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accession-icon SRP117331
Early NKT cell wave of IL-4 serves as an innate link to support initiation of B cell immunity during infection
  • organism-icon Mus musculus
  • sample-icon 222 Downloadable Samples
  • Technology Badge IconNextSeq 500

Description

IL-4/GFP- enhanced transcript (4Get) reporter mice were infected with 200 PFU of Influenza A virus PR8 strain. At day 3 of infection, mediastinal lymph nodes were harvested and GFP+ cells sorted and separated by their ability to bind a CD1d-tetramer (Tet+ n=133 , Tet- n=109 ). Single-cell RNA-Seq was used to identify subpopulations of IL-4 producing cells. Single-cell transcriptomes were clustered using Seurat and differentially expressed genes within each cluster were used to resolve IL-4+ subpopulations and aid in defining their role in initiating B cell immunity during influenza infection. Overall design: Examine cells involved in accute viral response in the lymph node after influenza infection

Publication Title

Initiation of Antiviral B Cell Immunity Relies on Innate Signals from Spatially Positioned NKT Cells.

Sample Metadata Fields

Specimen part, Subject

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accession-icon SRP212736
Gene expression data from IMR90 control, IMR90 shRRM2 and shRRM2/shp16
  • organism-icon Homo sapiens
  • sample-icon 9 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Transformed and tumorigenic cells require increased deoxyribonucleotide synthesis to fuel the genome replication that sustains their unregulated cell cycle and proliferation. Therefore, it is likely that the cell cycle and nucleotide metabolism are linked. The cell cycle inhibitor p16 is a critical tumor suppressor that is lost as an early event in many human cancers. While loss of p16 is known to play a role in deregulating the cell cycle, whether loss of p16 expression affects nucleotide metabolism is unknown. Overall design: mRNA profiles of IMR90 control, dNTP depletion-induced senesnce (shRRM2) and dNTP depletion-induced senescence bypass (shRRM2/shp16) were generated by deep sequencing, in triplicate, using HiSeq 2500 sequencer (Illumina)

Publication Title

Suppression of p16 Induces mTORC1-Mediated Nucleotide Metabolic Reprogramming.

Sample Metadata Fields

Cell line, Subject

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accession-icon GSE69688
Gene expression data from murine myeloid leukemia genomes induced by Sleeping Beauty transposon mutagenesis
  • organism-icon Mus musculus
  • sample-icon 47 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Transcriptome analysis of mRNA samples from a cohort of mice with histopathologically diagnosed Undifferentiated Myeloid Leukemia.

Publication Title

Analyzing tumor heterogeneity and driver genes in single myeloid leukemia cells with SBCapSeq.

Sample Metadata Fields

Sex, Age, Specimen part, Disease, Disease stage

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accession-icon SRP058917
Transcriptome sequencing of murine myeloid leukemia genome
  • organism-icon Mus musculus
  • sample-icon 5 Downloadable Samples
  • Technology Badge IconIon Torrent Proton

Description

Mus musculus (house mouse) Myeloid Leukemia RNA-Seq

Publication Title

Analyzing tumor heterogeneity and driver genes in single myeloid leukemia cells with SBCapSeq.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP066857
Single epicardial cell transcriptome sequencing identifies Caveolin-1 as an essential factor in zebrafish heart regeneration
  • organism-icon Danio rerio
  • sample-icon 40 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

By contrast with mammals, adult zebrafish have a high capacity to regenerate damaged or lost myocardium through proliferation of spared cardiomyocytes. The epicardial sheet covering the heart is activated by injury and aids muscle regeneration through paracrine effects and as a multipotent cell source, and has received recent attention as a target in cardiac repair strategies. While it is recognized that epicardium is required for muscle regeneration and itself has high regenerative potential, the extent of cellular heterogeneity within epicardial tissue is largely unexplored. In this study, we performed transcriptome analysis on dozens of epicardial lineage cells purified from zebrafish harboring a transgenic reporter for the pan-epicardial gene tcf21. Hierarchical clustering analysis suggested the presence of at least three epicardial cell subsets defined by expression signatures. We validated many new pan-epicardial and epicardial markers by alternative expression assays. Additionally, we explored the function of the scaffolding protein and main component of caveolae, caveolin-1 (cav1), which was present in each epicardial subset. In BAC transgenic zebrafish, cav1 regulatory sequences drove strong expression in ostensibly all epicardial cells and in coronary vascular endothelial cells. Moreover, cav1 mutant zebrafish generated by genome editing showed grossly normal heart development and adult cardiac anatomy, but displayed profound defects in injury-induced cardiomyocyte proliferation and heart regeneration. Our study defines a new platform for the discovery of epicardial lineage markers, genetic tools, and mechanisms of heart regeneration. Overall design: Deep sequencing of isolated single epicardial cells

Publication Title

Single epicardial cell transcriptome sequencing identifies Caveolin 1 as an essential factor in zebrafish heart regeneration.

Sample Metadata Fields

Age, Specimen part, Cell line, Subject

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accession-icon GSE8199
E18.5 Estrogen-related Receptor gamma Knockout Mouse Heart
  • organism-icon Mus musculus
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

3 ventricles from E18.5 male mice were pooled for each array. Three arrays per genotype.

