rapid Conversion of Fibroblasts into Functional Forebrain GABAergic Interneurons by Direct Genetic Reprogramming.

Sample Metadata Fields

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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