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accession-icon GSE138376
Expression data from HepG2 cells transfected with the Vitamin D Receptor (VDR) and activated by Vitamin D (calcitriol)
  • organism-icon Homo sapiens
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Clariom S Human array (clariomshuman)

Description

In the present study, we aimed to define the role of VDR in the overall lipid metabolism by transcriptomic and metabolomic analyses of human hepatocytes upon VDR activation by vitamin D (VitD)

Publication Title

The Vitamin D Receptor Regulates Glycerolipid and Phospholipid Metabolism in Human Hepatocytes.

Sample Metadata Fields

Specimen part, Cell line, Treatment

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accession-icon GSE101466
Type I IFN and not TNF, is essential for cyclic di-nucleotide-elicited CTL by a cytosolic cross-presentation pathway
  • organism-icon Mus musculus
  • sample-icon 70 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Dendritic cells are the initiators of the adaptive immune response, therefore its gene expression allow us to predict the responses to vaccination. We used bone marrow derived dendritic cells (BMDC) to analyze the gene expression that result from the exposure to adjuvants. We use model antigen OVA and cyclic di-AMP (CDA) as an adjuvant in order to characterize the genes involved in the activation of dendritic cells by CDA alone or when the antigen is present.

Publication Title

Type I IFN and not TNF, is Essential for Cyclic Di-nucleotide-elicited CTL by a Cytosolic Cross-presentation Pathway.

Sample Metadata Fields

Treatment, Time

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accession-icon SRP090801
Comparison of tbx5-positive ventricular cardiomyoctes with the rest of ventricular cardiomyocytes from adult zebrafish hearts
  • organism-icon Danio rerio
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2500

Description

In vertebrates, the heart has two main layers of cardiac muscle, a peripheral compact layer and an internal trabecular layer. Little is known on the differerences in gene expression between both layers. In zebrafish the outer layer is named cortical layer and the internal also trabecular layer. Here we used a double transgenic line labelling with GFP tbx5-positive cells and cardiomyoctes with nuclear DsRed (nucDsRed) to distinguish cortical from trabecular myocardium. Then, we compared the transcriptome of trabecular and cortical myocardium in the adult zebrafish. We describe that Tbx5a is a good marker of trabecular myocardium. Overall design: Four paired biological replicates consisting on Tbx5-positive and Tbx5-negative adult zebrafish ventricular cardiomyocytes were analysed by RNA-seq to compare their transcriptomic profiles.

Publication Title

Tbx5a lineage tracing shows cardiomyocyte plasticity during zebrafish heart regeneration.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP062067
Telomerase is essential for zebrafish heart regeneration
  • organism-icon Danio rerio
  • sample-icon 23 Downloadable Samples
  • Technology Badge IconIlluminaGenomeAnalyzerIIx

Description

Unlike human hearts, zebrafish hearts efficiently regenerate after injury. Regeneration is driven by the strong proliferation response of its cardiomyocytes to injury. In this study, we show that active telomerase is required for cardiomyocyte proliferation and full organ recovery, supporting the potential of telomerase therapy as a means of stimulating cell proliferation upon myocardial infarction. Overall design: Heart transcriptomes of WT and telomerase defective adult zebrafish animals were profiled by RNASeq, in control conditions and 3 days after heart cryoinjury.

Publication Title

Telomerase Is Essential for Zebrafish Heart Regeneration.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE32609
Transcriptional profiling of liver samples from Lmna Gly609Gly knock-in mice
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Hutchinson-Gilford Progeria Syndrome (HGPS) is caused by a point mutation in the LMNA gene that activates a cryptic donor splice site and yields a truncated form of prelamin A called progerin. Small amounts of progerin are also produced during normal aging. Studies with mouse models of HGPS have allowed the recent development of the first therapeutic approaches for this disease. However, none of these earlier works have addressed the aberrant and pathogenic LMNA splicing observed in HGPS patients because of the lack of an appropriate mouse model. We report herein a genetically modified mouse strain that carries the HGPS mutation. These mice accumulate progerin, present histological and transcriptional alterations characteristic of progeroid models, and phenocopy the main clinical manifestations of human HGPS, including shortened life span and bone and cardiovascular aberrations. By using this animal model, we have developed an antisense morpholinobased therapy that prevents the pathogenic Lmna splicing, dramatically reducing the accumulation of progerin and its associated nuclear defects. Treatment of mutant mice with these morpholinos led to a marked amelioration of their progeroid phenotype and substantially extended their life span, supporting the effectiveness of antisense oligonucleotidebased therapies for treating human diseases of accelerated aging.

