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accession-icon GSE30952
Microarray expression data from human renal mesangial cells (HMC) treated with a Cyclosporine A (CsA) time course.
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

HMCs were treated with CsA (4.2 M) for 0 12 and 48 hours. To exmaine global gene changes in the renal mesangium following CsA treatment in order to identify novel contributors to CsA-induced renal dysfunction

Publication Title

Cyclosporine A--induced oxidative stress in human renal mesangial cells: a role for ERK 1/2 MAPK signaling.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon SRP067960
Trascriptome of thyroid cancer-induced macrophages
  • organism-icon Homo sapiens
  • sample-icon 16 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq1500

Description

RNA sequencing data of macrophages after differentiation in the presence of TPC1 thyroid cancer cell line Overall design: Co-incubation in trans-well system between TPC1 cell lines and human primary macrophages

Publication Title

Transcriptional and metabolic reprogramming induce an inflammatory phenotype in non-medullary thyroid carcinoma-induced macrophages.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP113585
Therapeutic targeting of macrophages improves chemotherapy response and elicits neutrophil-dependent therapy resistance
  • organism-icon Mus musculus
  • sample-icon 27 Downloadable Samples
  • Technology Badge IconIllumina HiScanSQ

Description

Macrophages and neutrophils are almost invariably the most abundant intratumoral immune cells, and recent studies have revealed a sinister role for these cells in limiting chemotherapy efficacy. However, how these tumor-educated myeloid cells influence chemotherapy response is incompletely understood. Targeting tumor-associated macrophages by CSF-1 receptor (CSF-1R) blockade in a pre-clinical transgenic mouse model for breast cancer improved the anti-cancer efficacy of cisplatin. Importantly, our findings reveal that macrophage blockade in combination with cisplatin treatment evokes a compensatory neutrophil response limiting the therapeutic synergy of this therapy combination. Here we characterize neutrophils and macrophages gene expression profile from the tumor of mice treated with anti-CSF-1R, Control antibody, Cisplatin/anti-CSF-1R or cisplatin/control ab. Overall design: Intervention studies combining anti-CSF1R and chemotherapy in a transgenic mouse model for breast cancer.

Publication Title

Therapeutic targeting of macrophages enhances chemotherapy efficacy by unleashing type I interferon response.

Sample Metadata Fields

Specimen part, Cell line, Subject

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accession-icon SRP099453
RNA-sequencing of murine norovirus (MNV) infection and loxoribine (Lox) stimulation in RAW264.7 macrophages
  • organism-icon Mus musculus
  • sample-icon 48 Downloadable Samples
  • Technology Badge IconNextSeq 500

Description

This study aimed to generate a comprehensive analysis of changes in the transcriptome following MNV infection. Furthermore, we aimed to perform a differential gene expression analysis between MNV infection and loxoribine (tlr7 agonist) treatment to delineate features of the host modified directly by the MNV as opposed to indirect changes induced through IFN signalling. Overall design: Transcript expression profiles of RAW264.7 cells mock infected, infected with MNV (MOI 5) or treated with loxoribine (1 mM) for 12 hrs were generated using Illumina NextSeq500.

Publication Title

RNA Sequencing of Murine Norovirus-Infected Cells Reveals Transcriptional Alteration of Genes Important to Viral Recognition and Antigen Presentation.

Sample Metadata Fields

Cell line, Subject

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accession-icon SRP099423
RNA-sequencing of longitudinal murine norovirus (MNV) infection in RAW264.7 mouse macrophages
  • organism-icon Mus musculus
  • sample-icon 24 Downloadable Samples
  • Technology Badge IconNextSeq 500

Description

The transcriptome has an abundance of information about the function of individual cells, tissues and an organism in general. Characterising the transcriptome of virus infected cells can illuminate features of the viral-host relationship that are important for pathogenesis. This study broadly aimed to quantify the host gene expression changes that occur following MNV infection. Furthermore, we aimed to identify alterations in specific biological pathways by identifying alterations in transcript abundance that increase or decrease in intensity with MNV infection over time. Overall design: Transcript expression profiles of RAW264.7 cells mock infected or infected with MNV for 4, 8, 12, 16 and 20 hours (MOI 5) were generated by RNA-sequencing using Illumina NextSeq500.

Publication Title

RNA Sequencing of Murine Norovirus-Infected Cells Reveals Transcriptional Alteration of Genes Important to Viral Recognition and Antigen Presentation.

