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accession-icon GSE63827
Global gene transcriptional profiles in RAW 264.7 cells following mica fine particle stimulation
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina MouseWG-6 v2.0 expression beadchip

Description

We focused on how mica fine particle influences macrophage activities.

Publication Title

Modulation of macrophage activities in proliferation, lysosome, and phagosome by the nonspecific immunostimulator, mica.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon SRP124955
Combinatory RNA sequencing analyses reveal RNA editing-dependent and -independent gene regulation by ADAR1 in gastric cancer
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon

Description

To investigate the role of ADAR1 in gastric carcinogenesis, RNA sequencing and small RNA sequencing were performed in AGS and MKN-45 cells with stable ADAR1 knock-down. Changed frequencies of editing and messenger RNA (mRNA) and microRNA (miRNA) expression were then identified by bioinformatic analyses. Overall design: mRNA and miRNA sequencing were performed before and after stable knockdown of ADAR1 in AGS and MKN-45 cell line

Publication Title

Combinatory RNA-Sequencing Analyses Reveal a Dual Mode of Gene Regulation by ADAR1 in Gastric Cancer.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE63245
Gene expression data from murine M1 and M2 macrophages
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Macrophages have distinct characteristics depending on their microenvironment. We performed proteomic analysis between M1 and M2 macrophages and found that cellular metabolism is the key regulator of macrophage function.

Publication Title

Proteomic Analysis Reveals Distinct Metabolic Differences Between Granulocyte-Macrophage Colony Stimulating Factor (GM-CSF) and Macrophage Colony Stimulating Factor (M-CSF) Grown Macrophages Derived from Murine Bone Marrow Cells.

Sample Metadata Fields

Specimen part

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accession-icon SRP167107
Ferret animal model of severe fever with thrombocytopenia syndrome phlebovirus for human lethal infection and pathogenesis
  • organism-icon Mustela putorius furo
  • sample-icon 13 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Severe fever with thrombocytopenia syndrome phlebovirus (SFTSV), listed in the WHO most dangerous pathogens, has 12-30% fatality rates with a characteristic thrombocytopenia syndrome. With a majority of clinically diagnosed SFTSV patients older than ~50 years, age is a critical risk factor for SFTSV morbidity and mortality. Here, we report an age-dependent ferret model of SFTSV infection and pathogenesis that fully recapitulates the clinical manifestations of human infections. While young adult ferrets (=2 years old) did not show any clinical symptoms and mortality, SFTSV-infected aged ferrets (=4 years old) demonstrated severe thrombocytopenia, reduced white blood cells, and high fever with 93% mortality rate. Moreover, significantly higher viral load was observed in aged ferrets. Transcriptome analysis of SFTSV-infected young ferrets revealed strong interferon-mediated anti-viral signaling, whereas inflammatory immune responses were markedly upregulated and persisted in aged ferrets. Thus, this immunocompetent age-dependent ferret model should be useful for anti-SFTSV therapy and vaccine development. Overall design: Two groups of young adults (20-24 months, =2Y) and aged ferrets (48-50 months), =4 Y) were inoculated via the IM route with 107.6 TCID50 of the SFTSV CB1/2014 strain. PBMCs were isolated at 2 and 4 dpi from each group of ferrets (n=3) by density gradient centrifugation using Ficoll-Paque Plus according to the manufacture's protocol.

Publication Title

Ferret animal model of severe fever with thrombocytopenia syndrome phlebovirus for human lethal infection and pathogenesis.

Sample Metadata Fields

Specimen part, Subject

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accession-icon SRP144088
transcriptional response to endothelial cell-specific inactivation of Tspan12 in the mature retina
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 4000

Description

Blood-retina barrier (BRB) formation and retinal angiogenesis depend on beta-catenin signaling induced by the ligand norrin (NDP), the receptor frizzled4 (FZD4), co-receptor LRP5, and the tetraspanin TSPAN12. Impaired NDP/FZD4 signaling causes familial exudative vitreoretinopathy (FEVR), which may lead to blindness. Endothelial-cell specific inactivation of the Tspan12 gene at P28 using a Cdh5-CreERT2 driver shows that TSPAN12 functions in ECs to promote vascular morphogenesis and BRB formation in developing mice, and BRB maintenance in adult mice. 12 month after Tspan12 inactivation and loss of BRB maintenance with massive IgG and albumin extravasation we observe complement activation, cystoid edema, and impaired beta-wave in electroretinograms. RNA-Seq 6 month after Tspan12 inactivation provides a detailed view on the transcriptional response, including activation of antibody effector systems (complement and Fc receptors), inflammation and microglia responses, extracellular matrix organization and remodeling, and other responses. Overall design: Endothelial cell-specific inactivation of floxed Tspan12 was induced at P28 using a Cdh5-CreERT2 driver and total retina RNA (ribodepleted) from 4 control or ECKO retinas (8 samples) was subjected to RNA-Seq 6 months later

Publication Title

Endothelial Cell-Specific Inactivation of TSPAN12 (Tetraspanin 12) Reveals Pathological Consequences of Barrier Defects in an Otherwise Intact Vasculature.

