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accession-icon GSE39889
Neutrophil gene expression in response to Mycobacterium abscessus
  • organism-icon Homo sapiens
  • sample-icon 15 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

The response of human neutrophils to the emerging pathogen Mycobacterium abscessus has not been described. However, M. abscessus infections are frequently associated with neutrophil-rich abscesses. To better understand the reponse of neutrophils to M. abscessus we performed gene expression analysis using Affymetrix HG-U133A Plus 2.0 microarrays. Human neutrophils from healthy donors were stimulated with isogenic rough and smooth morphotypes of M. abscessus. Staphylococcus aureus was used as a control. Gene expression was compared to neutrophils left unstimulated. Neutrophils from four individual donors were isolated on separate days and stimulated with freshly prepared bacteria. Neutrophils (stimulated and control) were left for 2 hours before total RNA was isolated, and biotinylated cRNA was prepared by standard methods. Analysis indicates that M. abscessus morphotypes induce a limited number of genes, when compared to S. aureus, which are enriched in genes for cytokines and chemokines, including neutrophil-specific chemokines. These data suggest that neutrophils have a limited response to M. abscessus, which may contribute to neutrophil-rich abscess formation.overall_design = Human neutrophils from healthy donors were exposed to rough Mab (ATCC 19977T), smooth Mab (ATCC 19977T) and S. aureus (CF clinical strain) for two hours; control cells were exposed to saline.

Publication Title

Mycobacterium abscessus induces a limited pattern of neutrophil activation that promotes pathogen survival.

Alternate Accession IDs

E-GEOD-39889

Sample Metadata Fields

Specimen part, Disease, Treatment

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accession-icon GSE11496
Expression data from Gcn2 wild-type and knockout mouse liver perfused with or without methionine
  • organism-icon Mus musculus
  • sample-icon 16 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

In eukaryotes, regulation of mRNA translation enables a fast, localized and finely tuned expression of gene products. Within the translation process, the first stage of translation initiation is most rigorously modulated by the actions of eukaryotic initiation factors (eIFs) and their associated proteins. These 11 eIFs catalyze the joining of the tRNA, mRNA and rRNA into a functional translation complex. Their activity is influenced by a wide variety of extra- and intracellular signals, ranging from global, such as hormone signaling and unfolded proteins, to specific, such as single amino acid imbalance and iron deficiency. Their action is correspondingly comprehensive, in increasing or decreasing recruitment and translation of most cellular mRNAs, and specialized, in targeting translation of mRNAs with regulatory features such as a 5 terminal oligopyrimidine tract (TOP), upstream open reading frames (uORFs), or an internal ribosomal entry site (IRES). In mammals, two major pathways are linked to targeted mRNA translation. The target of rapamycin (TOR) kinase induces translation of TOP and perhaps other subsets of mRNAs, whereas a family of eIF2 kinases does so with mRNAs containing uORFs or an IRES. TOR targets translation of mRNAs that code for proteins involved in translation, an action compatible with its widely accepted role in regulating cellular growth. The four members of the eIF2 kinase family increase translation of mRNAs coding for stress response proteins such as transcription factors and chaperones. Though all four kinases act on one main substrate, eIF2, published literature demonstrates both common and unique effects by each kinase in response to its specific activating stress. This suggests that the activated eIF2 kinases regulate the translation of both a global and a specific set of mRNAs. Up to now, few studies have attempted to test such a hypothesis; none has been done in mammals.

Publication Title

eIF2alpha kinases GCN2 and PERK modulate transcription and translation of distinct sets of mRNAs in mouse liver.

Alternate Accession IDs

E-GEOD-11496

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE6193
Islet microarray on 2 days PERK wild type and knockout mice
  • organism-icon Mus musculus
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Expression 430A Array (moe430a)

Description

to study the proliferation of PERK knockout mice islets.

Publication Title

PERK EIF2AK3 control of pancreatic beta cell differentiation and proliferation is required for postnatal glucose homeostasis.

