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accession-icon GSE42538
Knockdown of mineralocorticoid receptor or glucocorticoid receptor on human endometrial stromal cells and decidualization
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

To clarify mineralcorticoid receptor and glucocorticoid receptor-dependent gene networks in decidualizing human endometrial stromal cells.

Publication Title

Induction of 11β-HSD 1 and activation of distinct mineralocorticoid receptor- and glucocorticoid receptor-dependent gene networks in decidualizing human endometrial stromal cells.

Sample Metadata Fields

Sex, Age, Specimen part, Treatment

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accession-icon GSE62210
Depletion of p62 reduces nuclear inclusions and paradoxically ameliorates disease phenotypes in Huntingtons model mice
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Huntingtons disease (HD) is a dominantly inherited genetic disease caused by mutant huntingtin (htt) protein with expanded polyglutamine tracts. A neuropathological hallmark of HD is the presence of neuronal inclusions of mutant htt. p62 is an important regulatory protein in selective autophagy, a process by which aggregated proteins are degraded, and it is associated with several neurodegenerative disorders including HD. Here we investigated the effect of p62 depletion in three HD model mice: R6/2, HD190QG and HD120QG mice. We found that loss of p62 in these models led to longer lifespans and reduced nuclear inclusions, although cytoplasmic inclusions increased with polyglutamine length. In mouse embryonic fibroblasts (MEFs) with or without p62, mutant htt with a nuclear localization signal (NLS) showed no difference in nuclear inclusion between the two MEF types. In the case of mutant htt without NLS, however, p62 depletion increased cytoplasmic inclusions. Furthermore, to examine the effect of impaired autophagy in HD model mice, we crossed R6/2 mice with Atg5 conditional knockout mice. These mice also showed decreased nuclear inclusions and increased cytoplasmic inclusions, similar to HD mice lacking p62. These data suggest that the genetic ablation of p62 in HD model mice enhances cytoplasmic inclusion formation by interrupting autophagic clearance of polyQ inclusions. This reduces polyQ nuclear influx and paradoxically ameliorates disease phenotypes by decreasing toxic nuclear inclusions.

Publication Title

Depletion of p62 reduces nuclear inclusions and paradoxically ameliorates disease phenotypes in Huntington's model mice.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE138725
Expression data from human epidermal keratinocytes treated with hydrolyzed wheat protein
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 2.0 ST Array (hugene20st)

Description

Hydrolyzed wheat proteins (HWPs) contained in cosmetics have occasionally caused immediate-type hypersensitivity following repeated skin exposure. Although the Cosmetic Ingredient Review Expert Panel concluded that <3,500 Da HWP is safe for use in cosmetics, it remains biologically unknown how allergenic HWPs evoke immediate-type allergy percutaneously. Keratinocyte-derived thymic stromal lymphopoietin (TSLP) induces type 2 immune responses, which play an essential role in the pathogenesis of immediate-type allergy. Previously, we demonstrated that protein allergens in cultured human keratinocytes strongly induced long-form TSLP (loTSLP) transcription. However loTSLP-regulating signaling by HWP is poorly understood.

Publication Title

An acid-hydrolyzed wheat protein activates the inflammatory and NF-κB pathways leading to long TSLP transcription in human keratinocytes.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon GSE153378
Expression data (U133 Plus 2.0) from fibroblast like synoviocytes from patients with rheumatoid arthritis (RA-FLS) stimulated by FasL
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Fas ligand (FasL)/TNFSF6, a member of the tumor necrosis factor (TNF) superfamily, can promote apoptosis in activated primary B cells, T cells, dendritic cells, and synovial fibroblasts through Fas and is involved in the pathogenesis of autoimmune diseases including rheumatoid arthritis (RA). Meanwhile, decoy receptor 3 (DcR3) competitively binds soluble FasL in addition to TL1A and LIGHT and inhibits the signaling of FasL via Fas. Therefore, FasL-DcR3/Fas signaling may be involved in the pathogenesis of RA.

Publication Title

Expression profiling of genes in rheumatoid fibroblast-like synoviocytes regulated by Fas ligand via cDNA microarray analysis.

Sample Metadata Fields

Specimen part

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accession-icon GSE61604
Effect of Drosophila immune proteins on gene expression in E. coli
  • organism-icon Escherichia coli
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix E. coli Genome 2.0 Array (ecoli2)

Description

Interaction between the host and invading pathogen determines the fate of both organisms during the infectious state. The host is equipped with a battery of immune reactions, while the pathogen displays a variety of mechanisms to compromise host immunity. Although bacteria alter their pattern of gene expression when they enter host organisms, studies to elucidate the mechanism behind this are only in their infancy. In the present study, we examined the possibility that host immune proteins directly participate in the change of gene expression in bacteria. To this end, Escherichia coli was treated with a mixture of the extracellular region of membrane-bound peptidoglycan recognition protein LC (PGRP-LC) and the antimicrobial peptide attacin of Drosophila, and subsequently subjected to DNA microarray analysis for the repertoire of mRNA. We identified nearly 200 genes whose mRNA increased after the treatment, and at least four of them were induced in response to PGRP-LC. One such gene, lipoprotein-encoding nlpI, showed a transient increase of its mRNA level in adult flies depending on PGRP-LC, and NlpI-lacking E. coli had a smaller pathogenic effect with lowered growth/viability than the parental strain in adult flies. These results suggest that a host immune receptor triggers a change of gene expression in bacteria simultaneously to their recognition of the invader and induction of immune responses.

