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accession-icon GSE13637
Influenza virus infected HUVEC
  • organism-icon Homo sapiens
  • sample-icon 29 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

To delineate specific patterns of signaling networks activated by H5N1 we used a comparative systems biology approach analyzing gene expression in endothelial cells infected with three different human and avian influenza strains of high and low pathogenicity.

Publication Title

Essential impact of NF-kappaB signaling on the H5N1 influenza A virus-induced transcriptome.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE27702
Highly Pathogenic Avian Influenza Viruses Avoid Effective Inflammatory Response of Human Macrophages
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A 2.0 Array (hgu133a2)

Description

Macrophages were infected with low (PR8) and high pathogenic influenza viruses (FPV and H5N1). To our surprise a genome-wide comparative systems biology approach revealed that in contrast PR8 infections with HPAIV H5N1 and FPV result in a reduced immune response of human macrophages contradicting a primary role of this cell type for the cytokine storm.

Publication Title

Highly pathogenic avian influenza viruses inhibit effective immune responses of human blood-derived macrophages.

Sample Metadata Fields

Specimen part

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accession-icon GSE40281
Signaling pathways of HPAIV
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Highly pathogenic avian influenza viruses (HPAIV) induce severe inflammation in poultry and men. There is still an ongoing threat that these viruses may acquire the capability to freely spread as novel pandemic virus strains that may cause major morbidity and mortality. One characteristic of HPAIV infections is the induction of a cytokine burst that strongly contributes to viral pathogenicity. It has been suggested, that this cytokine overexpression is an intrinsic feature of infected cells and involves hyperinduction of p38 mitogen activated protein kinase (MAPK). Here we investigate the role of MAPK p38 signaling in the antiviral response against HPAIV in mice as well as in endothelial cells, the latter a primary source for cytokines during systemic infections.

Publication Title

Inhibition of p38 mitogen-activated protein kinase impairs influenza virus-induced primary and secondary host gene responses and protects mice from lethal H5N1 infection.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE58771
Expression data from Arabidopsis thaliana root and piriformaspora indica during log and short term interaction
  • organism-icon Arabidopsis thaliana
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)

Description

Piriformospora indica, an endophytic fungus of Sebacinales, colonizes the roots of many plant species including Arabidopsis thaliana. The symbiotic interaction promotes plant per-formance, growth and resistance/tolerance against abiotic and biotic stress. We demonstrate that exudated compounds from the fungus activate stress and defense responses in the Arabidopsis roots and shoots before the two partners are in physical contact. They induce stomata closure, stimulate reactive oxygen species (ROS) production, stress-related phytohormone accumulation and activate defense and stress genes in the roots and/or shoots. Once a physical contact is established, the stomata re-open, ROS and phytohormone levels decline, and the gene expression pattern indicates a shift from defense to mutualistic interaction.

Publication Title

The interaction of Arabidopsis with Piriformospora indica shifts from initial transient stress induced by fungus-released chemical mediators to a mutualistic interaction after physical contact of the two symbionts.

Sample Metadata Fields

Age, Specimen part

View Samples
accession-icon GSE29458
Expression data from PDGF driven mouse tumors
  • organism-icon Mus musculus
  • sample-icon 23 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Background

Publication Title

Glioblastoma models reveal the connection between adult glial progenitors and the proneural phenotype.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE7355
Candida-induced expression profile in HUVEC
  • organism-icon Homo sapiens
  • sample-icon 7 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

Using oligonucleotide microarray analysis, we identified 56 genes that were transcriptionally up-regulated and 69 that were suppressed upon exposure of endothelial cells to C. albicans. Among the regulated genes those attributed to the categories chemotaxis, signaling, and transcription and translation were remarkably overrepresented.

