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accession-icon GSE13046
Microarray analysis of Huh7 cells treated with IFNa2, OSM or IFNa2 combined with OSM
  • organism-icon Homo sapiens
  • sample-icon 16 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A 2.0 Array (hgu133a2)

Description

OSM increases the antiviral effect of IFN in Huh7 cells infected with hepatitis A virus (HAV) or HCV replicon and synergizes with IFN in the induction of antiviral genes

Publication Title

Oncostatin M enhances the antiviral effects of type I interferon and activates immunostimulatory functions in liver epithelial cells.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE87403
The BET bromodomain inhibitor CPI203 improves lenalidomide activity in in vitro and in vivo models of multiple myeloma by synergistic blockade of Ikaros and c-Myc signaling
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U219 Array (hgu219)

Description

Multiple myeloma (MM) cells were treated with the BET inhibitor CPI203 alone and in combination with lenalidomide plus dexamethasone in vitro and in vivo (mouse xenograft).

Publication Title

The BET bromodomain inhibitor CPI203 improves lenalidomide and dexamethasone activity in <i>in vitro</i> and <i>in vivo</i> models of multiple myeloma by blockade of Ikaros and MYC signaling.

Sample Metadata Fields

Specimen part, Cell line, Treatment

View Samples
accession-icon GSE17301
The effect of IFN on human CD8 T cells_with other concomitant signals
  • organism-icon Homo sapiens
  • sample-icon 15 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A 2.0 Array (hgu133a2)

Description

IFN alpha mediated gene expression pattern. The effect of IFN alpha on human CD8 T cells responding to antigen (signal 1) and costimulatory signals (signal 2) provided by beads coated with anti-CD3 and anti-CD28 mAbs.

Publication Title

Effects of IFN-α as a signal-3 cytokine on human naïve and antigen-experienced CD8(+) T cells.

Sample Metadata Fields

Specimen part, Subject, Time

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accession-icon GSE89793
Loss of the Inhibitory Immune Checkpoint CD85j/LILRB1 on Malignant Plasma Cells Contributes to Immune Escape in Multiple Myeloma
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U219 Array (hgu219)

Description

Mechanisms of immune regulation may control proliferation of aberrant plasma cells (PCs) in patients with the asymptomatic monoclonal gammopathy of undetermined significance (MGUS) preventing progression to active multiple myeloma (MM). We investigated the role of CD85j (LILRB1), an inhibitory immune checkpoint for B cell function, in MM pathogenesis.

Publication Title

Loss of the Immune Checkpoint CD85j/LILRB1 on Malignant Plasma Cells Contributes to Immune Escape in Multiple Myeloma.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon SRP010038
Molecular Effects of Doxycycline Treatment on Pterygium as Revealed by Massive Transcriptome Sequencing
  • organism-icon Homo sapiens
  • sample-icon 40 Downloadable Samples
  • Technology Badge IconIllumina Genome Analyzer IIx

Description

A total of 332 genes were identified which modified their expression in a dose-dependent manner upon exposure to doxycycline. The more represented cellular pathways included all mitochondrial genes, the endoplasmic reticulum stress response, integrins and extracellular matrix components, and growth factors. Overall design: Examination of 4 different doses of doxycycline in ten human pterygium samples.

Publication Title

Transcriptomic profiling explains racial disparities in pterygium patients treated with doxycycline.

Sample Metadata Fields

Specimen part, Treatment, Subject

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accession-icon SRP043166
Molecular Effects of Doxycycline Treatment on Pterygium from Caucasian Patients as Revealed by Massive Transcriptome Sequencing
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIlluminaGenomeAnalyzerIIx

Description

Genes were identified which modified their expression in a dose-dependent manner upon exposure to doxycycline. The more represented cellular pathways included all mitochondrial genes, the endoplasmic reticulum stress response, integrins and extracellular matrix components, and growth factors. Overall design: Examination of 4 different doses of doxycycline in three human pterygium samples.

Publication Title

Transcriptomic profiling explains racial disparities in pterygium patients treated with doxycycline.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE8453
Expression data from yeast strain containing CDC34tm allele compared to WT
  • organism-icon Saccharomyces cerevisiae
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Yeast Genome 2.0 Array (yeast2)

Description

Cdc34 is an essential E2 ubiquitin conjugating enzyme found in nearly all eukaryotes. It contains a highly conserved motif composed of S73/S97/12 amino acid insert near the active site cysteine. This motif is unique to Cdc34/Ubc7 type E2s while other E2s contain K/D/no insert at these positions. To better understand the function of this motif we mutated Cdc34 S73/S97/insert to be K/D/no insert and observed changes in transcript levels in mid-log phase yeast cells. ABSTRACT [Cdc34 is a ubiquitin conjugating enzyme necessary for the ubiquitylation of substrates by the SCF family of ubiquitin ligases. Previous work has shown that the Cdc34 protein is phosphorylated in vivo on serine residues. Cdc34 contains two serines within its catalytic domain, S73 and S97, that together with a 12 amino acid acidic loop, constitute a highly conserved motif (serine, serine, insert) among all members of the Cdc34 family of E2 enzymes. Using phosphospecific antibodies, we show that the essential serine S97 is indeed phosphorylated in vivo. Furthermore, this phosphorylation event is regulated by treatment with pheromone in yeast. Consistently, expression of a Cdc34 mutant lacking this motif (serine, serine, insert) leads to misregulation of the SCF substrates, Sic1, Far1, Cln1 and Cln2 and suppresses the cell cycle arrest brought about by an activated mating pathway. We further explored the function of this motif by microarray analysis and show that the transcripts of nearly the entire Sic1 cluster of co-transcribed genes is altered in a strain the expresses Cdc34 lacking this motif. Our data reveals that this highly conserved motif in Cdc34 and its phosphorylation are important for modulating SCF substrate abundance both transcriptionally and post-transcriptionally.]

