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accession-icon GSE53716
IFNb-1a in-vivo treatment induces the expression and signaling of IFNAR1 and inhibits Th17 responses in PBMCs derived from CIS patients
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

IFNb has been used as a first line therapy for relapsing remitting multiple sclerosis (RRMS). Since only a few studies have addressed the role of endogenous IFNb in the pathogenesis of the disease, our objective was to characterize its role in the transcriptional regulation of pathogenic Th17 cytokines in patients with RRMS. In-vitro studies have demonstrated that IFNb inhibited IL-17A, IL-17F, IL-21, IL-22 and IFN-b secretion in CD4+ lymphocytes through the induction of suppressor of cytokine secretion (SOCS)1 and 3. We found that patients with RRMS have increased serum and cerebrospinal fluid (CSF) Th17 (IL-17A and IL-17F) cytokine levels in comparison to the control subjects, suggesting that deficient endogenous IFNbeta secretion and/or signaling may contribute to the dysregulation of those pathogenic cytokines in CD4+ cells. We identified that the endogenous IFNb from serum of RRMS patients induced a significantly lower IFN-inducible gene expression in comparison to healthy controls (HCs). In addition, in-vitro studies have revealed a deficient endogenous and exogenous IFNb signaling in CD4+ cells derived from MS patients. Interestingly, upon inhibition of the endogenous IFNb signaling by silencing interferon regulatory factor (IRF)7 gene expression, the resting CD4+ T cells secreted significantly higher level of IL-17A, IL-17F, IL-21, IL-22 and IL-9, suggesting that endogenous IFNb suppresses the secretion of these pathogenic cytokines. In-vivo recombinant IFNb-1a treatment induced IFNAR1 and its downstream signaling molecules gene expression, suggesting that treatment may reconstitute a deficient endogenous IFNbeta regulation of the CD4+ T-cells pathogenic cytokine production in MS patients.

Publication Title

The role of endogenous IFN-β in the regulation of Th17 responses in patients with relapsing-remitting multiple sclerosis.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon GSE58268
MicroRNA-15/16 Antagonizes c-Myb to Control Natural Killer Cell Maturation (c-Myb overexpression)
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

NK cells develop in the bone marrow and complete their maturation in peripheral organs, but the molecular events controlling maturation are incompletely understood. Utilizing an NK cell-specific miR-15/16 deficient genetic model (15aKO), we identified a critical role for miR-15/16 family microRNAs in the normal maturation of NK cells in vivo, with a specific reduction in mature CD11b+CD27- NK cells in multiple tissues. The mechanism responsible was a block in differentiation, since accelerated NK cell death was not evident, and earlier intermediates of NK cell maturation were expanded. Further, we identified Myb as a direct target of miR-15/16 in NK cells, with Myb expression increased in immature 15aKO NK cells. Following adoptive transfer, immature 15aKO NK cells exhibited defective maturation, which was rescued by ectopic miR-15/16 expression or Myb knockdown. Moreover, Myb overexpression resulted in defective NK cell maturation. Thus, miR-15/16 regulation of Myb controls the normal NK cell maturation program.

Publication Title

MicroRNA-15/16 Antagonizes Myb To Control NK Cell Maturation.

Sample Metadata Fields

Cell line

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accession-icon GSE55033
MicroRNA-15/16 Antagonizes c-Myb to Control Natural Killer Cell Maturation
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

NK cells develop in the bone marrow and complete their maturation in peripheral organs, but the molecular events controlling maturation are incompletely understood. Utilizing an NK cell-specific miR-15/16 deficient genetic model (15aKO), we identified a critical role for miR-15/16 family microRNAs in the normal maturation of NK cells in vivo, with a specific reduction in mature CD11b+CD27- NK cells in multiple tissues. The mechanism responsible was a block in differentiation, since accelerated NK cell death was not evident, and earlier intermediates of NK cell maturation were expanded. Further, we identified Myb as a direct target of miR-15/16 in NK cells, with Myb expression increased in immature 15aKO NK cells. Following adoptive transfer, immature 15aKO NK cells exhibited defective maturation, which was rescued by ectopic miR-15/16 expression or Myb knockdown. Moreover, Myb overexpression resulted in defective NK cell maturation. Thus, miR-15/16 regulation of Myb controls the normal NK cell maturation program.

