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accession-icon SRP093990
Retinoic Acid Induced Transcriptional Repressor HIC1 is Required for Suppressive Function of Human Induced Regulatory T cells [RNA-Seq 2]
  • organism-icon Homo sapiens
  • sample-icon 57 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Human CD4 positive T cells were isolated from cord blood using CD4 positive isolation kit from Dynal. Cells were activated with plate bound anti-CD3 and soluble anti-CD28 in presence (iTreg) or absence (Th0) of IL2, TGF beta and ATRA. The cells were harvested at 0, 0.5, 1, 2, 4, 6, 12, 24, 48, and 72 hours. Overall design: Comparing the gene expression in activated CD4+ cells and iTreg differentiated cells in human. 9 time points, 3 replicates for each time point.

Publication Title

Transcriptional Repressor HIC1 Contributes to Suppressive Function of Human Induced Regulatory T Cells.

Sample Metadata Fields

Specimen part, Subject

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accession-icon GSE53795
Th17 pathway is activated in early inflamed acne lesions
  • organism-icon Homo sapiens
  • sample-icon 24 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

The mechanisms of inflammation in acne are not well understood. This study performed in two separate patient populations focused on the activation of adaptive and innate immunity in early inflamed acne. Biopsies were collected from lesional and non-lesional skin of acne patients. Psoriasis patients and healthy volunteers were included in the study for comparison (not included in the records). Using Affymetrix Genechips, we observed significant elevation of the signature cytokines of the Th17 lineage in acne lesions compared to non-lesional skin. The increased expression of IL-17 was confirmed with real-time qPCR (RT-PCR) in two separate patient populations. Cytokines involved in Th17 lineage differentiation (IL-1beta, IL-6, TGF-beta; IL23p19) were remarkably induced at the RNA level. In addition, pro-inflammatory cytokines (IL-8, TNF-), Th1 markers (IL12p40, CXCR3, T-bet, IFN-gamma), T regulatory cell markers (Foxp3, IL-10, TGF-) and antimicrobial peptides (S100A7, S100A9, LNC2, hBD2, hBD3, hCAP18) were induced. Importantly, immunohistochemistry revealed significantly increased numbers of IL-17A positive T cells and CD83 dendritic cells in the acne lesions. In summary our results demonstrate the presence of IL17A positive T cells and the activation of Th17-related cytokines in acne lesions, indicating that the Th17 pathway may play a pivotal role in the disease process, offering new targets of therapy.

Publication Title

IL-17/Th17 pathway is activated in acne lesions.

Sample Metadata Fields

Specimen part

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accession-icon SRP092552
Transcriptional profiling of cortex and striatal tissue following chronic dosing of PDE10A inhibitor PF-02545920 in a Q175 homozygous knock-in mouse model of Huntington’s disease
  • organism-icon Mus musculus
  • sample-icon 86 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Huntington’s disease (HD) symptoms are driven to a large extent by dysfunction of the basal ganglia circuitry. HD patients exhibit reduced striatal phoshodiesterase 10 (PDE10) levels. Using HD mouse models that exhibit reduced PDE10, we demonstrate the benefit of pharmacologic PDE10 inhibition to acutely correct basal ganglia circuitry deficits. PDE10 inhibition restored corticostriatal input and boosted cortically driven indirect pathway activity. Cyclic nucleotide signaling is impaired in HD models and PDE10 loss may represent a homeostatic adaptation to maintain signaling. Elevation of both cAMP and cGMP by PDE10 inhibition were required for rescue. Phosphoproteomic profiling of striatum in response to PDE10 inhibition highlighted plausible neural substrates responsible for the improvement. Early chronic PDE10 inhibition in Q175 mice showed improvements beyond those seen with acute administration after symptom onset, including partial reversal of striatal deregulated transcripts and the prevention of the emergence of HD neurophysiological deficits. Overall design: Transcriptional profiling of cortex and striatal tissue following chronic dosing of either vehicle or the  PDE10A inhibitor PF-02545920 (0.32, 1 and 3.2 mg/kg po qd) in the Q175 homozygous knock-in mouse model of Huntington’s disease (dosing from 5-weeks to 9 months of age).

Publication Title

Phosphodiesterase 10A Inhibition Improves Cortico-Basal Ganglia Function in Huntington's Disease Models.

Sample Metadata Fields

Sex, Age, Specimen part, Cell line, Treatment, Subject

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accession-icon GSE4616
Time series of diabetes and exercise training induced expression changes in cardiac muscle of mice
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Murine Genome U74A Version 2 Array (mgu74av2)

Description

We investigated the effects of diabetes, physical training, and their combination on the gene expression of cardiac muscle. Mice were divided to control (C), training (T), streptozotocin-induced diabetic (D), and diabetic training (DT) groups. Training groups performed 1, 3, or 5 weeks of endurance training on a motor-driven treadmill. Muscle samples from T and DT groups together with respective controls were collected 24 hours after the last training session. Gene expression of cardiac muscles were analyzed using Affymetrix Gene chip MG U74Av2 (Affymetrix , Inc., Santa Clara, CA).

