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accession-icon GSE29946
Genome wide transcriptional analysis of P. aeruginosa PAO1 response to kappa-opioid U-50,488 in poor nutrient medium
  • organism-icon Pseudomonas aeruginosa pao1
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Pseudomonas aeruginosa Array (paeg1a)

Description

Here we examined virulence activation in Pseudomonas aeruginosa in response to the synthetic kappa opioid agonist U-50, 488 in nutrient poor media where growth conditions are limited and density dependent quorum sensing is not activated.

Publication Title

Pseudomonas aeruginosa overrides the virulence inducing effect of opioids when it senses an abundance of phosphate.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE29789
Genome wide transcriptional analysis of P. aeruginosa PAO1 response to pH at 25 mM phosphate background
  • organism-icon Pseudomonas aeruginosa pao1
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Pseudomonas aeruginosa Array (paeg1a)

Description

During extreme physiological stress, the intestinal tract can be transformed into a harsh environment characterized by regio- spatial alterations in oxygen, pH, and phosphate concentration. When the human intestine is exposed to extreme medical interventions, the normal flora becomes replaced by pathogenic species whose virulence can be triggered by various physico-chemical cues leading to lethal sepsis. We previously demonstrated that phosphate depletion develops in the mouse intestine following surgical injury and triggers intestinal P. aeruginosa to express a lethal phenotype that can be prevented by oral phosphate ([Pi]) supplementation.

Publication Title

Prevention of siderophore- mediated gut-derived sepsis due to P. aeruginosa can be achieved without iron provision by maintaining local phosphate abundance: role of pH.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE34729
Gene expression changes induced by overexpression of EVI1 in Lin- hematopoietic cells [Lin]
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

The transcription factor Evi1 is essential for the formation and maintenance of hematopoietic stem cells, and induces clonal dominance with malignant progression upon constitutive activation by chromosomal rearrangements or transgene integration events. To understand the immediate and adaptive response of primary murine hematopoietic cells to the transcriptional upregulation of Evi1, we developed an inducible lentiviral vector system with a robust expression switch. We found that Evi1 delays differentiation and promotes survival in myeloid culture conditions, orchestrating a battery of genes involved in stemness (Aldh1a1, Ly6a [Sca1], Abca1, Epcam, among others). Importantly, Evi1 suppresses Cyclins and Cyclin-dependent kinases (Cdk), while it upregulates Cdk inhibitors, inducing quiescence in various proliferation-inducing cytokine conditions and operating in a strictly dose-dependent manner. Hematopoietic cells with persisting Evi1-induction tend to adopt a relatively low expression level. We thus classify Evi1 as a dormancy-inducing oncogene, likely requiring epigenetic and genetic compensation for cell expansion and malignant progression.

Publication Title

Activation of Evi1 inhibits cell cycle progression and differentiation of hematopoietic progenitor cells.

Sample Metadata Fields

Specimen part

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accession-icon GSE39103
Gene expression changes induced by overexpression of EVI1 in Lin- hematopoietic cells [EVI1_ST]
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

The transcription factor Evi1 is essential for the formation and maintenance of hematopoietic stem cells, and induces clonal dominance with malignant progression upon constitutive activation by chromosomal rearrangements or transgene integration events. To understand the immediate and adaptive response of primary murine hematopoietic cells to the transcriptional upregulation of Evi1, we developed an inducible lentiviral vector system with a robust expression switch. We found that Evi1 delays differentiation and promotes survival in myeloid culture conditions, orchestrating a battery of genes involved in stemness (Aldh1a1, Ly6a [Sca1], Abca1, Epcam, among others). Importantly, Evi1 suppresses Cyclins and Cyclin-dependent kinases (Cdk), while it upregulates Cdk inhibitors, inducing quiescence in various proliferation-inducing cytokine conditions and operating in a strictly dose-dependent manner. Hematopoietic cells with persisting Evi1-induction tend to adopt a relatively low expression level. We thus classify Evi1 as a dormancy-inducing oncogene, likely requiring epigenetic and genetic compensation for cell expansion and malignant progression.