Publication Title

Peptidoglycan recognition protein-triggered induction of Escherichia coli gene in Drosophila melanogaster.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP006578
X chromosome dosage compensation via enhanced transcriptional elongation in Drosophila males (Control & MSL2 RNAi)
  • organism-icon Drosophila melanogaster
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina Genome Analyzer II

Description

MSL (Male-specific lethal) complex increases transcription on the single X chromosome of Drosophila males in order to equalize expression of X-linked genes between males (XY) and females (XX). The increase in transcript levels correlates with MSL- dependent acetylation of histone H4 at K16 within the bodies of active genes, but identification of the transcriptional step affected has not been possible. In this study, we use global run-on sequencing (GRO-seq) to examine the specific effect of MSL complex on RNA Polymerase II (RNAP II) on a genome-wide level. Results indicate that MSL complex enhances transcription by facilitating the progression of RNAP II across the bodies of active X-linked genes. Improving transcriptional output downstream of typical gene-specific control may explain how dosage compensation can be imposed on the diverse set of genes along an entire chromosome. Overall design: Global Run-On Sequencing (GRO-Seq) reads, i.e., RNA-Seq of nascent RNA transcripts, from D. Melanogaster SL2 cells. Two biological replicates of cells treated with control GFP RNAi and cells treated with MSL2 RNAi were analyzed.

Publication Title

X chromosome dosage compensation via enhanced transcriptional elongation in Drosophila.

Sample Metadata Fields

Subject

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accession-icon GSE63332
Hydroxypropyl--cyclodextrin spikes local inflammation that induces Th2 and Tfh responses to the coadministered antigen
  • organism-icon Mus musculus
  • sample-icon 30 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Gene expression data from mouse organs after hydroxypropyl--cyclodextrin injection

Publication Title

Hydroxypropyl-β-cyclodextrin spikes local inflammation that induces Th2 cell and T follicular helper cell responses to the coadministered antigen.

Sample Metadata Fields

Sex, Specimen part

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accession-icon SRP061033
Recovery and analysis of nascent RNA
  • organism-icon Homo sapiens
  • sample-icon 14 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2500

Description

Nascent transcription profiles are shown for scaled megadomains and 100kb flanking regions before BRD4-NUT induction (0h) and at different time points (2h, 3h, 7h) following induction in 293T cells. Increase of the transcription from 0h to 7h after induction. Average level of transcriptional activity is reduced within the megadomains and their flanking regions following JQ1 treatment of TC-797 cells. Profile of nascent RNA-seq is shown for cells without JQ1 treatment, and for cells 1hr, 2.5hr and 4hr following JQ1 treatment. Overall design: Recovery and analysis of nascent RNA

Publication Title

The oncogenic BRD4-NUT chromatin regulator drives aberrant transcription within large topological domains.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE80985
Expresion data from primary retinal pigment epithelium (RPE) and immortalized RPE
  • organism-icon Homo sapiens
  • sample-icon 30 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

We used microarrays to detail the global gene expression of primary RPE and immortalized RPE.

Publication Title

Identification of a Gene Encoding Slow Skeletal Muscle Troponin T as a Novel Marker for Immortalization of Retinal Pigment Epithelial Cells.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon SRP156330
Next generation sequencing facilities quantitative analysis of KMST6 cells expressing AUG-initiated c-Myc and CUG-initiated c-Myc.
  • organism-icon Homo sapiens
  • sample-icon 9 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 4000

Description

To investigate the differences of transcriptional activities between AUG-initiated c-Myc and CUG-initiated c-Myc , we performed a transcriptomic analysis using high throoughput RNA sequencing (RNA-seq). Overall design: Total RNA extracted from KMST6 fibroblast cells stably expressing AUG-initiated c-Myc, CUG-initiated c-Myc, and empty vector (negative control) was subjected to RNA-seq analysis. The sequencing libraries generated from the RNA were analyzed by Illumina Hiseq 4000. The sequencing reads were trimmed for adaptor sequence, and low-complexity or low-quality reads were removed. Subsequently, the sequencing reads were aligned to the human reference GRCh38 genome using Gencode v27 annotations by STAR. Read counts per gene were quantified using the HTSeq Python package.

Publication Title

Novel oncogene 5MP1 reprograms c-Myc translation initiation to drive malignant phenotypes in colorectal cancer.

Sample Metadata Fields

Subject

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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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