Publication Title

Splicing-directed therapy in a new mouse model of human accelerated aging.

Sample Metadata Fields

Sex, Age, Specimen part

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accession-icon GSE15743
IFN alpha-induced gene expression in human NK cells
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

NK cells are believed to contribute to the control of hepatitis C virus infection and pathogenesis of liver disease. Standard treatment of both acute and chronic hepatitis C is based on the administration of interferon alpha, however, the effects of type I interferons on human NK cells have not been studied in the context of hepatitis C. We therefore first performed a microarray screen for genes differentially regulated in human NK cells after stimulation of PBMC with recombinant interferon alpha-2b. One of the genes upregulated was TRAIL which was confirmed in vitro on the protein level.

Publication Title

Interferon-alpha-induced TRAIL on natural killer cells is associated with control of hepatitis C virus infection.

Sample Metadata Fields

Sex, Specimen part, Treatment

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accession-icon SRP077452
SHARPIN regulates collagen architecture and ductal invasion in the developing mouse mammary gland
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Primary mammary gland stromal fibroblasts from pubertal SHARPIN-deficient cpdm/cpdm -mice and their littermate controls Overall design: mRNA seq data from 3 wt and 3 Sharpincpdm mouse mammary gland stromal fibroblast cell samples

Publication Title

SHARPIN regulates collagen architecture and ductal outgrowth in the developing mouse mammary gland.

Sample Metadata Fields

Age, Specimen part, Cell line, Subject

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accession-icon GSE85473
Role of DmSTING in fly
  • organism-icon Drosophila melanogaster
  • sample-icon 16 Downloadable Samples
  • Technology Badge Icon Affymetrix Drosophila Genome 2.0 Array (drosophila2)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Analysis of Drosophila STING Reveals an Evolutionarily Conserved Antimicrobial Function.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon GSE47751
Early tissue responses to etanercept in psoriasis lesions
  • organism-icon Homo sapiens
  • sample-icon 34 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Anti-TNF-alpha therapy has made a significant impact on the treatment of psoriasis. Despite being designed to neutralize TNF-alpha activity, the mechanism of action of these agents in the resolution of psoriasis remains unclear. The aim of this study was to better understand the mechanism of action of etanercept by examining very early changes in the lesional skin of psoriasis patients. 20 chronic plaque psoriasis patients were enrolled and received 50mg etanercept twice weekly. Skin biopsies were obtained before treatment and on days 1, 3, 7 and 14 post-treatment. Skin mRNA expression was analysed by microarray.

Publication Title

Early tissue responses in psoriasis to the antitumour necrosis factor-α biologic etanercept suggest reduced interleukin-17 receptor expression and signalling.

Sample Metadata Fields

Specimen part, Disease, Subject

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accession-icon SRP045665
Impact of Tcf1 and Lef1 deficiency on HSCs
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Comparison of transcriptome between control and Tcf1/Lef1-deficient hematopoietic stem cells (HSCs). Overall design: Flt3-negative, lineage-negative, Sca1+ and cKit+ cells (Flt3-LSKs) were sorted from bone marrow cells from control mice or those are deficient for Tcf1 and Lef1 transcription factors. Both genes were conditionally deleted using Vav-Cre

Publication Title

Prostaglandin E1 and Its Analog Misoprostol Inhibit Human CML Stem Cell Self-Renewal via EP4 Receptor Activation and Repression of AP-1.

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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