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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

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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

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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

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accession-icon GSE67603
Untreated and iron-treated ARPE-19 cell gene expression
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 2.0 ST Array (hugene20st)

Description

To characterize the potential molecular pathway(s) affected by iron treatment and identify the one(s) responsible for C3 induction, we performed a whole genome microarray on untreated ARPE-19 cells and cells treated with 250 M FAC for 48h/2d.

Publication Title

Iron-induced Local Complement Component 3 (C3) Up-regulation via Non-canonical Transforming Growth Factor (TGF)-β Signaling in the Retinal Pigment Epithelium.

Sample Metadata Fields

Cell line, Treatment

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accession-icon GSE14753
Mammary tumors from K14-cre; ApcCKO/+ mice vs control mammary glands
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Many components of Wnt/-catenin signaling pathway also play critical roles in mammary tumor development. To study the role of Apc in mammary tumorigensis, we introduced conditional Apc mutations specifically into two different mammary epithelial populations using K14-Cre (progenitor) and WAP-cre (lactaing luminal) transgenic mice. Only the K14-cre mediated Apc heterozygosity developed mammary adenocarcinomas demonstrating histological and molecular heterogeneity, suggesting the progenitor cell origin of these tumors. These tumors harbored truncation mutation in a very defined region in the remaining wild-type allele of Apc that would retain some down-regulating activity of -catenin signaling. Our results suggest that not only the epithelial origin but also a certain Apc mutations are selected to achieve a specific level of -catenin signaling optimal for mammary tumor development.

Publication Title

Genetic mechanisms in Apc-mediated mammary tumorigenesis.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE37773
Retinal light damage microarray
  • organism-icon Mus musculus
  • sample-icon 16 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Microarray analysis of murine retinal light damage reveals changes in iron regulatory, complement, and antioxidant genes in the neurosensory retina and isolated retinal pigment epithelium (RPE). With the advent of microarrays representing most of the transcriptome and techniques to obtain RNA from the isolated RPE monolayer, we have probed the response of the RPE and neurosensory retina (NSR) to light damage.

Publication Title

Microarray analysis of murine retinal light damage reveals changes in iron regulatory, complement, and antioxidant genes in the neurosensory retina and isolated RPE.

Sample Metadata Fields

Sex, Specimen part, Treatment

View Samples
accession-icon SRP050061
Discovery of cis-spliced chimeric RNAs between adjacent genes in human prostate cells
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2000

Description

Total RNA extracted from prostate cancer LNCaP cells transfected with siRNA against CTCF(siCTCF), or negative control siRNA (si-)were processed, and sequenced by two different companies using Illumina Hi-seq 2000 platform to generate RNA sequencing with two output sequences: paired-end 50bp and 101bp in read length. Nearly 100 million and 50 million raw reads were yielded from each sample respectively. We used FastQC to confirm the quality of raw fastq sequencing data, and SOAPfuse software to detect fusion transcripts. Overall design: Discovering fusion genes from siCTCF and si- in LNCaP cells.

Publication Title

Discovery of CTCF-sensitive Cis-spliced fusion RNAs between adjacent genes in human prostate cells.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE103622
Gene expression data from irradiated mouse liver
  • organism-icon Mus musculus
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 2.0 ST Array (mogene20st)

Description

In previous studies, it was observed that survivors who received stem cell transplantation and whole body irradiation showed development of NAFLD as a chronic effect.

Publication Title

Decreased Hepatic Lactotransferrin Induces Hepatic Steatosis in Chronic Non-Alcoholic Fatty Liver Disease Model.

Sample Metadata Fields

Sex, Age, Specimen part

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accession-icon GSE13298
Rb1 deficient Apc1638N cecal tumors vs duodenal tumors
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)

Description

To examine the role of Rb1 in gastrointestinal (GI) tumors we generated mice with an Apc1638N allele, Rbtm2brn floxed alleles, and a villlin-cre transgene (RBVCA). These mice had reduced median survival due to an increase in tumor incidence and multiplicity in the cecum and the proximal colon; they differed from murine intestinal tumors of the Apc1638N type which normally arise solely in the small intestine. We have examined by micro-array analysis three cecal tumors from these mice (probable adenomas), and compared them to three duodenal tumors (probable adenocarcinomas). Expression profiles of duodenal and cecal tumors relative to each other show unique gene subsets up and down regulated. The two tumor types were subsequently shown to differentially regulate distinct sets of genes over expressed in a majority of human colorectal carcinomas.

Publication Title

Loss of Rb1 in the gastrointestinal tract of Apc1638N mice promotes tumors of the cecum and proximal colon.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE37397
Global Transcriptional Analysis of Nuclear Reprogramming in the Transition from MEFs to iPSCs
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Here, we focused on the intermediate stages of SCR by comparing the somatic cell line induced by OCT4, SOX2, and KLF4 (OSK) for 7 days with mouse embryonic fibroblasts (MEFs), iPSCs, and embryonic stem cells (ESCs). Transcriptional profiles of these four cell lines were analyzed by microarray, and we found that the transition process from day 7 to the formation of iPSCs is crucial for SCR and that the reverse expression patterns can provide more candidate markers to distinguish ESCs and somatic cells iPSC. Data confirmed that the viral infection results in defense innate immunity, DNA damage, and apoptosis in MEFs, which slows down cell proliferation and immortalization to inhibit SCR. Although SCR is initiated by OSK, the p53 signaling pathway can affect the transcriptional regulatory networks through cell cycle and genomic instability as a powerful core node.

Publication Title

Global transcriptional analysis of nuclear reprogramming in the transition from MEFs to iPSCs.

Sample Metadata Fields

Sex, 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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