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accession-icon GSE91393
Glioblastoma cell malignancy and drug sensitivity are affected by the cell of origin
  • organism-icon Mus musculus, Homo sapiens
  • sample-icon 71 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Transcriptome Array 2.0 (hta20), Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Glioblastoma Cell Malignancy and Drug Sensitivity Are Affected by the Cell of Origin.

Sample Metadata Fields

Specimen part

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accession-icon GSE91392
Human expression data from Glioblastoma cell malignancy and drug sensitivity are affected by the cell of origin.
  • organism-icon Homo sapiens
  • sample-icon 59 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st), Affymetrix Human Transcriptome Array 2.0 (hta20)

Description

The cell of origin in glioblastoma is not formally proven but generally accepted to be a neural stem cell or glial precursor cell. In addition, there is also limited knowledge about the functional consequences of the cell of origin for glioblastoma development and response to therapy.

Publication Title

Glioblastoma Cell Malignancy and Drug Sensitivity Are Affected by the Cell of Origin.

Sample Metadata Fields

Specimen part

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accession-icon GSE91391
Mouse expression data from Glioblastoma cell malignancy and drug sensitivity are affected by the cell of origin.
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

The cell of origin in glioblastoma is not formally proven but generally accepted to be a neural stem cell or glial precursor cell. In addition, there is also limited knowledge about the functional consequences of the cell of origin for glioblastoma development and response to therapy.

Publication Title

Glioblastoma Cell Malignancy and Drug Sensitivity Are Affected by the Cell of Origin.

Sample Metadata Fields

Specimen part

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accession-icon SRP101719
Zoledronic acid inhibits NFAT and IL-2 signaling pathways in regulatory T cells and diminishes their suppressive function in patients with metastatic cancer
  • organism-icon Homo sapiens
  • sample-icon 60 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

In order to identify the processes altered in T regulatory cells (Treg) by Zoledronic acid (ZA), we examined RNA expression by RNA-seq in Treg treated with and without ZA. We identified gene expression alterations in ZA-treated Treg that were essential to Treg function. Overall design: Human T regulatory cells isolated from healthy donors (n=6) were cultured overnight with IL-2 and OKT3 (anti-CD3) in the presence or absence of ZA. RNA sequencing (Illumina HiSeq2500) was performed to identify differential gene expression induced by ZA treatment of Treg.

Publication Title

Zoledronic acid inhibits NFAT and IL-2 signaling pathways in regulatory T cells and diminishes their suppressive function in patients with metastatic cancer.

Sample Metadata Fields

Specimen part, Disease, Treatment, Subject

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accession-icon GSE75824
Expression data from pam48 (mterf6-1) mutants
  • organism-icon Arabidopsis thaliana
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)

Description

Of the members of mitochondrial transcription termination factors (mTERFs) found in metazoans and plants known to regulate organellar gene expression at various levels, plant mTERF6 promotes maturation of a tRNA

Publication Title

Definition of a core module for the nuclear retrograde response to altered organellar gene expression identifies GLK overexpressors as gun mutants.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP173260
Functional relationship of GUN1 and FUG1 in plastid proteostasis
  • organism-icon Arabidopsis thaliana
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

GUN1 integrates retrograde signals in the chloroplast but the underlying mechanism is elusive. FUG1, a chloroplast translation initiation factor, and GUN1 are co-expressed at the transcript level, and FUG1 co-immunoprecipitates with GUN1. We used mutants of GUN1 (gun1-103) and FUG1 (fug1-3) to analyse their functional relationship at the physiological and systems-wide level, the latter including transcriptome and proteome analyses. Absence of GUN1 aggravates the effects of decreased FUG1 levels on chloroplast protein translation, resulting in transient additive phenotypes with respect to photosynthesis, leaf coloration, growth and cold acclimation. Variegation of the var2 mutant is enhanced by gun1-103 in terms of increasing the fraction of white sectors, in contrast to fug1-3 that acts as suppressor. The transcriptomes of fug1-3 and gun1-103 are very similar, but absence of GUN1 alone has almost no effects on protein levels, whereas chloroplast protein accumulation is markedly decreased in fug1-3. In gun1 fug1 double mutants, effects on transcriptomes and particularly proteomes are enhanced. Our results show that GUN1 function becomes critical when chloroplast proteostasis is perturbed by decreased translation (fug1) or degradation (var2) of chloroplast proteins. The functions of FUG1 and GUN1 appear to be related, corroborating the view that GUN1 operates in chloroplast proteostasis. Overall design: Examination of differential gene expression in the Arabdidopsis thaliana gun1, fug1 and gun1 fug1 mutants compared to wild type in three replicates

Publication Title

Relationship of GUN1 to FUG1 in chloroplast protein homeostasis.

