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accession-icon GSE7332
Comparison of human embryonic stem cell (hESC) derived mesenchymal precursor cell populations
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

We have developed efficient protocols for the derivation of mesenchymal precursors from hESCs. While previous protocols were based on mesodermal induction via co-culture of hESCs on OP9 mouse stroma (Barberi et al., PLoS Biology, 2005), our recent work shows the derivation of hESC derived mesenchymal precurors under feeder-free conditions. The data presented here show a large and highly signficant overlap in global gene expression profiles between hESC derived mesenchymal precursors derived under feeder-free conditions with those derived via OP9 co-culure and mesenchymal precurosrs isolated directly from the adult bone marrow.

Publication Title

Derivation of engraftable skeletal myoblasts from human embryonic stem cells.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE9118
A screen to identify novel tumor suppressor genes silenced by methylation in melanoma
  • organism-icon Homo sapiens
  • sample-icon 14 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

Malignant melanoma is a common and frequently lethal disease. Current therapeutic interventions have little effect on survival, emphasizing the need for a better understanding of the genetic, epigenetic, and phenotypic changes in melanoma formation and progression. We identified genes that were not previously known to be silenced by methylation in melanoma using a microarray-based screen following treatment of melanoma cell lines with the DNA methylation inhibitor 5-Aza-2'-deoxycytidine.

Publication Title

Epigenetic silencing of novel tumor suppressors in malignant melanoma.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE10343
Murine Acute Lung Injury
  • organism-icon Mus musculus
  • sample-icon 18 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

With advances in supportive therapy in the last two decades, mortality rates from ALI/ARDS have improved somewhat, but remain around 30 to 40% with significant morbidity in survivors. Several promising treatments are in various stages of evaluation, but many have failed to prove beneficial in large randomized clinical trials (RCT). The first definitive step forward in ALI therapeutics occurred recently as a result of a large RCT demonstrating a mortality decrease from 40 to 31% with the use of low-volume ventilation strategies. From this, it is clear that the opportunity for successful intervention in ALI exists. However, therapeutic advances remain frustrated by the lack of complete understanding of ALI pathophysiology. This stresses the importance of integrating basic and clinical research of the molecular pathogenesis of this disease. The conclusions of a recent National Heart, Lung, and Blood Institute (NHLBI) Working Group on ALI support this type of research as a priority for future investigations of ALI. One of the areas of research given priority by this ALI Working Group is the issue of ALI severity progression and the role of cells of innate immunity in this process. Currently, the processes that determine which ALI patients progress to ARDS and which do not are unclear. As with many phenotype differences, there is most likely a genetic component involved. The basis for this has been demonstrated. For example, a surfactant protein B (SP-B) polymorphism appears to increase a patients risk of developing ALI from pneumonia. Additionally, a polymorphism in the promoter region of the gene for interleukin-6 (IL-6) has been associated with a poor prognosis in patients with ARDS. Understanding the intracellular processes of these genes and the cells expressing them in ALI progression could lead to the identification of molecular markers of ALI severity and eventually to the development of targeted therapies. An examination of genetically uniform animals will provide a clearer insight into the interaction between immune cells in ALI progression as well as guide future human experiments.

Publication Title

Sepsis alters the megakaryocyte-platelet transcriptional axis resulting in granzyme B-mediated lymphotoxicity.

Sample Metadata Fields

Specimen part

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accession-icon GSE48258
Changes in gene expression induced by CDK9 inhibition alone and in combination with fludarabine
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Using a transcriptomics approach we explored the mechanism(s) of synergy observed between CDKI-73 and fludarabine in primary CLL cells. The cytotoxic effects of CDKI-73 were associated with transcriptional inhibition of cdk9 target genes including MCL1 and XIAP. In contrast, fludarabine induced the transcription of these genes, an effect that was reversed by the combination of CDKI-73 and fludarabine.

