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accession-icon GSE1923
Identification of PDGF-dependent patterns of gene expression in U87 glioblastoma cells
  • organism-icon Homo sapiens
  • sample-icon 15 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U95 Version 2 Array (hgu95av2)

Description

Overall study: Identification of PDGF-dependent patterns of gene expression in U87 glioblastoma cells.

Publication Title

Autocrine platelet-derived growth factor-dependent gene expression in glioblastoma cells is mediated largely by activation of the transcription factor sterol regulatory element binding protein and is associated with altered genotype and patient survival in human brain tumors.

Alternate Accession IDs

E-GEOD-1923

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE108649
Transcriptomic Predictors of Paradoxical Cryptococcosis-Associated Immune Reconstitution Inflammatory Syndrome
  • organism-icon Homo sapiens
  • sample-icon 162 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip

Description

Paradoxical cryptococcosis-associated immune reconstitution inflammatory syndrome

Publication Title

Transcriptomic Predictors of Paradoxical Cryptococcosis-Associated Immune Reconstitution Inflammatory Syndrome.

Alternate Accession IDs

E-GEOD-108649

Sample Metadata Fields

Specimen part

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accession-icon GSE52256
Deletion of the Saccharomyces cerevisiae ARO8 gene, encoding an aromatic amino acid transaminase, enhances phenylethanol production from glucose
  • organism-icon Saccharomyces cerevisiae
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Yeast Genome S98 Array (ygs98)

Description

Its characteristic rose-like aroma makes phenylethanol a popular ingredient in foods, beverages and cosmetics. Microbial production of phenylethanol currently relies on whole-cell bioconversion of phenylalanine with yeasts that harbor an Ehrlich pathway for phenylalanine catabolism. Complete biosynthesis of phenylethanol from a cheap carbon source such as glucose provides an economically attractive alternative for phenylalanine bioconversion. In this study, a Synthetic Genetic Array screening was applied to identify genes involved in regulation of phenylethanol synthesis in Saccharomyces cerevisiae. The screen focused on transcriptional regulation of ARO10, which encodes the major decarboxylase involved in conversion of phenylpyruvate to phenylethanol. A deletion in ARO8, which encodes an aromatic amino acid transaminase, was found to cause a transcriptional upregulation of ARO10 during growth with ammonium sulfate as the sole nitrogen source. Physiological characterization revealed that the aro8 mutation led to substantial changes in the absolute and relative intracellular concentrations of amino acids. Moreover, deletion of ARO8 led to de novo production of phenylethanol during growth on a glucose synthetic medium with ammonium as the sole nitrogen source. The aro8 mutation also stimulated phenylethanol production when combined with other, previously documented mutations that deregulate aromatic amino acid biosynthesis in S. cerevisiae. The resulting engineered S. cerevisiae strain produced over 3 mM of phenylethanol from glucose during growth on a simple synthetic medium. The strong impact of a transaminase deletion on intracellular amino acid concentrations opens new possibilities for yeast-based production of amino acid-derived products.

Publication Title

Deletion of the Saccharomyces cerevisiae ARO8 gene, encoding an aromatic amino acid transaminase, enhances phenylethanol production from glucose.

Alternate Accession IDs

E-GEOD-52256

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon SRP075535
Single cell gene expression profiling in normal HSCs and CML stem cells
  • organism-icon Homo sapiens
  • sample-icon 181 Downloadable Samples
  • Technology Badge Icon

Description

CML stem cells (CMLSCs) and normal hematopoietic stem cells (HSCs) display the same set of surface markers (CD34+CD38-CD90+CD45RA-), making it infeasible to separate these two populations within the same sample. To overcome this challenge, and to minimize variations in gene expression due to individual variation, here we perform single-cell RNA-seq to compare expression profiles of CMLSCs and HSCs isolated from the same patient. We captured ~600 HSCs (CD34+CD38-CD90+CD45RA-) (~200 from each of three CML patient samples), separated them into CMLSCs (BCR-ABL+) or normal HSCs (BCR-ABL-) based on the presence of the BCR-ABL transcript, and performed paired-end deep sequencing. Typically, we obtained ~2.5 million mapped reads (>70% average mapping efficiency) and detected ~5,000 genes (transcript per million [TPM]>1) per cell. Despite the heterogeneity of the gene expression pattern, we were able to identify genes that were significantly more highly expressed in CMLSCs than in normal HSCs. Notably, among these genes are two cell surface markers, CD33 and CD47, that could potentially be used to distinguish CMLSCs from normal HSCs. We also found genes, such as PIM2, that could be targeted for CML therapy using available small molecule inhibitors. Overall design: Hematopoietic stem cell population from three chronic phase CML patients with no detectable BCR-ABL mutation.

Publication Title

Prosurvival kinase PIM2 is a therapeutic target for eradication of chronic myeloid leukemia stem cells.

Alternate Accession IDs

GSE81730

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE119061
Reovirus infection induces stabilization and up-regulation of cellular transcripts that encode regulators of TGF-beta signaling
  • organism-icon Mus musculus
  • sample-icon 46 Downloadable Samples
  • Technology Badge Icon Affymetrix Murine Genome U74A Version 2 Array (mgu74av2)

Description

We utilized oligonucleotide microarrays to measure cellular mRNA decay rates in mock- or reovirus-infected murine L929 cells to determine if changes in host mRNA expression are a consequence of reovirus-induced alterations in cellular mRNA stability.