Sample Metadata Fields

Subject

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accession-icon GSE54573
Identification of target genes of translation-dependent signalling in Arabidopsis
  • organism-icon Arabidopsis thaliana
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)

Description

Changes ins organellar gene expression trigger retrograde signalling. Prolyl-tRNA synthetase (PRORS1) is located in chloroplasts and mitochondria. Thus, prors1-2 mutants are impaired in chloroplast and mitochondrial gene expression.

Publication Title

Identification of target genes and transcription factors implicated in translation-dependent retrograde signaling in Arabidopsis.

Sample Metadata Fields

Age, Specimen part

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accession-icon GSE94521
Identification of transcriptome signatures and biomarkers specific for potential developmental toxicants inhibiting human neural crest cell migration
  • organism-icon Homo sapiens
  • sample-icon 57 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

The in vitro test battery of the European research consortium ESNATS (novel stem cell-based test systems) has been used to screen for potential human developmental toxicants. As part of this effort, the migration of neural crest (MINC) assay has been used to evaluate chemical effects on neural crest function. It identified some drug-like compounds in addition to known environmental toxicants. The hits included the HSP90 inhibitor geldanamycin, the chemotherapeutic arsenic trioxide, the flame-retardant PBDE-99, the pesticide triadimefon and the histone deacetylase inhibitors valproic acid and trichostatin A. Transcriptome changes triggered by these substances in human neural crest cells were recorded and analysed here to answer three questions: (1) can toxicants be individually identified based on their transcript profile; (2) how can the toxicity pattern reflected by transcript changes be compacted/ dimensionality-reduced for practical regulatory use; (3) how can a reduced set of biomarkers be selected for large-scale follow up? Transcript profiling allowed clear separation of different toxicants and the identification of toxicant types in a blinded test study. We also developed a diagrammatic system to visualize and compare toxicity patterns of a group of chemicals by giving a quantitative overview of altered superordinate biological processes (e.g. activation of KEGG pathways or overrepresentation of gene ontology terms). The transcript data were mined for potential markers of toxicity, and 39 transcripts were selected to either indicate general developmental toxicity or distinguish compounds with different modes-of-action in read-across. In summary, we found inclusion of transcriptome data to largely increase the information from the MINC phenotypic test.

Publication Title

Identification of transcriptome signatures and biomarkers specific for potential developmental toxicants inhibiting human neural crest cell migration.

Sample Metadata Fields

Sex, Specimen part

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accession-icon E-MTAB-375
Transcription profiling by array of Arabidopsis after exposure to different temperatures and light levels
  • organism-icon Arabidopsis thaliana
  • sample-icon 175 Downloadable Samples
  • Technology Badge Icon Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)

Description

High-density kinetic analysis of the metabolomic and transcriptomic response of Arabidopsis to temperature and light

Publication Title

High-density kinetic analysis of the metabolomic and transcriptomic response of Arabidopsis to eight environmental conditions.

Sample Metadata Fields

Specimen part, Time

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accession-icon E-MTAB-1344
Transcription profiling by array of Arabidopsis thaliana Col-0 and RAP2.4a mutants under time dependent light stress by transfer to high light
  • organism-icon Arabidopsis thaliana
  • sample-icon 24 Downloadable Samples
  • Technology Badge Icon Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)

Description

Comparison of expression of Arabidopsis thaliana Col-0 and T-DNA insertion line of RAP2.4a under time dependent light stress by transfer to high light

Publication Title

Meta-analysis of retrograde signaling in Arabidopsis thaliana reveals a core module of genes embedded in complex cellular signaling networks.

Sample Metadata Fields

Specimen part

View Samples
...

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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