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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

View Samples
accession-icon E-MEXP-401
Transcription profiling of mouse myoblast samples treated with a panel of compounds known to affect cellular differentiation or its reversal
  • organism-icon Mus musculus
  • sample-icon 16 Downloadable Samples
  • Technology Badge Icon Affymetrix Murine Genome U74A Version 2 Array (mgu74av2)

Description

A Single Cell Analysis of Myogenic Dedifferentiation Induced by Small Molecules An important direction in chemical biology is the derivation of compounds that affect cellular differentiation or its reversal. The fragmentation of multinucleate myofibers into viable mononucleates (called cellularisation) occurs during limb regeneration in urodele amphibians and the isolation of myoseverin, a tri-substituted purine that could apparently activate this pathway of myogenic dedifferentiation in mammalian cells, generated considerable interest. We have explored the mechanism and outcome of cellularisation at a single cell level, and report findings that significantly extend the previous work with myoseverin. Using a panel of compounds, including a novel triazine compound called 109 with structural similarity and comparable activity to myoseverin, we have identified microtubule disruption as critical for activation of the response. Our analysis has included the related control triazine compound 401, and the microtubule disrupting agent nocodazole. Time-lapse microscopy has enabled us to analyse the fate of identified mononucleate progeny, and directly assess the extent of dedifferentiation.

Publication Title

A single-cell analysis of myogenic dedifferentiation induced by small molecules.

Sample Metadata Fields

Specimen part, Cell line, Compound, Time

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accession-icon GSE101046
Identification of target mRNAs of amyotrophic lateral sclerosis associated miR-1825 in HEK293 cells
  • organism-icon Homo sapiens
  • sample-icon 3 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 2.0 ST Array (hugene20st)

Description

In previous studies, miR-1825 has been found to be downregulated in the serum of familial and sporadic patients with amyotrophic lateral sclerosis (ALS). In this study, we aim to identify the target mRNAs of miR-1825 using a combination of proteomic and transcriptomic approaches.

Publication Title

Dysregulation of a novel miR-1825/TBCB/TUBA4A pathway in sporadic and familial ALS.

Sample Metadata Fields

Cell line

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accession-icon GSE53514
Coexpression of CD49b and LAG-3 identifies human and mouse T regulatory type 1 cells
  • organism-icon Homo sapiens
  • sample-icon 34 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

CD4(+) type 1 T regulatory (Tr1) cells are induced in the periphery and have a pivotal role in promoting and maintaining tolerance. The absence of surface markers that uniquely identify Tr1 cells has limited their study and clinical applications. By gene expression profiling of human Tr1 cell clones, we identified the surface markers CD49b and lymphocyte activation gene 3 (LAG-3) as being stably and selectively coexpressed on mouse and human Tr1 cells. We showed the specificity of these markers in mouse models of intestinal inflammation and helminth infection and in the peripheral blood of healthy volunteers. The coexpression of CD49b and LAG-3 enables the isolation of highly suppressive human Tr1 cells from in vitro anergized cultures and allows the tracking of Tr1 cells in the peripheral blood of subjects who developed tolerance after allogeneic hematopoietic stem cell transplantation. The use of these markers makes it feasible to track Tr1 cells in vivo and purify Tr1 cells for cell therapy to induce or restore tolerance in subjects with immune-mediated diseases.

Publication Title

Coexpression of CD49b and LAG-3 identifies human and mouse T regulatory type 1 cells.

Sample Metadata Fields

Specimen part, Treatment, Time

View Samples
accession-icon SRP057639
Tracking the fate of pathogenic CD4 T helper cells in vivo.
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Inflammation is a beneficial host response to infection, but it also contributes to inflammatory disease if unregulated. The Th17 lineage of T helper (Th) cells can cause severe human inflammatory diseases. These cells exhibit both instability (i.e., they can cease to express their signature cytokine, IL-17A) and plasticity (i.e., they can start expressing cytokines typical of other lineages) upon in vitro re-stimulation. However technical limitations prevented the transcriptional profiling of pre- and post-conversion Th17 cells ex vivo during immune responses. Thus, it is unknown whether Th17 cell plasticity merely reflects change in expression of a few cytokines, or if Th17 cells physiologically undergo global genetic reprogramming driving their conversion from one T helper cell type to another, a process known as “transdifferentiation”. Furthermore, while Th17 cell instability/plasticity has been associated with pathogenicity, it is unknown whether this could present a therapeutic opportunity, whereby formerly pathogenic Th17 cells could adopt an anti-inflammatory fate. Here we used two novel fate-mapping mouse models to track Th17 cells during immune responses to show that CD4+ T cells that formerly expressed IL-17A go on to acquire an anti-inflammatory phenotype. The transdifferentiation of Th17 into regulatory T cells was illustrated by a global change in their transcriptome and the acquisition of potent regulatory capacity. Comparisons of the transcriptional profiles of pre- and post-conversion Th17 cells also revealed a role for canonical TGF- ß signaling and the aryl hydrocarbon receptor (AhR) in conversion. Thus, Th17 transdifferentiate into regulatory cells, and contribute to the resolution of inflammation. Our data suggest Th17 cell instability and plasticity is a therapeutic opportunity for inflammatory diseases. Overall design: We isolated intestinal lymphocytes from two independent experiments, each using 5 mice injected with anti-CD3 mAb. Th17, exTh17, Tr1 exTh17, Tr1, Foxp3 Treg and Foxp3 IL-10+ Treg cell populations were FACS-sorted from these two independent experiments and the cells of each population were pooled before the analysis. Around 5,000 cells for each population were processed.