Publication Title

Effects of streptozotocin-induced diabetes and physical training on gene expression of titin-based stretch-sensing complexes in mouse striated muscle.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE1659
Time series of diabetes and exercise training induced expression changes in skeletal muscle of mice
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Murine Genome U74A Version 2 Array (mgu74av2)

Description

Experiment protocol:

Publication Title

Effects of streptozotocin-induced diabetes and physical training on gene expression of extracellular matrix proteins in mouse skeletal muscle.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP110277
Transcriptomic analysis of neuroepithelium and sorted neural progenitors in the murine cortex duirng early stages of development
  • organism-icon Mus musculus
  • sample-icon 10 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500, Illumina HiSeq 2000

Description

Relatively little is known about how the identity of early neuronal stem cells changes before and after neural tube closure (neurulation). We performed RNA sequencing on microdissected forebrain precursors and revealed sharp reductions in expresion of protein biosynthetic machinery after neurulation. These reductions were paralleled by down-regulation of Myc, which regulated forebrain precursor ribosome ribosome biogenesis. To study consequences of Myc dysregulation, we overexpressed Myc in Nestin+ neural progenitors, sorted these progenitors for RNA sequencing, and identified 135 genes that are differentially expressed between Myc-overexpressed embryos and their wildtype littermates. Overall design: The first RNA sequencing dataset contains micordissected neuroepithelium from E8.5 and E10.5 mouse embryos, two biological replicates for each age. The second RNA sequencing dataset contain FACS isolated Pax6+ neural progenitors form the cortex of E13.5 MYC-overexpressed embryos and their wildtype littermates, three biological replicates for each genotype.

Publication Title

Downregulation of ribosome biogenesis during early forebrain development.

Sample Metadata Fields

Specimen part, Cell line, Subject

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accession-icon GSE28536
Expression data from the Finnish Nodular Lymphocyte Predominant Hodgkin Lymphoma (NLPHL) family and ten controls
  • organism-icon Homo sapiens
  • sample-icon 18 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Gene expression was studied from the blood derived RNAs of the Finnish family members as well as from 10 controls using GeneChip Human Genome U133 Plus2 (Affymetrix). Eight out of 10 family members in the expression analysis are heterozygous for the NPAT c.2437-2438delAG, three of which are NLPHL cases.

Publication Title

Exome sequencing reveals germline NPAT mutation as a candidate risk factor for Hodgkin lymphoma.

Sample Metadata Fields

Specimen part, Disease, Disease stage, Subject

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accession-icon GSE64420
Multi-level omics analysis of dystrophin loss and therapeutic restoration in a murine model
  • organism-icon Mus musculus
  • sample-icon 22 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.1 ST Array (mogene11st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Multi-level omics analysis in a murine model of dystrophin loss and therapeutic restoration.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon GSE64418
Multi-level omics analysis of gene expression in a murine model of dystrophin loss and therapeutic restoration [mRNA]
  • organism-icon Mus musculus
  • sample-icon 11 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.1 ST Array (mogene11st)

Description

Duchenne muscular dystrophy (DMD) is a classical monogenic disorder, a model disease for genomic studies and a priority candidate for regenerative medicine and gene therapy. Although the genetic cause of DMD is well known, the molecular pathogenesis of disease and the response to therapy are incompletely understood. Here,we describe analyses of protein, mRNA and microRNA expression in the tibialis anterior of the mdx mouse model of DMD. Notably, 3272 proteins were quantifiable and 525 identified as differentially expressed in mdx muscle (P < 0.01). Therapeutic restoration of dystrophin by exon skipping induced widespread shifts in protein and mRNA expression towards wild-type expression levels, whereas the miRNome was largely unaffected. Comparison analyses between datasets showed that protein and mRNA ratios were only weakly correlated (r = 0.405), and identified a multitude of differentially affected cellular pathways, upstream regulators and predicted miRNAtarget interactions. This study provides fundamental new insights into gene expression and regulation in dystrophic muscle.

Publication Title

Multi-level omics analysis in a murine model of dystrophin loss and therapeutic restoration.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon GSE72351
Cells release subpopulations of exosomes with distinct molecular and functional properties
  • organism-icon Mus musculus
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 2.1 ST Array (mogene21st)

Description

Cells release nano-sized membrane vesicles that are involved in intercellular communication by transferring biological information between cells. It is generally accepted that cells release at least three types of these extracellular vesicles (EVs): apoptotic bodies, microvesicles and exosomes. Whilst exosomes are assumed to be a homogenous population of EVs, they have a wide range of putative functions. Therefore, we hypothesized that cells release subpopulations of exosomes with distinct molecular compositions and functional properties. Exosomes were isolated from conditioned medium by differential ultracentrifugation. Sucrose density gradient centrifugation of the resulting exosome pellet revealed the presence of two distinct subpopulations, one smaller, slow migrating population (HD-Exo), and one fast migrating, larger population (LD-Exo).

Publication Title

Cells release subpopulations of exosomes with distinct molecular and biological properties.

Sample Metadata Fields

Specimen part

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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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