Sample Metadata Fields

Cell line, Subject, Time

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accession-icon SRP033417
Snapshots of pre-rRNA structural flexibility reveal eukaryotic 40S assembly dynamics at nucleotide resolution
  • organism-icon Saccharomyces cerevisiae
  • sample-icon 35 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Ribosome assembly in eukaryotes involves the activity of hundreds of assembly factors that direct the hierarchical assembly of ribosomal proteins and numerous ribosomal RNA folding steps. However, detailed insights into the function of assembly factors and ribosomal RNA folding events are lacking. To address this, we have developed ChemModSeq, a method that combines structure probing, high throughput sequencing and statistical modeling, to quantitatively measure RNA structural rearrangements during the assembly of macromolecular complexes. By applying ChemModSeq to purified 40S assembly intermediates we obtained nucleotide-resolution maps of ribosomal RNA flexibility revealing structurally distinct assembly intermediates and mechanistic insights into assembly dynamics not readily observed in cryo-electron microscopy reconstructions. We show that RNA restructuring events coincide with the release of assembly factors and predict that completion of the head domain is required before the Rio1 kinase enters the assembly pathway. Collectively, our results suggest that 40S assembly factors regulate the timely incorporation of ribosomal proteins by delaying specific folding steps in the 3’ major domain of the 20S pre-ribosomal RNA. Overall design: Three datasets of yeast ribosomal samples subjected to different chemical modifications; 1M7 dataset contains 8 different modified samples and 2 control samples; NAI dataset contains 3 different modified samples and 2 control samples; DMS dataset contains 1 modified sample and 1 control sample. Each sample consists of at least two replicates.

Publication Title

Snapshots of pre-rRNA structural flexibility reveal eukaryotic 40S assembly dynamics at nucleotide resolution.

Sample Metadata Fields

Disease, Cell line, Treatment, Subject

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accession-icon E-MEXP-922
Transcription profiling of yeast with a fumarase point mutation or knock-out to model hereditary leiomyomatosis and renal cell cancer
  • organism-icon Saccharomyces cerevisiae
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Yeast Genome S98 Array (ygs98)

Description

Effect of fumarase point mutation or knock-out on transcriptional profile in yeast to model hereditary leiomyomatosis and renal cell cancer (HLRCC).

Publication Title

Modeling tumor predisposing FH mutations in yeast: effects on fumarase activity, growth phenotype and gene expression profile.

Sample Metadata Fields

Sex, Subject

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accession-icon SRP155036
RNA-seq analysis of canonical and adaptive human NK cell and CD8+ T cell subsets from HCMV seropositive donors
  • organism-icon Homo sapiens
  • sample-icon 42 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

We report our results of RNA-seq analysis on freshly isolated, sorted subsets of cytotoxic lymphocytes Overall design: RNA was isolated from sorted cells. Libraries were created using standard Illumina reagents and analyzed using a HiSeq2500.

Publication Title

ARID5B regulates metabolic programming in human adaptive NK cells.

Sample Metadata Fields

Specimen part, Subject

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accession-icon E-MEXP-268
Transcription profiling of asymptomatic and symptomatic atherosclerotic plaques from the same patient
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U95 Version 2 Array (hgu95av2)

Description

We compared gene expression profiles between asymptomatic and symptomatic atherosclerotic plaques from the same patient. This was accomplished by analyzing carotid plaques from four patients with bilateral high-grade carotid artery stenoses one being symptomatic (TIA or stroke) and the other asymptomatic.

Publication Title

Microarray analysis reveals overexpression of CD163 and HO-1 in symptomatic carotid plaques.

Sample Metadata Fields

Sex, Age, Specimen part, Disease, Disease stage, Subject, Time

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accession-icon GSE63848
Akt-Induced Mitochondrial Dysfunction in the Heart
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Sustained Akt activation induces cardiac hypertrophy (LVH), which may lead to heart failure. This study tested the hypothesis that Akt activation contributes to mitochondrial dysfunction in pathological LVH. Akt activation induced LVH and progressive repression of mitochondrial fatty acid oxidation (FAO) pathways. Preventing LVH by inhibiting mTOR failed to prevent the decline in mitochondrial function but glucose utilization was maintained. Akt activation represses expression of mitochondrial regulatory, FAO, and oxidative phosphorylation genes in vivo that correlate with the duration of Akt activation in part by reducing FOXO-mediated transcriptional activation of mitochondrial-targeted nuclear genes in concert with reduced signaling via PPAR/PGC-1 and other transcriptional regulators. In cultured myocytes Akt activation disrupted mitochondrial bioenergetics, which could be partially reversed by maintaining nuclear FOXO, but not by increasing PGC-1. Thus, although short-term Akt activation may be cardioprotective during ischemia by reducing mitochondrial metabolism and increasing glycolysis, long-term Akt activation in the adult heart contributes to pathological LVH in part by reducing mitochondrial oxidative capacity.

Publication Title

Enhanced cardiac Akt/protein kinase B signaling contributes to pathological cardiac hypertrophy in part by impairing mitochondrial function via transcriptional repression of mitochondrion-targeted nuclear genes.

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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