Publication Title

New insight into the role of the Cdc34 ubiquitin-conjugating enzyme in cell cycle regulation via Ace2 and Sic1.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE104849
New role of ID3 in melanoma adaptive drug-resistance
  • organism-icon Homo sapiens
  • sample-icon 28 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip

Description

Adaptive resistance to targeted therapy such as BRAF inhibitors represents in melanoma a major drawback to this otherwise powerful treatment. Some of the underlying molecular mechanisms have recently been described: hyperactivation of the BRAF-MAPK pathway, of the AKT pathway, of the TGF/EGFR/PDGFRB pathway, or the low MITF/AXL ratio. Nevertheless, the phenomenon of early resistance is still not clearly understood. In this report, we show that knockdown of neural crest-associated gene ID3 increases the melanoma sensitivity to vemurafenib short-term treatment. In addition, we observe an ID3-mediated regulation of cell migration and of the expression of resistance-associated genes such as SOX10 and MITF. In sum, these data suggest ID3 as a new key actor of melanoma adaptive resistance to vemurafenib and as a potential drug target. Molecular mechanisms that are responsible for the development of human skin epithelial cells are not completely understood so far. As a consequence, the efficiency to establish a pure skin epithelial cell population from human induced pluripotent stem cells (hiPSC) remains poor. Using an approach including RNA interference and high-throughput imaging of early epithelial cells, we could identify candidate kinases which are involved in skin epithelial differentiation. Among them, we found HIPK4 to be an important inhibitor of this process. Indeed, its silencing increased the amount of generated skin epithelial precursors, increased the amount of generated keratinocytes and improved growth and differentiation of organotypic cultures, allowing for the formation of a denser basal layer and stratification with the expression of several keratins. Our data bring substantial input in the regulation of human skin epithelial differentiation and for improving differentiation protocols from pluripotent stem cells.

Publication Title

New role of ID3 in melanoma adaptive drug-resistance.

Sample Metadata Fields

Cell line, Treatment

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accession-icon SRP126788
Single-cell RNA-sequencing reveals distinct populations of glucagon-like peptide-1 producing cells in the mouse upper small intestine
  • organism-icon Mus musculus
  • sample-icon 288 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Enteroendocrine L-cells release hormones that control metabolism and appetite and are targets under investigation for the treatment of diabetes and obesity. Understanding L-cell diversity and expression profiles is critical for identifying target receptors that will translate into altered hormone secretion. We performed single cell RNA sequencing of mouse L-cells from the upper small intestine to distinguish cellular populations, revealing that L-cells form 3 major clusters: a group with typical characteristics of classical L-cells, including high expression of Gcg and Pyy; a cell type overlapping with Gip-expressing K-cells; and a unique cluster expressing Tph1 and Pzp that was predominantly located in duodenal villi and co-produced 5HT. Expression of G-protein coupled receptors differed between clusters, suggesting the cell types are differentially regulated, and would be differentially targetable. Our findings support the emerging concept that many enteroendocrine cell populations are highly overlapping, with individual cells producing a range of peptides previously assigned to distinct cell types. Overall design: Single cell RNA sequencing of mouse duodenal L-cells cells

Publication Title

Single-cell RNA-sequencing reveals a distinct population of proglucagon-expressing cells specific to the mouse upper small intestine.

Sample Metadata Fields

Specimen part, Subject

View Samples
accession-icon GSE102067
An RNAi screen reveals an essential role for HIPK4 in human skin epithelial differentiation from iPSCs
  • organism-icon Homo sapiens
  • sample-icon 21 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip

Description

Molecular mechanisms that are responsible for the development of human skin epithelial cells are not completely understood so far. As a consequence, the efficiency to establish a pure skin epithelial cell population from human induced pluripotent stem cells (hiPSC) remains poor. Using an approach including RNA interference and high-throughput imaging of early epithelial cells, we could identify candidate kinases which are involved in skin epithelial differentiation. Among them, we found HIPK4 to be an important inhibitor of this process. Indeed, its silencing increased the amount of generated skin epithelial precursors, increased the amount of generated keratinocytes and improved growth and differentiation of organotypic cultures, allowing for the formation of a denser basal layer and stratification with the expression of several keratins. Our data bring substantial input in the regulation of human skin epithelial differentiation and for improving differentiation protocols from pluripotent stem cells.

Publication Title

An RNAi Screen Reveals an Essential Role for HIPK4 in Human Skin Epithelial Differentiation from iPSCs.

Sample Metadata Fields

Specimen part, Time

View Samples
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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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