Publication Title

Candida albicans triggers activation of distinct signaling pathways to establish a proinflammatory gene expression program in primary human endothelial cells.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon SRP106907
BRCA1 Regulates Carbohydrate Metabolism Through its RING Domain and Transcription Factor Oct1
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

The tumor suppressor BRCA1 regulates DNA damage responses and multiple other processes. Among these, BRCA1 heterodimerizes with BARD1 to ubiquitylate targets via its N-terminal RING domain. Here we show that BRCA1 promotes oxidative metabolism via degradation of Oct1, a transcription factor with pro-glycolytic/tumorigenic effects. BRCA1 E3 ubiquitin ligase mutation skews cells towards a glycolytic metabolic profile while elevating Oct1 protein. CRISPR-mediated Oct1 deletion reverts the glycolytic phenotype. RNAseq confirms the deregulation of metabolic genes. BRCA1 mediates direct Oct1 ubiquitylation and degradation, and mutation of two ubiquitylated Oct1 lysines insulates the protein against BRCA1-mediated destabilization. Oct1 deletion in MCF-7 breast cancer cells does not perturb growth in standard culture, but inhibits growth in soft agar and xenografts. Oct1 protein levels correlate positively with tumor aggressiveness, and inversely with BRCA1, in primary breast cancer samples. These results identify BRCA1 as an Oct1 ubiquitin ligase that catalyzes Oct1 degradation to promote oxidative metabolism. Overall design: mRNA profiles of BRCA1-I26A mutant MEFs treated with control CRISPR lentiviral vector, or an Oct1-specific CRISPR construct

Publication Title

BRCA1 through Its E3 Ligase Activity Regulates the Transcription Factor Oct1 and Carbohydrate Metabolism.

Sample Metadata Fields

Specimen part, Cell line, Subject

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accession-icon SRP134235
Poly(A)+ RNA-seq from H226 cells expressing doxycycline-inducible Control (non-targeting) and p63-targeting shRNAs
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

To determine the impact of ?Np63a knockdown on steady-state mRNA levels, we performed poly(A)-enriched RNA-seq analysis of lung squamous cell carcinoma line H226 (inducible shControl and shp63) in the presence of 1µg/mL doxycycline to induce shRNA expression. Overall design: Poly(A)+ RNA for two independent biological replicates was purified from H226 cells (inducible shControl and shp63) incubated treated for six days with 1 µg/mL doxycycline. a TruSeq Stranded mRNA Library Prep Kit (Illumina). Libraries were sequenced on an Illumina HiSeq 2000 system at the University of Colorado Cancer Center Genomics and Microarray Core facility. Reads were aligned (TopHat2) to the Human reference genome (GRCh37/hg19) and gene-level counts (HTseq-count) were used for differential expression analysis (DESeq2).

Publication Title

ΔNp63α Suppresses TGFB2 Expression and RHOA Activity to Drive Cell Proliferation in Squamous Cell Carcinomas.

Sample Metadata Fields

Specimen part, Cell line, Treatment, Subject

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accession-icon GSE5847
Tumor and stroma from breast by LCM
  • organism-icon Homo sapiens
  • sample-icon 95 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

Tumor epithelium and surrounding stromal cells were isolated using laser capture microdissection of human breast cancer to examine differences in gene expression based on tissue types from inflammatory and non-inflammatory breast cancer

Publication Title

A stromal gene signature associated with inflammatory breast cancer.

Sample Metadata Fields

Specimen part, Disease, Race, Subject

View Samples
accession-icon E-MEXP-254
Plasmodiophora brassicae infection of Arabidopsis thaliana
  • organism-icon Arabidopsis thaliana
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)

Description

Arabipdosis thaliana (ecotype Col-0) was infected with the root pathogen Plasmodiophora brassicae. Gene expression of the host plant has been analyzed at two time points after inoculation (10 and 23 days after inoculation) compared to the correspondend control plants.

Publication Title

Transcriptome analysis of Arabidopsis clubroots indicate a key role for cytokinins in disease development.

Sample Metadata Fields

Age, Specimen part, Cell line, 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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