Publication Title

ERRgamma directs and maintains the transition to oxidative metabolism in the postnatal heart.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE81959
Effects of Sex, Strain, and Energy Intake on Hallmarks of Aging in Mice
  • organism-icon Mus musculus
  • sample-icon 72 Downloadable Samples
  • Technology Badge IconIllumina MouseRef-8 v2.0 expression beadchip

Description

Calorie restriction (CR) is the most robust non-genetic intervention to universally delay the onset of age-related diseases and extend mean and maximum lifespan. However, species, strain, sex, diet, age of onset, and level of CR are emerging as important variables to consider for a successful CR response. Here, we investigated the role of strain, sex and level of CR on outcomes of health and survival in mice. Response to CR varied from lifespan extension to no effect on survival, while consistently delaying the onset and impact of diseases independently of strain, sex and level of dietary restriction. CR led to transcriptional and metabolomics changes in the liver indicating anaplerotic filling of the Krebs cycle together with fatty acid fueling of mitochondria. Additionally, CR prevented the age-associated decline in the proteostasis network. Further, CR increased mitochondrial number and preserved their ultrastructure and function with age. Abrogation of mitochondrial function by deletion of fumarate hydratase or malate dehydrogenase 2 negated the life-prolonging effects of CR in yeast and worms. In F1 hybrid strains of mice, the lifespan response to CR tracked with the dam, indicating that the mitochondrial haplotype is an important regulator of CR. Our data illustrate the complexity of the CR responses within a single animal species in the context of aging, with a clear separation of outcomes related to health and survival, highlighting the complexities of translation of CR into human interventions.

Publication Title

Effects of Sex, Strain, and Energy Intake on Hallmarks of Aging in Mice.

Sample Metadata Fields

Sex, Specimen part

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accession-icon SRP167975
An Optofluidic Real-Time Cell Sorter for Longitudinal CTC Studies in Mouse Models of Cancer
  • organism-icon Mus musculus
  • sample-icon 756 Downloadable Samples
  • Technology Badge IconNextSeq 500

Description

Circulating tumor cells (CTCs) play a fundamental role in cancer progression. However, in mice, limited blood volume and the rarity of CTCs in the bloodstream preclude longitudinal, in-depth studies of these cells using existing liquid biopsy techniques. Here, we present an optofluidic system that continuously collects fluorescently-labeled CTCs from a genetically-engineered mouse model for several hours per day over multiple days or weeks. The system is based on a microfluidic cell-sorting chip connected serially to an un-anesthetized mouse via an implanted arteriovenous shunt. Pneumatically-controlled microfluidic valves capture CTCs as they flow through the device and CTC-depleted blood is returned back to the mouse via the shunt. To demonstrate the utility of our system, we profile CTCs isolated longitudinally from animals over a four-day treatment with the BET inhibitor JQ1 using single-cell RNA-Seq (scRNA-Seq) and show that our approach eliminates potential biases driven by inter-mouse heterogeneity that can occur when CTCs are collected across different mice. The CTC isolation and sorting technology presented here provides a research tool to help reveal details of how CTCs change over time, allowing studies to credential changes in CTCs as biomarkers of drug response and facilitating future studies to understand the role of CTCs in metastasis. Overall design: Single-cell RNA-Sequencing of CTCs and primary tumors from a murine model of non-small cell-lung cancer

Publication Title

Optofluidic real-time cell sorter for longitudinal CTC studies in mouse models of cancer.

Sample Metadata Fields

Specimen part, Subject, Time

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accession-icon GSE46988
Expression data from rat spinal cord injury and mesenchymal stromal cells (MSC) or olfactory ensheathing cells (OEC) transplantation
  • organism-icon Rattus norvegicus
  • sample-icon 52 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Gene 1.1 ST Array (ragene11st)

Description

We analyzed the changes in the spinal cord transcriptome after a spinal cord contusion injury and MSC or OEC transplantation. The cells were injected immediately or 7 days after the injury. The mRNA of the spinal cord injured segment was extracted and analyzed by microarray at 2 and 7 days after cell grafting.

Publication Title

Gene expression changes in the injured spinal cord following transplantation of mesenchymal stem cells or olfactory ensheathing cells.

Sample Metadata Fields

Treatment

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accession-icon GSE27328
Transcriptome analysis on ovarian cancer
  • organism-icon Homo sapiens
  • sample-icon 17 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

We are studying signaling pathways and growth properties of cultured human ovarian cancer cells that are expressing the G protein-coupled receptor, luteinizing hormone receptor (LHR),particularly interested in the changes that occur when the receptor is activated by its cognate ligand, gonadotropin (LH). To investigate these questions, we have employed the SKOV3 ovarian cancer cell line that has been stably transfected with LHR, and can then test the response of these cells in culture following exposure to LH.

Publication Title

Regulation of gene expression in ovarian cancer cells by luteinizing hormone receptor expression and activation.

Sample Metadata Fields

Cell line, Treatment, Time

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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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