Publication Title

Th17 cells transdifferentiate into regulatory T cells during resolution of inflammation.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE8024
Murine ES cells, neural precursor cells and embryonic fibroblasts
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Expression profiles for isogenic (129SvJae x C57BL/6) murine embryonic stem (ES) cells, neural precursors (NPC) obtained through in vitro differentiation of the ES cells, and embryonic fibroblasts (MEF) obtained at day 13.5.

Publication Title

Genome-wide maps of chromatin state in pluripotent and lineage-committed cells.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE4885
Role of coactivator SRC-1/NcoA-1 for IL-6 target gene induction in HepG2 cells
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

This experiment series addresses the role of coactivator SRC-1/NcoA-1 for the induction of interleukin-6 (IL-6) target genes in HepG2 cells. For that purpose, HepG2 human hepatocellular carcinoma cells were manipulated to stably express an shRNA that knocks down SRC-1 expression yielding the HepG2-Src1 cells. Either unmanipulated HepG2 or HepG2-Src1 cells were then treated for various periods with IL-6.

Publication Title

Co-activator SRC-1 is dispensable for transcriptional control by STAT3.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE4817
Sphingosine 1-phosphate effect on glioblastoma cells in vitro
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

Abstract

Publication Title

Text mining of full-text journal articles combined with gene expression analysis reveals a relationship between sphingosine-1-phosphate and invasiveness of a glioblastoma cell line.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP165794
Molecular and functional heterogeneity of IL-10-producing CD4+ T cells [Mouse Bulk-seq]
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

IL-10 is a prototypical anti-inflammatory cytokine, which is fundamental to the maintenance of immune homeostasis, especially in the intestine. There is an assumption that cells producing IL-10 have an immunoregulatory function. However, here we report that IL-10-producing CD4+ T cells are phenotypically and functionally heterogeneous. By combining single cell transcriptome and functional analyses, we identified a subpopulation of IL-10-producing Foxp3Neg CD4+ T cells that displays regulatory activity unlike other IL-10-producing CD4+ T cells, which are unexpectedly pro-inflammatory. The combinatorial expression of co-inhibitory receptors is sufficient to discriminate IL-10-producing CD4+ T cells with regulatory function from others and to identify them across different tissues and disease models in mice and humans. These regulatory IL-10-producing Foxp3Neg CD4+ T cells have a unique transcriptional program, which goes beyond the regulation of IL-10 expression. Finally, we found that patients with Inflammatory Bowel Disease (IBD), demonstrate a deficiency in this specific regulatory T-cell subpopulation. Overall design: We carried out high troughput RNA sequencing of RNA isolated from IL-10 producing Foxp3- CD4+ T-cells, which were isolated from the spleen of mice treated with anti-CD3 antibody.

Publication Title

Molecular and functional heterogeneity of IL-10-producing CD4<sup>+</sup> T cells.

Sample Metadata Fields

Subject

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accession-icon GSE40438
Gene expression profiling of resistant and vulnerable motor neuron subtypes in amyotrophic lateral sclerosis
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

A consistent clinical feature of amyotrophic lateral sclerosis (ALS) is the sparing of eye movements. Pathological studies have confirmed that there is relative sparing of the cranial motor nuclei of the oculomotor, trochlear and abducens nerves, although pathological changes resembling those seen in anterior horn cells are present to a lesser degree. The aim of the present study is to combine LCM and microarray analysis to study the differences between motor neurons that are selectively resistant (oculomotor neurons) and those that are vulnerable (lumbar spinal motor neurons) to the disease process in amyotrophic lateral sclerosis.

Publication Title

Unravelling the enigma of selective vulnerability in neurodegeneration: motor neurons resistant to degeneration in ALS show distinct gene expression characteristics and decreased susceptibility to excitotoxicity.

Sample Metadata Fields

Specimen part, Disease, Disease stage

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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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