Publication Title

A novel Cdk9 inhibitor preferentially targets tumor cells and synergizes with fludarabine.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon SRP047126
Transcriptomic profiling of bone marrow cells from healthy individuals
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconIlluminaGenomeAnalyzerIIx

Description

We performed whole-genome transcriptomic profiling of RNA from mononuclear cells from bone marrow aspirates taken from healthy individuals. This study complements GSE58335: transcriptomic profiling of peripheral blood mononuclear cells from healthy individuals. Overall design: High-throughput sequencing was done using the Illumina GA IIx. The RNA is from previously published samples (Stirewalt et al., Genes Chromosomes Cancer, 2008, PMID:17910043)

Publication Title

Widespread intron retention diversifies most cancer transcriptomes.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE135182
Microarray data for Bhlhe40WT and Bhlhe40KO small intestine lamina propria CD4+ T cells
  • organism-icon Mus musculus
  • sample-icon 10 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

The cytokines GM-CSF and IL-5 are thought to possess largely divergent functions despite a shared dependence on the common beta (βC) chain to initiate signaling. Although IL-5 is part of the core type 2 cytokine signature and is required for protection against some helminths, it is dispensable for immunity to others, such as Heligmosomoides polygyrus bakeri (H. polygyrus). Whether this is due to compensatory mechanisms is unclear. The transcription factor Bhlhe40 has been shown to control GM-CSF production and is proposed to be a novel regulator of T helper type 2 cells.

Publication Title

BHLHE40 Promotes T<sub>H</sub>2 Cell-Mediated Antihelminth Immunity and Reveals Cooperative CSF2RB Family Cytokines.

Sample Metadata Fields

Sex, Specimen part, Treatment

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accession-icon GSE49166
Expression data from mouse differentiated T helper cell lineages
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Microarray data on TH cell subsets from WT C57BL/6 and Bhlhe40 KO mice

Publication Title

Bhlhe40 controls cytokine production by T cells and is essential for pathogenicity in autoimmune neuroinflammation.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon SRP050137
RNA-seq analysis of the eight Drosophila SR protein family members
  • organism-icon Drosophila melanogaster
  • sample-icon 24 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Using RNA-seq, we characterize the global AS regulation of the eight Drosophila SR protein family members Overall design: RNA-seq experiments on two replicate samples from 8 individual SR protein knockdown (exptGroup=S), two replicates of simultaneous SR protein knockdown (XL6:B52 & SC35:B52) (exptGroup=D). Each exptGroup includes duplicate of its own non-specific (NS) controls.

Publication Title

SR proteins control a complex network of RNA-processing events.

Sample Metadata Fields

Specimen part, Subject

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accession-icon SRP090916
UPF1 knockdown in differentiating human myoblasts
  • organism-icon Homo sapiens
  • sample-icon 2 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Human myoblast cell line 54-1 is transfected with either a srambled control siRNA or siRNA against UPF1. Two days after transfection, cell were induced to differentiate by changing grow meida to differentiation media. 2 days after induction of differentiation, cells are collected for extraction of RNA. Overall design: Human myoblast cell line 54-1 is transfected with either a srambled control siRNA or siRNA against UPF1. Two days after transfection, cell were induced to differentiate by changing grow meida to differentiation media. 2 days after induction of differentiation, cells are collected for extraction of RNA.

Publication Title

The RNA Surveillance Factor UPF1 Represses Myogenesis via Its E3 Ubiquitin Ligase Activity.

Sample Metadata Fields

Specimen part, Cell line, Treatment, Subject, Time

View Samples
accession-icon GSE26631
Effect of biotin deficiency on gene expression in Aravbidopsis leaves
  • organism-icon Arabidopsis thaliana
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)

Description

In addition to its essential metabolic functions biotin is suggested a critical role in regulating gene expression. The first committed enzyme in biotin biosynthesis in Arabidopsis, 7-keto-8-aminopelargonic acid synthase is encoded by At5g04620 (BIO4). We isolated a novel T-DNA insertion mutant of BIO4 (bio4-1) showing a spontaneous cell death phenotype that could be rescued both by exogenous biotin and genetic complementation. The bio4-1 plants exhibited massive accumulation of hydrogen peroxide.

Publication Title

Biotin deficiency causes spontaneous cell death and activation of defense signaling.

Sample Metadata Fields

Age, 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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