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accession-icon SRP149347
Kidney compartment specific eQTL studies highlight causal genes and pathways for renal disease development
  • organism-icon Homo sapiens
  • sample-icon 20 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Expression quantitative trait loci (eQTL) analyses were conducted separately on the glomerular and tubular portions of healthy human kidney samples obtained from subjects of European descent. Overall design: We aimed to define genotype driven gene expression changes in the glomerular and tubular compartments of human kidneys, identifying genetic variants (eVariants) that influence the expression of genes (eGenes). Later, we integrated this information with genotype and phenotype association studies (GWAS) to identify genes for which expression in the kidney shows differences in patients with GWAS variants.

Publication Title

Mapping eGFR loci to the renal transcriptome and phenome in the VA Million Veteran Program.

Sample Metadata Fields

Specimen part, Disease, Disease stage, Subject

View Samples
accession-icon SRP124942
Identification of immune-activated Hematopoietic Stem Cells
  • organism-icon Mus musculus
  • sample-icon 24 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

We utilized our transgenic Fgd5-mCherry mouse to sort and RNAseq for HSCs under acute immune activation (with pIC) to reveal a complex cell cycle gene expression and an upregulated IFN I/II signature Overall design: RNAseq of bone marrow Lineage-Sca1+cKit+CD150+mCherry+ cells (1000) 24hrs after pIC was administered and control (PBS treated)

Publication Title

Identification of immune-activated hematopoietic stem cells.

Sample Metadata Fields

Specimen part, Cell line, Treatment, Subject

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accession-icon GSE27718
MiR-30b/30d regulation of GalNAc transferases enhances invasion and immunosuppression during metastasis
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

To metastasize, a tumor cell must acquire abilities such as the capacity to colonize new tissue and evade immune surveillance. Recent evidence suggests that microRNAs can promote the evolution of malignant behaviors by regulating multiple targets simultaneously. We performed a microRNA analysis of human melanoma, an aggressively invasive cancer, and found that miR-30b/30d upregulation correlates with stage, metastatic potential of primary tumors, shorter time to recurrence and reduced overall survival. Ectopic expression of miR-30b/30d promoted the metastatic behavior of melanoma cells by directly targeting the GalNAc transferase GALNT7, resulted in increased synthesis of the immunosuppressive cytokine IL-10, and reduced immune cell activation and recruitment. These data point to a key role of miR-30b/30d and GalNAc transferases in metastasis, by simultaneously promoting cellular invasion and immune suppression.

Publication Title

miR-30b/30d regulation of GalNAc transferases enhances invasion and immunosuppression during metastasis.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon GSE40278
A multiply redundant genetic switch locks in the transcriptional signature of T regulatory cells
  • organism-icon Mus musculus
  • sample-icon 60 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

A multiply redundant genetic switch 'locks in' the transcriptional signature of regulatory T cells.

Sample Metadata Fields

Sex, Age, Specimen part

View Samples
accession-icon GSE40274
Gene profiling data of CD4+ T cells transduced with FOXP3 and candidate cofactors
  • organism-icon Mus musculus
  • sample-icon 33 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

The transcription factor FoxP3 partakes dominantly in the specification and function of FoxP3+ CD4+ T regulatory cells (Tregs), but is neither strictly necessary nor sufficient to determine the characteristic Treg transcriptional signature. Computational network inference and experimental testing assessed the contribution of several other transcription factors (TFs). Enforced expression of Helios or Xbp1 elicited specific signatures, but Eos, Irf4, Satb1, Lef1 and Gata1 elicited exactly the same outcome, synergizing with FoxP3 to activate most of the Treg signature, including key TFs, and enhancing FoxP3 occupancy at its genomic targets. Conversely, the Treg signature was robust to inactivation of any single cofactor. A redundant genetic switch thus locks-in the Treg phenotype, a model which accounts for several aspects of Treg physiology, differentiation and stability.

Publication Title

A multiply redundant genetic switch 'locks in' the transcriptional signature of regulatory T cells.