Publication Title

Reovirus infection induces stabilization and up-regulation of cellular transcripts that encode regulators of TGF-β signaling.

Alternate Accession IDs

E-GEOD-119061

Sample Metadata Fields

Cell line, Time

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accession-icon GSE2485
Gene expression of pseudopalisading cells in human glioblastoma
  • organism-icon Homo sapiens
  • sample-icon 17 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

By comparing to common tumor cells, genes were differencially expressed in pseudopalisading cells in human glioblastoma

Publication Title

Histology-based expression profiling yields novel prognostic markers in human glioblastoma.

Alternate Accession IDs

E-GEOD-2485

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE4717
5`aza-dC demethylation of three short term cultured glioblastomas
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

Glioblastoma, the most aggressive and least treatable form of malignant glioma, is the most common human brain tumor. Although many regions of allelic loss occur in glioblastomas, relatively few tumor suppressor genes have been found mutated at such loci. To address the possibility that epigenetic alterations are an alternative means of glioblastoma gene inactivation, we coupled pharmacological manipulation of methylation with gene profiling to identify potential methylation-regulated, tumor-related genes. Triplicates of three short-term cultured glioblastomas were exposed to 5M 5-aza-dC for 96 hours followed by cRNA hybridization to an oligonucleotide microarray (Affymetrix U133A). We based candidate gene selection on bioinformatics, RT-PCR, bisulfite sequencing, methylation-specific PCR and matrix-assisted laser desorption/ionization time-of-flight mass spectrometry. Two genes identified in this manner, RUNX3 and Testin (TES), were subsequently shown to harbor frequent tumor-specific epigenetic alterations in primary glioblastomas. This overall approach therefore provides a powerful means to identify candidate tumor suppressor genes for subsequent evaluation and may lead to the identification of genes whose epigenetic dysregulation is integral to glioblastoma tumorigenesis.

Publication Title

Downregulation of RUNX3 and TES by hypermethylation in glioblastoma.

Alternate Accession IDs

E-GEOD-4717

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon SRP115925
The hepatitis C viral protein NS5A stabilizes growth-regulatory human transcripts
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon

Description

Numerous mammalian proto-oncogene and other growth-regulatory transcripts are upregulated in malignancy due to abnormal mRNA stabilization. In hepatoma cells expressing a hepatitis C virus (HCV) subgenomic replicon, we found that the viral nonstructural protein 5A (NS5A), a protein known to bind to viral RNA, also bound specifically to human cellular transcripts that encode regulators of cell growth and apoptosis, and this binding correlated with transcript stabilization. An important subset of human NS5A-target transcripts contained GU-rich elements, sequences known to destabilize mRNA. We found that NS5A bound to GU-rich elements in vitro and in cells. Mutation of the NS5A zinc finger abrogated its GU-rich element-binding and mRNA stabilizing activities. Overall, we identified a molecular mechanism whereby HCV manipulates host gene expression by stabilizing host transcripts in a manner that would promote growth and prevent death of virus-infected cells, allowing the virus to establish chronic infection and lead to the development of hepatocellular carcinoma. Overall design: Calculate mRNA decay rate by examining RNA-seq expression levels of 2 samples (Huh and Huh-HCV) at 3 time points (0h, 3h, and 6h) after transcription arrest. RNA-IP followed by RNA-seq on 2 samples (Huh and Huh-HCV).

Publication Title

The hepatitis C viral nonstructural protein 5A stabilizes growth-regulatory human transcripts.

Alternate Accession IDs

GSE102910

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE25763
Comparative expression profiling identifies differential roles for Myogenin and p38 MAPK signaling in myogenesis
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Mitogen activated protein kinase (MAPK) signaling regulates differentiation of many cell types. During myogenesis in particular, p38a MAPK (MAPK14) phosphorylates multiple transcriptional regulators to modulate muscle-specific gene expression. Among the p38a MAPK modulated genes is the muscle-specific transcriptional regulator Myogenin (Myog) that is also essential to complete the muscle differentiation program, and while it is known that both p38a MAPK and Myog are critically required for myogenesis, the individual contribution of each of these proteins is poorly defined. Here we show that Myog expression (in the absence of p38a MAPK signaling) is sufficient to establish expression of many late markers of muscle differentiation and to mediate cell migration. However, Myog expression alone did not led to the formation of multinucleated muscle cells, highlighting a critical role for p38a MAPK in myoblast fusion. Using comparative microarray analysis we identified p38a MAPK-dependent genes that are not regulated by Myog

Publication Title

Comparative expression profiling identifies differential roles for Myogenin and p38α MAPK signaling in myogenesis.

Alternate Accession IDs

E-GEOD-25763

Sample Metadata Fields

Cell line

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accession-icon GSE46016
Epigenomic profiling of glioblastoma stem cells
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

An aberrant transcription factor network essential for Wnt signaling and stem cell maintenance in glioblastoma.

Alternate Accession IDs

E-GEOD-46016

Sample Metadata Fields

Specimen part, Cell line

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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