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accession-icon GSE137998
Expression profiling of cervical cancer cells with IGF2R knock down
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

From comprehensive expression analysis of RNAseq data, IGF2R was found to correlate with poor prognosis in cervical cancer. Gene knockdown of IGF2R lead to cell death in cervical cancer. To reveal its biological function, we performed microarray analysis using IGF2R knockdown cervical cancer cells.

Publication Title

Upregulation of IGF2R evades lysosomal dysfunction-induced apoptosis of cervical cancer cells via transport of cathepsins.

Sample Metadata Fields

Cell line

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accession-icon GSE69925
Gene expression profiling of esophageal squamous cell carcinomas
  • organism-icon Homo sapiens
  • sample-icon 256 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

To identify the specific genes for subtyping.

Publication Title

Discovery of a Good Responder Subtype of Esophageal Squamous Cell Carcinoma with Cytotoxic T-Lymphocyte Signatures Activated by Chemoradiotherapy.

Sample Metadata Fields

Specimen part, Disease, Disease stage

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accession-icon GSE49469
Oncogenic Ras inhibits IRF1 to promote viral oncolysis
  • organism-icon Mus musculus
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Oncolytic viruses exploit common molecular changes in cancer cells, which are not present in normal cells, to target and kill cancer cells. Ras transformation and defects in type I interferon (IFN)-mediated antiviral responses are known to be the major mechanisms underlying viral oncolysis. Previously, we demonstrated that oncogenic RAS/Mitogen-activated protein kinase kinase (Ras/MEK) activation suppresses the transcription of many IFN-inducible genes in human cancer cells, suggesting that Ras transformation underlies type I IFN defects in cancer cells. Here, we investigated how Ras/MEK downregulates IFN-induced transcription. By conducting promoter deletion analysis of IFN-inducible genes, namely guanylate-binding protein 2 and IFN gamma inducible protein 47 (Ifi47), we identified the IFN regulatory factor 1 (IRF1) binding site as the promoter region responsible for the regulation of transcription by MEK. MEK inhibition promoted transcription of the IFN-inducible genes in wild type mouse embryonic fibroblasts (MEFs), but not in IRF1/ MEFs, showing that IRF1 is involved in MEK-mediated downregulation of IFN-inducible genes. Furthermore, IRF1 protein expression was lower in RasV12 cells compared with vector control NIH3T3 cells, but was restored to equivalent levels by inhibition of MEK. Similarly, the restoration of IRF1 expression by MEK inhibition was observed in human cancer cells. IRF1 re-expression in human cancer cells caused cells to become resistant to infection by the oncolytic vesicular stomatitis virus strain. Together, this work demonstrates that Ras/MEK activation in cancer cells downregulates transcription of IFN-inducible genes by targeting IRF1 expression, resulting in increased susceptibility to viral oncolysis.

Publication Title

Oncogenic Ras inhibits IRF1 to promote viral oncolysis.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE31019
Suppression of IFN-induced transcription underlies IFN defects generated by activated Ras/MEK in human cancer cells
  • organism-icon Homo sapiens
  • sample-icon 30 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Certain oncolytic viruses exploit activated Ras signalling in order to replicate in cancer cells. Constitutive activation of the Ras/MEK pathway is known to suppress the effectiveness of the interferon (IFN) antiviral response, which may contribute to Ras-dependent viral oncolysis. Here, we identified 10 human cancer cell lines (out of 16) with increased sensitivity to the anti-viral effects of IFN- after treatment with the MEK inhibitor U0126, suggesting that the Ras/MEK pathway underlies their reduced sensitivity to IFN. To determine how Ras/MEK suppresses the IFN response in these cells, we used DNA microarrays to compare IFN-induced transcription in IFN-sensitive SKOV3 cells, moderately resistant HT1080 cells, and HT1080 cells treated with U0126. We found that 267 genes were induced by IFN in SKOV3 cells, while only 98 genes were induced in HT1080 cells at the same time point. Furthermore, the expression of a distinct subset of IFN inducible genes, that included RIGI, GBP2, IFIT2, BTN3A3, MAP2, MMP7 and STAT2, was restored or increased in HT1080 cells when the cells were co-treated with U0126 and IFN. Bioinformatic analysis of the biological processes represented by these genes revealed increased representation of genes involved in the anti-viral response, regulation of apoptosis, cell differentiation and metabolism. Furthermore, introduction of constitutively active Ras into IFN sensitive SKOV3 cells reduced their IFN sensitivity and ability to activate IFN-induced transcription. This work demonstrates for the first time that activated Ras/MEK in human cancer cells induces downregulation of a specific subset of IFN-inducible genes.