Sample Metadata Fields

Sex, Age, Specimen part

View Samples
accession-icon GSE40273
Gene expression profiling in Treg cells deficient or mutant in candidate FoxP3 cofactors
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

The transcription factor FoxP3 partakes dominantly in the specification and function of FoxP3+ CD4+ T regulatory cells (Tregs), but is neither strictly necessary nor sufficient to determine the characteristic Treg transcriptional signature. Computational network inference and experimental testing assessed the contribution of several other transcription factors (TFs). Enforced expression of Helios or Xbp1 elicited specific signatures, but Eos, Irf4, Satb1, Lef1 and Gata1 elicited exactly the same outcome, synergizing with FoxP3 to activate most of the Treg signature, including key TFs, and enhancing FoxP3 occupancy at its genomic targets. Conversely, the Treg signature was robust to inactivation of any single cofactor. A redundant genetic switch thus locks-in the Treg phenotype, a model which accounts for several aspects of Treg physiology, differentiation and stability.

Publication Title

A multiply redundant genetic switch 'locks in' the transcriptional signature of regulatory T cells.

Sample Metadata Fields

Sex, Age, Specimen part

View Samples
accession-icon GSE40277
Gene profiling data of CD4+ T cells doubly transduced with EOS+LEF1 or GATA1+SATB1
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

The transcription factor FoxP3 partakes dominantly in the specification and function of FoxP3+ CD4+ T regulatory cells (Tregs), but is neither strictly necessary nor sufficient to determine the characteristic Treg transcriptional signature. Computational network inference and experimental testing assessed the contribution of several other transcription factors (TFs). Enforced expression of Helios or Xbp1 elicited specific signatures, but Eos, Irf4, Satb1, Lef1 and Gata1 elicited exactly the same outcome, synergizing with FoxP3 to activate most of the Treg signature, including key TFs, and enhancing FoxP3 occupancy at its genomic targets. Conversely, the Treg signature was robust to inactivation of any single cofactor. A redundant genetic switch thus locks-in the Treg phenotype, a model which accounts for several aspects of Treg physiology, differentiation and stability.

Publication Title

A multiply redundant genetic switch 'locks in' the transcriptional signature of regulatory T cells.

Sample Metadata Fields

Sex, Age, Specimen part

View Samples
accession-icon GSE40276
Gene profiling data of CD4+ T cells transduced with FOXP3 and GATA1, then sorted into different fractions, based on the expression of Thy1.1 (FOXP3)
  • organism-icon Mus musculus
  • sample-icon 7 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

The transcription factor FoxP3 partakes dominantly in the specification and function of FoxP3+ CD4+ T regulatory cells (Tregs), but is neither strictly necessary nor sufficient to determine the characteristic Treg transcriptional signature. Computational network inference and experimental testing assessed the contribution of several other transcription factors (TFs). Enforced expression of Helios or Xbp1 elicited specific signatures, but Eos, Irf4, Satb1, Lef1 and Gata1 elicited exactly the same outcome, synergizing with FoxP3 to activate most of the Treg signature, including key TFs, and enhancing FoxP3 occupancy at its genomic targets. Conversely, the Treg signature was robust to inactivation of any single cofactor. A redundant genetic switch thus locks-in the Treg phenotype, a model which accounts for several aspects of Treg physiology, differentiation and stability.

Publication Title

A multiply redundant genetic switch 'locks in' the transcriptional signature of regulatory T cells.

Sample Metadata Fields

Sex, Age, Specimen part

View Samples
accession-icon GSE22010
TMPRSS2:ERG promotes invasiveness and epithelial to mesenchymal transition in prostate cancer model
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Recently, a frequent chromosomal aberration fusing Androgen regulated TMPRSS2 promoter and the ERG gene (T/ERG) was discovered in prostate cancer. Several studies demonstrated cooperation between the T/ERG and other defective pathways in cancer progression however, the biological mechanism by which the T/ERG operates is yet to be determined. Using immortalized prostate epithelial cells (EP) model we were able to show that EP with the combination of androgen receptor(AR) and T/ERG(EP-AR T/ERG cell line) demonstrate an Epithelial to Mesenchymal Transition (EMT) manifested by a mesenchyme-like morphological appearance and behavior.

Publication Title

TMPRSS2/ERG promotes epithelial to mesenchymal transition through the ZEB1/ZEB2 axis in a prostate cancer model.

Sample Metadata Fields

Specimen part, Cell line

View Samples
accession-icon GSE30852
Expression data from Bmi1 mutant versus wild-type lung cells
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Bmi1 is an important stem cell regulator in multiple tissues, including the lung.

Publication Title

Lung stem cell self-renewal relies on BMI1-dependent control of expression at imprinted loci.

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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