Sample Metadata Fields

Specimen part, Cell line, Subject

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accession-icon SRP063949
RNA-seq identified KLF16 as a negative regulator of adipogenesis
  • organism-icon Mus musculus
  • sample-icon 2 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

We performed high throughput RNA sequencing at preadipocyte (D0) and differentiated adipocyte (D7) of primary brown preadipocyte and found that Kruppel-like factor 16 (KLF11) gene that was downregulated in D7 was a novel negative regulator of adipogenesis. Overall design: To explore global view of gene expression during adipogenesis, RNA-seq was performed in the primary cultured brown preadipocyte (D0) and brown adipocyte after 7 day differentiation (D7). Compared with D0, 6,668 genes were identified as 2 fold differentially expressed genes (DEGs) at D7 including 2,836-upregulated genes and 3,832 down-regulated genes.

Publication Title

RNA-Seq Analysis Reveals a Negative Role of KLF16 in Adipogenesis.

Sample Metadata Fields

Specimen part, Cell line, Subject

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accession-icon GSE92948
GPCR19 agonist increases in number of immune-regulatory myeloid cells and their expression of immune checkpoint molecule
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

GPCR19 pathway has been implicated in regulating various inflammation. However, the exact mechanism of immune regulation by GPCR19 pathway has not been elucidated in detail.

Publication Title

Taurodeoxycholate Increases the Number of Myeloid-Derived Suppressor Cells That Ameliorate Sepsis in Mice.

Sample Metadata Fields

Sex, Specimen part

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accession-icon GSE61049
Nervous system developmental genes are altered in fetal hippocampus by ethanol.
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Prenatal alcohol exposure can cause long-lasting changes in functional and genetic programs of the brain, which may underlie behavioral alterations found in FASD.

Publication Title

Ethanol-related alterations in gene expression patterns in the developing murine hippocampus.

Sample Metadata Fields

Specimen part

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accession-icon GSE63270
Expression profiles of normal hematopoietic stem and progenitor cells and acute myeloid leukemia sub-populations
  • organism-icon Homo sapiens
  • sample-icon 98 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Acute Myeloid Leukemia AML is a cancer in which the process of normal cell hematopoietic differentiation is disrupted. Evidence exists that AML comprises a hierarchy with leukemic stem cells giving rise to more differentiated, but immature and functionally incompetent populations. The similarity of these AML subpopulations to normal stages of hematopoietic differentiation has not been dissected comprehensively at the transcriptional level. Here we introduce Normal Memory Analysis (NorMA), a data analysis method that extracts from omic data the remnants of the healthy normal-like phenotype. Applying NorMA to gene expression data from AML uncovered a wealth of information in the normal-like component of data: the normal hematopoietic memory of AML tumor cells. We found significant variation within the patient population, and we found strong association of this normal hematopoietic memory with survival. We found that undifferentiated NorMA phenotype has significantly worse survival than differentiated NorMA phenotype, showing that the NorMA classification of tumors captures a biologically meaningful stratification of patients, with highly significant survival association. Patients with NorMA phenotype in the undifferentiated Hematopoietic Stem Cell HSC stage had the worst survival, with median survival time under 6 months. We further found significant survival differences between tumor groups with differentiated NorMA phenotype, depending on their hematopoietic path: AML patients with NorMA phenotype in megakaryocyte-erythroid progenitor MEP stage had significantly better survival than those with NorMA phenotype in granulocyte-macrophage progenitor GMP stage. Thus NorMA produced a stratification of AML cohorts by differentiation stage, with significant outcome differences. It also provided clean molecular signatures for these stages. NorMA can be used in many other contexts, to explore for example the tumor cell of origin, or disease predisposition.

Publication Title

An LSC epigenetic signature is largely mutation independent and implicates the HOXA cluster in AML pathogenesis.

Sample Metadata Fields

Specimen part

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accession-icon GSE54189
Luteolin attenuates lipid dysregulation and insulin resistance thorough interplay of liver and adipose tissue in diet-induced obese mice
  • organism-icon Mus musculus
  • sample-icon 18 Downloadable Samples
  • Technology Badge IconIllumina MouseWG-6 v2.0 expression beadchip

Description

Analysis of effect of luteolin on lipid metabolism at gene expression level. The hypothesis tested in the present study was that luteolin treatment with obesogenic diet suppressed the hepatic lipogenesis pathways. Conversely, in adipose tissue, luteolin stimulated the lipogenesis pathway and it also simultaneously increased the expression of genes controlling lipolysis and TCA cycle. Results provide important information about the effect on diet-induced obesity and its metabolic complications.

Publication Title

Luteolin attenuates hepatic steatosis and insulin resistance through the interplay between the liver and adipose tissue in mice with diet-induced obesity.

Sample Metadata Fields

Sex, 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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