Alternate Accession IDs

E-GEOD-6193

Sample Metadata Fields

Sex

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accession-icon GSE33442
The target genes of EGFR activity in glioma cells
  • organism-icon Homo sapiens
  • sample-icon 7 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

As a first step towards identifying the target genes of EGFR activity in glioma cells, genome-wide expression analyses were performed using the Affymetrix GeneChip Human Genome U133A array.

Publication Title

Guanylate binding protein 1 is a novel effector of EGFR-driven invasion in glioblastoma.

Alternate Accession IDs

E-GEOD-33442

Sample Metadata Fields

Cell line, Treatment

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accession-icon SRP043271
Embryonic stem cell-derived cerebral cortex largely reproduces the in vivo epigenetic control of imprinted gene expression [RNA-seq]
  • organism-icon Mus musculus
  • sample-icon 31 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

In vitro differentiation of embryonic stem cells (ESC) provides models that reproduce in vivo development and cells for therapy. Whether the epigenetic signatures that are crucial for brain development and function and that are sensitive to in vitro culture are similar between native brain tissues and their artificial counterpart generated from ESC is largely unknown. Here, using RNA-seq we have compared the parental origin-dependent expression of imprinted genes (IGs), a model of epigenetic regulation, in cerebral cortex generated either in vivo, or from ESCs using in vitro corticogenesis, a model that reproduces the landmarks of in vivo corticogenesis. For a majority of IGs, the expressed parental alleles were the same for in vivo and in vitro cortex. In most cases, this choice was already set in ESCs and faithfully maintained during the 3 weeks of in vitro corticogenesis. Confirming these findings, methylation, which selects the parental allele to be transcribed, was also largely equivalent between the 2 types of cortex and ESCs. Our results thus indicate that the allele specific expression of imprinted transcripts, a model of epigenetic regulation resulting from a differential methylation of parental genomes, is mostly mimicked in cortical cells derived from ESC. Overall design: We have crossed two strains of mice (B6 and JF1) that display more than 12 million of SNPs (Takada et al., Genome Res. 2013 Aug;23(8):1329-38. doi: 10.1101/gr.156497.113). We have then analyzed allele specific expression transcriptome-wide using RNA-seq on hybrid F1 cortex generated either in vivo or in vitro from ESCs. In addition, we have used 2 different developmental stages of in vivo cortex (E13.5, P0) and three stages in vitro (undiffererentiated ESC, and differentiated into cortex for 12 and 21 days) to measure the dynamics of parental expression. Please note that [1] the same raw data files were used to generate the ''*allele-specific_sense_read_bases_by_gene_withoutContamination.txt'' processed data files. [2] The samples associated with each file are indicated in the file column header (as their GSM accession numbers). [3] The readme.txt file contains the data processing steps, file description.

Publication Title

In Vitro Corticogenesis from Embryonic Stem Cells Recapitulates the In Vivo Epigenetic Control of Imprinted Gene Expression.

Alternate Accession IDs

GSE58523

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE7688
Genome-wide mapping and analysis of active promoters in mouse ES cells and adult organs
  • organism-icon Mus musculus
  • sample-icon 5 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

The analysis of several mammalian genomes has revealed between 20,000 to 30,000 genes in each genome, a number that may seem hard to reconcile with the large number of cell types and complex functions of these organisms. The solution to this paradox partly lies in the large array of transcripts that each gene can potentially generate through usage of alternative promoters and the variable levels of transcripts that each gene produces in different tissues and cell types. Thus, in order to understand the mechanisms that control diverse patterns of gene expression in mammals, it is necessary to accurately define the active promoters and monitor their cell or tissue-dependent activity. Previous high throughput strategies for assaying tissue-specific gene expression have primarily relied on measurements of steady-state transcript levels by microarrays or tag sequencing. Here, we employ a new experimental strategy to identify and characterize tissue specific promoters by integrating genome-wide maps of RNA polymerase II (Pol II) binding, chromatin modifications and gene expression profiles. We applied this strategy to mouse embryonic stem cells (mES), and adult brain, heart, kidney, and liver. Our results delineated 24,363 Pol II binding sites throughout the genome, 91% of which correspond to 5 end annotation based on known transcripts and cap-analysis of gene expression (CAGE) and can be regarded as promoters. A majority of these experimentally defined promoters are active in all tissues, while only 4,396 can be characterized as tissue-specific using a quantitative measure of Pol II occupancy. In general, Pol II occupancy at these tissue specific promoters is correlated with the presence of active histone modification marks. However, a set of mES- specific promoters display persistent levels of H3K4me3 in non-ES tissues despite undetectable Pol II binding and transcript. Broadly, our results expand the knowledge of tissue-specific mammalian genes and provide a resource for understanding the transcriptional programs in mammalian development and differentiation.