Publication Title

Suppression of IFN-induced transcription underlies IFN defects generated by activated Ras/MEK in human cancer cells.

Sample Metadata Fields

Cell line, Treatment, Time

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accession-icon GSE69105
Expression data from WT and Fezf2 KO mTECs
  • organism-icon Mus musculus
  • sample-icon 10 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Fezf2 is highly and specifically expressed in mTECs in mouse thymus and Fezf2 deficiency (Fezf2 KO) in the thymus leads to autoimmunity. However, it is unclear how Fezf2 contributes to thymic gene expression.

Publication Title

Fezf2 Orchestrates a Thymic Program of Self-Antigen Expression for Immune Tolerance.

Sample Metadata Fields

Age, Specimen part

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accession-icon GSE48428
Expression data from Th17 cells of different origins
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Foxp3 is indispensable for Treg suppressive function, but the stability of Foxp3 has been controversial. In autoimmune arthritis, Th17 cells play a critically important pathological role, but the origin of Th17 cells remains unknown

Publication Title

Pathogenic conversion of Foxp3+ T cells into TH17 cells in autoimmune arthritis.

Sample Metadata Fields

Specimen part

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accession-icon GSE15046
Transcriptome analysis of gibberellin-signaling mutants in rice [Oryza sativa]
  • organism-icon Oryza sativa
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Rice Genome Array (rice)

Description

Gibberellins control a wide range of aspects of plant growth and development. Although a series of mutant of the signaling pathway has been identified, the global regulatory network underlying gibberellin signal transduction has not been revealed. To address this issue, we performed microarray analysis with rice gibberellin signaling mutants, gid1, gid2, slr, and the parental cultivar Taichung 65.

Publication Title

Highly sensitive and high-throughput analysis of plant hormones using MS-probe modification and liquid chromatography-tandem mass spectrometry: an application for hormone profiling in Oryza sativa.

Sample Metadata Fields

Specimen part

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accession-icon GSE29485
Expression data from Mouse embryo
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Mice lacking the function of the PcG protein CBX2 (also known as M33) show defects in gonadal, adrenal, and splenic development. In particular, XY knockout mice develop ovaries but not testes, and the gonads are hypoplastic in both sexes.

Publication Title

Cbx2, a polycomb group gene, is required for Sry gene expression in mice.

Sample Metadata Fields

Specimen part

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accession-icon GSE53521
Expression data in mouse liver expressing or not the adapter Grb14
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Grb14 is an endogenous inhibitor of insulin signaling

Publication Title

Novel Grb14-Mediated Cross Talk between Insulin and p62/Nrf2 Pathways Regulates Liver Lipogenesis and Selective Insulin Resistance.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon GSE28574
Transcriptome expressed in the mouse suprachiasmatic nucleus
  • organism-icon Mus musculus
  • sample-icon 1 Downloadable Sample
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

This array set was used to identify the genes that are highly expressed in the mouse suprachiasmatic nucleus (SCN). Because pharmacological inhibition of Gai/o activity with pertussis toxin hampers intercellular synchronization and causes dampened rhythms of the entire SCN, we hypothesized that member(s) of the Regulator of G protein Signaling (RGS) family might contribute to synchronized cellular oscillations in the SCN. To test this hypothesis, we surveyed all known mouse Rgs genes for their expression by using GeneChip and selected the genes that are highly expressed in the SCN for further analysis.

Publication Title

Circadian regulation of intracellular G-protein signalling mediates intercellular synchrony and rhythmicity in the suprachiasmatic nucleus.

Sample Metadata Fields

Sex, Age, Specimen part, Disease, Treatment, Time

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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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