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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 GSE94504
RNA expression data from mouse endothelial cells isolated from tumors that were exposed to interferon gamma (IFN) in vivo
  • organism-icon Mus musculus
  • sample-icon 26 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 2.0 ST Array (mogene20st)

Description

While it is clear that T cell derived IFN has to act on tumor stroma cells for rejection of solid tumors, it is not clear which tumor stroma cells are targets. We studied how IFN affects gene expression in tumor blood vessels in vivo. To study the effect on endothelial cells, we either used a model of ectopic IFN (MCA313 tumors) or IFN-GFP fusion protein (J558L tumors) expression in tumors, or we used T cell derived IFN in large vascularized 16.113 tumours. Tumors were grown in mice that were expressing the IFN receptor ubiquitously (J558L tumors + IFN-GFP treatment and 16.113 tumors + T cell treatment) or in some experiments the IFN-receptor was expressed exclusively in endothelial cells (MCA313 tumor + IFN treatment).

Publication Title

Tumour ischaemia by interferon-γ resembles physiological blood vessel regression.

Sample Metadata Fields

Sex, Specimen part, Time

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accession-icon SRP109826
Transcriptional impact of MTHFD2 in Human Aortic Endothelial Cells
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 4000

Description

We performed transcriptome analysis of Human Aortic Endothelial Cells after siRNA mediated knockdown of MTHFD2. We identified MTHFD2 as a key driver for a gene cluster which integrates mitochondrial one-carbon metabolism, serine synthesizing enzymes as well as common amino acid and ER stress response genes. Overall design: Human Aortic Endothelial Cells were treated with three different siRNAs against MTHFD2 or scramble for 72 h

Publication Title

Oxidized phospholipids regulate amino acid metabolism through MTHFD2 to facilitate nucleotide release in endothelial cells.

Sample Metadata Fields

Treatment, Subject

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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 GSE145697
The role of lncRNA Sarrah in human cardiomyocytes
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Exon 1.0 ST Array [transcript (gene) version (huex10st)

Description

Long non-coding RNAs (lncRNAs) contribute to (patho)physiological processes in the heart. Aging is the major risk factor for cardiovascular disease and cardiomyocyte apoptosis is an underlying cause for age-related cardiac dysfunction. RNA sequencing of cardiomyocytes from young and aged mouse hearts revealed several aging-regulated lncRNAs. An siRNA screen for caspase activity identified the aging-regulated lncRNA Sarrah (ENSMUST00000140003) as anti-apoptotic, which we confirmed in human cells (human SARRAH is annotated as OXCT1-AS1). Importantly, human engineered heart tissue showed impaired contractile force development upon SARRAH knockdown compared with controls. Computational prediction of RNA-DNA triple helix formation showed that SARRAH may directly bind the promoters of genes downregulated after SARRAH silencing, which mainly consist of cell survival genes. Indeed, nuclear magnetic resonance spectroscopy confirmed RNA-DNA triple helix formation and cardiomyocytes lacking the triple helix-forming domain of Sarrah showed an increase in apoptosis. One of the key direct SARRAH targets is NRF2, an anti-oxidant transcription factor. Restoration of NRF2 levels after SARRAH silencing partially rescues the reduction in cell viability. RNA affinity purification mass spectrometry analysis identified CRIP2 as main protein interaction partner. Furthermore, SARRAH associates with acetyltransferase p300 and acetylated histone H3K27. Finally, Sarrah was also profoundly downregulated after acute myocardial infarction (AMI) in mice. Adeno-associated virus-mediated overexpression of Sarrah in mice showed better recovery of cardiac contractile function after AMI compared to control mice, as measured by echocardiography and magnetic resonance imaging, consistent with a decrease in cardiomyocyte cell death and an increase in endothelial cell proliferation. In summary, we identified the anti-apoptotic evolutionary conserved lncRNA Sarrah, which is downregulated by aging, as a pivotal regulator of cardiomyocyte survival. Sarrah overexpression has beneficial effects on AMI recovery highlighting it as a potential therapeutic approach against heart failure.

Publication Title

Aging-regulated anti-apoptotic long non-coding RNA Sarrah augments recovery from acute myocardial infarction.

Sample Metadata Fields

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

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accession-icon GSE65168
Cellular and molecular characterization of the altered metabolism in RCC
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

RCC cells (786-O) were transfected with VHL. The parental cell line should be compared to the transfectant (+VHL) under nomoxia as well as under hypoxia conditions.

Publication Title

Distinct von Hippel-Lindau gene and hypoxia-regulated alterations in gene and protein expression patterns of renal cell carcinoma and their effects on metabolism.

Sample Metadata Fields

Cell line

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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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