Publication Title

Activation of Evi1 inhibits cell cycle progression and differentiation of hematopoietic progenitor cells.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE30967
Genome wide transcriptional analysis of P. aeruginosa PAO1, response to phosphate limitation
  • organism-icon Pseudomonas aeruginosa pao1
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Pseudomonas aeruginosa Array (paeg1a)

Description

P. aeruginosa PAO1 grown as lawns on Nematode Growth Medium prepared without supplementation (NGM Pi<0.1 mM) has high killing ability against C. elegans, however, no mortality in worms has been observed during 48 hrs when feeding on PAO1 lawns grown on phosphate supplemented full NGM Pi 25 mM, pH 6.0 medium.

Publication Title

Red death in Caenorhabditis elegans caused by Pseudomonas aeruginosa PAO1.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE36279
Expression data from murine liver tissue upon depletion of regulatory T cells
  • organism-icon Mus musculus
  • sample-icon 11 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Regulatory T cells (Treg) play a pivotal role in modulating immune responses and were shown to decrease atherosclerosis in murine models. How this effect is brought about remains elusive.

Publication Title

Depletion of FOXP3+ regulatory T cells promotes hypercholesterolemia and atherosclerosis.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon SRP057134
Transcriptome analysis of thymic APC subsets, mTECs and thymic DCs in comparison to splenic DCs
  • organism-icon Mus musculus
  • sample-icon 9 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Thymic antigen-presenting cells (APCs), including thymic dendritic cells (t-DCs) and medullary thymic epithelial cells (mTECs) have been described to play a critical role in thymic Treg generation. Our findings could show that both these thymic APCs can induce a more pronounced demethylation of Foxp3 and other Treg-specific epigenetic signature genes in developing Tregs when compared to splenic DCs. In order to elucidate the unique properties of thymic APCs, gene expression profiling was performed in comparison to splenic DCs. Transcriptome analysis of thymic APCs revealed differential expression of costimulatory molecules that could be involved in stable Treg generation. Importantly, both mTEC- and t-DC- induced alloantigen-specific Tregs displayed significantly higher efficacy in prolonging skin allograft acceptance when compared to alloantigen-specific Tregs generated by splenic DCs. Overall design: Thymic APCs, including mTECs and t-DCs and splenic DCs were isolated ex vivo from thymus as CD45-EpCAM+Ly51- (mTECs) and CD45+EpCAM-CD11chiLin- (t-DCs) and from spleen as CD11chiLin- (splenic DCs) (Lin is defined as CD90, CD49b, F4/80 and CD19), respectively.

Publication Title

Unique properties of thymic antigen-presenting cells promote epigenetic imprinting of alloantigen-specific regulatory T cells.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE9452
Definition of an ulcerative colitis preinflammatory state
  • organism-icon Homo sapiens
  • sample-icon 26 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

The samples are a part of a study aiming at diagnosing ulcerative colitis from genome-wide gene expression analysis of the colonic mucosa. Colonic mucosal samples were collected as endoscopic pinch biopsies from ulcerative colitis patients and from control subjects. Samples with and without macroscopic signs of inflammation were collected from the patients.

Publication Title

Diagnosis of ulcerative colitis before onset of inflammation by multivariate modeling of genome-wide gene expression data.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE31595
Gene Expression Profiles in Stage II and III Colon Cancer. Application of a 128-gene signature
  • organism-icon Homo sapiens
  • sample-icon 34 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Purpose: A 128-gene signature has been proposed to predict poor outcomes in patients with stage II and III colorectal cancer. In the present study we aimed to validate this previously published 128-gene signature on external and independent data from patients with stage II and III colon cancer.

Publication Title

Gene expression profiles in stages II and III colon cancers: application of a 128-gene signature.

Sample Metadata Fields

Sex, Age, Disease stage, Race

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accession-icon GSE38681
Lyl-1 knockout vs wildtype Lymphoid Primed Multipotent Progenitors (LMPPs)
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

We compared gene expression differences in Lyl-1 knockout vs wildtype LMPPs

Publication Title

The transcription factor Lyl-1 regulates lymphoid specification and the maintenance of early T lineage progenitors.

Sample Metadata Fields

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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