Publication Title

MicroRNA-15/16 Antagonizes Myb To Control NK Cell Maturation.

Sample Metadata Fields

Specimen part

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accession-icon SRP066729
Muscle transcriptome analysis following Total Knee Arthroplasty with Tourniquet
  • organism-icon Homo sapiens
  • sample-icon 20 Downloadable Samples
  • Technology Badge IconNextSeq500

Description

Transcriptome profiling was performed on muscle biopsies from patients immediately before Total Knee Arthroplasty and two hours after TKA and tourniquet application. Overall design: RNA was isolated from 10 patients who were give vastus lateralis muscle biopsies immediately before surgery and 2 hours post surgery with tourniquet

Publication Title

Transcriptional profiling and muscle cross-section analysis reveal signs of ischemia reperfusion injury following total knee arthroplasty with tourniquet.

Sample Metadata Fields

No sample metadata fields

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accession-icon E-MEXP-1407
Transcription profiling by array of S. cerevisiae wild type, SNF1, SNF4, and double knock outs to investigate SNF1/4 dependent gene expression
  • organism-icon Saccharomyces cerevisiae
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Yeast Genome 2.0 Array (yeast2)

Description

The protrotophic laboratory strain CEN.PK113-7D (MAT a) and three knock-out strains snf1, snf4 and snf1snf4 were grown in laboratory fermentors with a working volume of 1 litre at dilution rate (D) of 0.10 per hour (in triplicate for each strain). At steady state, samples from each of the 12 continuous cultures were taken and cooled below 2 degree C within ten seconds by mixing 40% sample and 60% crushed ice.

Publication Title

Reconstruction of the yeast Snf1 kinase regulatory network reveals its role as a global energy regulator.

Sample Metadata Fields

Sex

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accession-icon E-MTAB-78
Transcription profiling of yeast grown in a three-factor design to study the relationship between specific growth rate and genome-wide gene expression
  • organism-icon Saccharomyces cerevisiae
  • sample-icon 36 Downloadable Samples
  • Technology Badge Icon Affymetrix Yeast Genome S98 Array (ygs98)

Description

A three-factor design was applied to study the relationship between specific growth rate and genome-wide gene expression in 36 steady-state chemostat cultures of Saccharomyces cerevisiae.

Publication Title

Transcription factor control of growth rate dependent genes in Saccharomyces cerevisiae: a three factor design.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE4709
Gcn4p-mediated transcriptional stress response
  • organism-icon Saccharomyces cerevisiae
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Yeast Genome 2.0 Array (yeast2)

Description

The transcriptional data from an integrative analysis of transcriptional and metabolic stress responses that provides a more complete understanding of the mechanisms by which genetic regulatory circuits mediate metabolic phenotype.

Publication Title

Linking high-resolution metabolic flux phenotypes and transcriptional regulation in yeast modulated by the global regulator Gcn4p.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP066118
Generation of Patient-Matched Malignant and Normal Primary Cell Cultures from Clear Cell Renal Cell Carcinoma Patients
  • organism-icon Homo sapiens
  • sample-icon 54 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2500

Description

Transcriptome profiling of de novo-derived ccRCC cell cultures and their matching parental tumours. VHL-mutant and VHL wild-type cultures were established by isolating CA9+ and CA9- cells from tumor samples using FACS. Overall design: RNASeq expression profiling of 18 renal cell carcinoma samples, including 6 patient tumours, 6 VHL mutant and 6 VHL WT derivative cell cultures

Publication Title

Efficient generation of patient-matched malignant and normal primary cell cultures from clear cell renal cell carcinoma patients: clinically relevant models for research and personalized medicine.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE62203
Effect of glucose, endothelin-1 and cortisol on human iPS-derived cardiomyocytes
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Analysis of human iPS-derived cardiomyocytes exposed to glucose, endothelin-1 and cortisol in vitro. Treatment produces a surrogate diabetic cardiomyopathic phenotype. Results provide insight into the pathways regulated by the treatment in the cardiomyocyte.

Publication Title

Disease modeling and phenotypic drug screening for diabetic cardiomyopathy using human induced pluripotent stem cells.

Sample Metadata Fields

Specimen part, 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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