refine.bio
  • Search
      • Normalized Compendia
      • RNA-seq Sample Compendia
  • Docs
  • About
  • My Dataset
github link
Showing
of 12 results
Sort by

Filters

Technology

Platform

accession-icon GSE104509
Expression data from keratinocytes treated either with IL-22 or combination of tofacitinib (JAK1/3 inhibitor) and IL-22 at 6 hours
  • organism-icon Homo sapiens
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 2.1 ST Array (hugene21st)

Description

JAK inhibitors like tofacitinib were thought to act primarily on T cells. However, our data and recent research suggest that JAK receptors are also present on keratinocytes. Here, we show effect of tofacitinib on primary keratinocytes, which could explain effects of topical tofacitinib treatment in psoriasis.

Publication Title

Tofacitinib Represses the Janus Kinase-Signal Transducer and Activators of Transcription Signalling Pathway in Keratinocytes.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE78057
Expression data from IMQ-induced psoriasis-like skin inflammation in miR-146a-/- and C57BL6J mice
  • organism-icon Mus musculus
  • sample-icon 16 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 2.1 ST Array (mogene21st)

Description

miR-146a acts as a negative feedback regulator of inflammation. To investigate the role of miR-146a in psoriasis psoriasiform skin inflammation was indeuced in Mir-146a-/- and wild type mice (C57BL6J) by topical applciation of imiquimod (IMQ)-cream (Aldara).

Publication Title

MicroRNA-146a suppresses IL-17-mediated skin inflammation and is genetically associated with psoriasis.

Sample Metadata Fields

Age, Specimen part

View Samples
accession-icon GSE41905
A global transcriptome analysis of keratinocytes upon suppression of endogenous microRNA-31
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.1 ST Array (hugene11st)

Description

MiR-31 is one of the most highly overexpressed miRNAs in psoriasis skin; however, its biological role in the disease has not been studied. Here we show that miR-31 is markedly overexpressed in psoriasis keratinocytes. To study the biological role of miR-31 in keratinocytes, we transfected miR-31 hairpin inhibitor (anti-miR-31) into primary human keratinocytes to inhibit endogenous miR-31. We performed a global transcriptome analysis of keratinocytes upon suppression of endogenous miR-31 using Affymetrix arrays.

Publication Title

MicroRNA-31 is overexpressed in psoriasis and modulates inflammatory cytokine and chemokine production in keratinocytes via targeting serine/threonine kinase 40.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE114203
A microarray analysis of human epidermal keratinocytes upon depletion of the long non-coding RNA LOC100130476
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Clariom S Pico Assay HT (clariomshumanht)

Description

The lncRNA LOC100130476 (named as WAKMAR2) was found to be down-regulated in epidermal keratinocytes in human chronic non-healing wounds compared to normal acute wounds and the intact skin. However, its biological role in keratinocytes during wound repair has not been studied.

Publication Title

WAKMAR2, a Long Noncoding RNA Downregulated in Human Chronic Wounds, Modulates Keratinocyte Motility and Production of Inflammatory Chemokines.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE84584
NorUrsodeoxycholic Acid Ameliorates Cholemic Nephropathy in Common Bile Duct Ligated Mice
  • organism-icon Mus musculus
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 2.0 ST Array (mogene20st)

Description

Cholestasis may cause cholemic nephropathy that can be modelled in common bile duct ligated (CBDL) mice. We aimed to explore the therapeutic efficacy and mechanisms of norursodeoxycholic acid (norUDCA) in cholemic nephropathy. To determine whether norUrsodeoxycholic acid (norUDCA) prevents cholemic nephropathy in long-term CBDL mice, a norUDCA-enriched diet (0.125% w/v, corresponding to 200 mg/kg/day for a mouse of 25 g body weight eating about 4g daily) or a standard mouse diet (Sniff, Soest, Germany) were started 5 days prior to CBDL and were continued until harvesting 3 weeks thereafter. For transcriptional profiling using microarray technology, we compared sham-operated (SOP) mice and 3-week CBDL mice that were either fed 0.125% norUDCA-enriched or standard mouse diets.

Publication Title

NorUrsodeoxycholic acid ameliorates cholemic nephropathy in bile duct ligated mice.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE27975
HL-1 cardiomyocyte response to hypoxia
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Expression profiling of cultured HL-1 cardiomyocytes subjected to hypoxia for 8 hours.

Publication Title

The VLDL receptor promotes lipotoxicity and increases mortality in mice following an acute myocardial infarction.