Publication Title

Genome-wide mapping and analysis of active promoters in mouse embryonic stem cells and adult organs.

Alternate Accession IDs

E-GEOD-7688

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE29008
Human colon epithelial cells treated with Clostridium difficile Toxins A and B
  • organism-icon Homo sapiens
  • sample-icon 19 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Toxin A and B from Clostridium difficile are the primary virulence factors in Clostridium difficile disease. The changes in gene transcription of human colon epithelial cells were investigated in vitro in order to better understand the many effects of both toxins.

Publication Title

Systems analysis of the transcriptional response of human ileocecal epithelial cells to Clostridium difficile toxins and effects on cell cycle control.

Alternate Accession IDs

E-GEOD-29008

Sample Metadata Fields

Cell line

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accession-icon GSE8332
Death receptor O-glycosylation controls tumor-cell sensitivity to the proapoptotic ligand Apo2L/TRAIL
  • organism-icon Homo sapiens
  • sample-icon 117 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Apo2L/TRAIL stimulates cancer-cell death through the proapoptotic receptors DR4 and DR5, but the determinants of tumor susceptibility to this ligand are not fully defined. mRNA expression of the peptidyl O-glycosyl transferase GALNT14 correlated with Apo2L/TRAIL sensitivity in pancreatic carcinoma, non-small cell lung carcinoma and melanoma cell lines (P < 0.00009; n=83), and up to 30% of samples from various human malignancies displayed GALNT14 overexpression. RNA interference of GALNT14 reduced cellular Apo2L/TRAIL sensitivity, whereas overexpression increased responsiveness. Biochemical analysis of DR5 identified several ectodomain O-GalNAc-Gal-Sialic acid structures. Sequence comparison predicted conserved extracellular DR4 and DR5 O-glycosylation sites; progressive mutation of the DR5 sites attenuated apoptosis signaling. O-glycosylation promoted ligand-stimulated clustering of DR4 and DR5, which mediated recruitment and activation of the apoptosis-initiating protease caspase-8. These results uncover a novel link between death receptor O-glycosylation and apoptosis signaling, providing potential predictive biomarkers for Apo2L/TRAIL-based cancer therapy.

Publication Title

Death-receptor O-glycosylation controls tumor-cell sensitivity to the proapoptotic ligand Apo2L/TRAIL.

Alternate Accession IDs

E-GEOD-8332

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE12790
Gene expression profiling of human breast cancers and cancer cell lines
  • organism-icon Homo sapiens
  • sample-icon 96 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

In vivo antitumor activity of MEK and phosphatidylinositol 3-kinase inhibitors in basal-like breast cancer models.

Alternate Accession IDs

E-GEOD-12790

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE12777
Gene expression profiling of 51 human breast cancer cell lines
  • organism-icon Homo sapiens
  • sample-icon 50 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Basal gene expression levels were determined by global gene expression profiling of breast cancer cell lines.

Publication Title

In vivo antitumor activity of MEK and phosphatidylinositol 3-kinase inhibitors in basal-like breast cancer models.

Alternate Accession IDs

E-GEOD-12777

Sample Metadata Fields

No sample metadata fields

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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