Sample Metadata Fields

Cell line

View Samples
accession-icon SRP076944
RNA-seq transcriptome analysis of epidermal CD8+CD103+CD49a+ and CD8+CD103+CD49- T cells from healthy human skin
  • organism-icon Homo sapiens
  • sample-icon 53 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

We report the transcriptome analysis of epidermal CD8 tissue resident memory T (TRM) cells from healthy human skin. Specifically, epidermal CD8+CD103+CD49a+ and CD8+CD103+CD49- TRM cells from healthy human skin were sorted by FACS. Differential gene expression analysis revealed functional dichotomy of epidermal CD8+CD103+CD49a+ and CD8+CD103+CD49- TRM cells. Overall design: Analysis of differentially expressed genes between epidermal CD8+CD103+CD49a+ and CD8+CD103+CD49- T cells from healthy human skin, biological replicates (n=7) (healthy skin donors).

Publication Title

CD49a Expression Defines Tissue-Resident CD8<sup>+</sup> T Cells Poised for Cytotoxic Function in Human Skin.

Sample Metadata Fields

Specimen part, Subject

View Samples
accession-icon GSE73489
Gene expression profiling from pooled samples of liver tissue of liver MyD88 WT mice and MyD88 liver specific KO mice fed either with a control diet or a high-fat diet.
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 2.0 ST Array (mogene20st)

Description

Mice wild type or knocked-out for the MyD88 gene specifically in liver, were recruited for this expression profiling experiment. Each group of mice (WT versus LKO) were fed with a control diet or a high fat diet. Then mice were sacrificed and liver samples form were processed for RNA extraction. Total liver RNA of each sample was then pooled with those of the same group and treatment for microarray hybridization.

Publication Title

Hepatocyte MyD88 affects bile acids, gut microbiota and metabolome contributing to regulate glucose and lipid metabolism.

Sample Metadata Fields

Age, Specimen part

View Samples
accession-icon SRP040622
The age and genomic integrity of neurons after cortical stroke in humans
  • organism-icon Homo sapiens
  • sample-icon 13 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2000

Description

It has been unclear whether ischemic stroke induces neurogenesis or neuronal DNA-rearrangements in the human neocortex. We show here that neither is the case, using immunohistochemistry, transcriptome-, genome- and ploidy-analyses, and determination of nuclear bomb test-derived 14C-concentration in neuronal DNA. A large proportion of cortical neurons display DNA-fragmentation and DNA-repair short time after stroke, whereas neurons at chronic stages after stroke show DNA-integrity, demonstrating the relevance of an intact genome for survival. Overall design: Analyze of potential fusion transcripts in 13 samples, seven cortical ischemic stroke tissue and six control cortex, by deep sequencing using Illumina HiSeq 2000

Publication Title

The age and genomic integrity of neurons after cortical stroke in humans.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE29674
Differential pancreatic islet global gene expression in young heterozygous Men1 mice and wildtype littermates
  • organism-icon Mus musculus
  • sample-icon 10 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Multiple Endocrine Neoplasia Tumor Syndrome type 1 (MEN 1) is an autosomal dominant tumor syndrome affecting individuals with a heterozygous germline mutaion of the MEN1 gene. MEN 1 carriers commonly develop parathyroid, anterior pituitary, duodenal and pancreatic endocrine tumors. The phenotype of existing mouse models for the MEN 1 syndrome, with a germline heterozygous (hz) Men1 gene inactivation, show close resemblance to the human MEN 1 syndrome. Menin, the protein encoded for by the MEN1/Men1 gene, lacks homology with known proteins, and evidence of its involvement in different cellular processes is steadily growing. Several interaction partners have been identified, involving different interaction sites on the menin protein. Accumulating evidence suggests a role for menin in transcriptional regulation, cell cycle control, apoptosis, chromatin modification and DNA damage response and repair. Loss of heterozygosity (LOH) of the MEN1 gene precedes tumor formation in the MEN 1 heterozygous pancreas. We set out to determine if there is a change in gene expression early on in the hz islet, as compared with islets in wildtype (wt) littermates, long before the LOH events occur. We performed a global mRNA expression microarray on islets from young, five-week-old, hz Men1 mice and their wt littermates, and we have subsequently corroborated a subset of the findings on the qPCR and protein level.

Publication Title

Accelerated proliferation and differential global gene expression in pancreatic islets of five-week-old heterozygous Men1 mice: Men1 is a haploinsufficient suppressor.

Sample Metadata Fields

Sex, Age, Specimen part

View Samples

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)

fund-icon Fund the CCDL

Developed by the Childhood Cancer Data Lab

Powered by Alex's Lemonade Stand Foundation

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.

BSD 3-Clause LicensePrivacyTerms of UseContact