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accession-icon GSE142544
Nerve injury induced protein 1 (Ninjurin1) deletion effect on peritoneal macrophages
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 2.0 ST Array (mogene20st)

Description

We used microarrays to investigate gene expression from peritoneal macrophages associated with Ninjurin1 expression.

Publication Title

Detrimental Role of Nerve Injury-Induced Protein 1 in Myeloid Cells under Intestinal Inflammatory Conditions.

Sample Metadata Fields

Sex

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accession-icon GSE3583
Huntington's disease: Gene expression changes caused by Hdh CAG mutation or 3-nitropropionic acid in striatal cells
  • organism-icon Mus musculus
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Affymetrix MG430 2.0 expression levels of wild-type (STHdhQ7/Q7), 3NP-treated wild-type (STHdhQ7/Q7+3-NP), and mutant (STHdhQ111/Q111) striatal cells

Publication Title

Unbiased gene expression analysis implicates the huntingtin polyglutamine tract in extra-mitochondrial energy metabolism.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE12007
Identification of Sox10 target genes by comparative expression profiling
  • organism-icon Rattus norvegicus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Genome 230 2.0 Array (rat2302)

Description

RT4D6 Schwannoma cells were treated with siRNA specific for Sox10 and a mutant siRNA. Total RNA from the cells were used to screen for differentially expressed genes.

Publication Title

Identification of direct regulatory targets of the transcription factor Sox10 based on function and conservation.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE21182
Curcumin Extends Lifespan, Improves Healthspan, and Modulates the Expression of Age-Associated Aging Genes in Drosophila melanogaster
  • organism-icon Drosophila melanogaster
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Drosophila Genome 2.0 Array (drosophila2)

Description

Curcumin, a yellow pigment extracted from the rhizome of the plant Curcuma longa (turmeric) has been widely used as a spice and herbal medicine in Asia. It has been suggested to have many biological activities such as anti-oxidative, anti-inflammatory, anti-cancer, chemopreventive, and anti-neurodegenerative properties. We evaluated the impact of curcumin on lifespan, fecundity, feeding rate, oxidative stress, locomotion and gene expression in two different wild type Drosophila melanogaster strains, Canton-S and Ives, under two different experimental conditions. We report that curcumin extended the lifespan of two different strains of Drosophila and was accompanied by protection against oxidative stress, improvement in locomotion and chemopreventive effects. Curcumin also modulated the expression of several aging related genes (genes with age-dependent changes in gene expression) such as mth, thor, InR, and JNK.

Publication Title

Curcumin extends life span, improves health span, and modulates the expression of age-associated aging genes in Drosophila melanogaster.

Sample Metadata Fields

Sex, Age

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accession-icon GSE9038
Gene expression profiles of striatum and cerebellum from knock-in mouse model of Huntington's disease
  • organism-icon Mus musculus
  • sample-icon 24 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Huntingtons disease (HD) involves marked early neurodegeneration in the striatum whereas the cerebellum is relatively spared despite the ubiquitous expression of full-length mutant huntingtin, implying that inherent tissue-specific differences determine susceptibility to the HD CAG mutation. To understand this tissue specificity, we compared early mutant huntingtin-induced gene expression changes in striatum to those in cerebellum in young Hdh CAG knock-in mice, prior to onset of evident pathological alterations. Endogenous levels of full-length mutant huntingtin caused qualitatively similar, but quantitatively different gene expression changes in the two brain regions. Importantly, the quantitatively different responses in striatum and cerebellum in mutant mice were well accounted for by the intrinsic molecular differences in gene expression between striatum and cerebellum in wild-type animals. Tissue-specific gene expression changes in response to the HD mutation, therefore, appear to reflect the different inherent capacities of these tissues to buffer qualitatively similar effects of mutant huntingtin. These findings highlight a role for intrinsic quantitative tissue differences in contributing to HD pathogenesis, and likely to other neurodegenerative disorders exhibiting tissue-specificity, thereby guiding the search for effective therapeutic interventions.

Publication Title

Differential effects of the Huntington's disease CAG mutation in striatum and cerebellum are quantitative not qualitative.

Sample Metadata Fields

Specimen part

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accession-icon SRP162023
HantavaxTM vaccinated peripheral blood mononuclear cells (PBMCs) and sera analyses by transcriptomic and metabolomic profilings
  • organism-icon Homo sapiens
  • sample-icon 74 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Purpose: To annotate vaccine-induced protective immunity following vaccination and identify the dynamics of enriched modules over time, and determine whether and how transcriptomics and metabolomics data correlates. charge ratio) within a range of ions set from 50 to 1,000 from mass spectral data. The data from triplicate run were averaged and statistically analysed using SIMCA 14.1 Results: Based on neutralizing antibody titers, subjects were subsequently classified into three groups; non responders (NRs), low responders (LRs) and high responders (HRs). Post vaccination differentially expressed genes (DEGs) associated with innate immunity and cytokine pathways were highly upregulated. DEG analysis revealed a significant induction of CD69 expression in the HRs. High resolution metabolomics (HRM) analysis showed that correlated to the antibody response, cholesteryl nitrolinoleate and octanoyl-carnitine were significantly elevated in HRs, while chenodeoxycholic acid and methyl palmitate were upregulated in NRs and LRs, but not HRs. Additionally, gene-metabolite interaction revealed upregulated gene-metabolite couplings in, folate biosynthesis, nicotinate and nicotinamide, arachidonic acid, thiamine and pyrimidine metabolism in a dose dependent manner in HR group. Conclusions: Our data provide new insight into the underlying mechanisms of the HantavaxTM-mediated immunogenicity in humans. Our study illustrate the potential for transcriptomics and untargeted metabolomics to identify genes and metabolites involved in immune responses which may propose a targeted vaccine design in future. Overall design: Systems vaccinology analyses were performed based on two different approaches: vaccination instance and responsiveness to the vaccine. In our study we vaccinated a total of 20 subjects with 4 doses. However, 1 subject (subject or sample # 3) was excluded from transcriptomic study after first vaccination due to abnormal antibody titer. Hence, we have 19 subjects vaccinated 4 time but the samples were collected before 1st and after 2nd, 3rd and 4th vaccination (i.e., sample collections was performed at 4 time points). This Series contains a total of 76 samples (19 x 4).

Publication Title

A Systems Vaccinology Approach Reveals the Mechanisms of Immunogenic Responses to Hantavax Vaccination in Humans.

Sample Metadata Fields

Sex, Age, Specimen part, Subject

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accession-icon GSE90121
Identification Of Neuroblastoma Metastasis Associated Genes
  • organism-icon Homo sapiens
  • sample-icon 16 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Metastatic relapse is the major cause of death in neuroblastoma (NB), yet there are no therapies to specifically target metastases. To understand the molecular mechanisms mediating NB metastasis, we developed a mouse model using intracardiac injection and in vivo selection to isolate metastatic subpopulations that exhibited a higher propensity for bone and central nervous system metastases. Gene expression profiling revealed two distinct subtypes, primary and metastatic, with differential regulation of 412 genes and multiple pathways including CADM1, SPHK1, and YAP/TAZ whose expression independently predicted survival. Loss- and gain-of-function experiments with these genes demonstrated a rescue of metastatic phenotypes in multiple NB cell lines in vitro or in vivo. Treatment with the compounds SKI II and Verteporfin that target SPHK1 and YAP/TAZ, respectively, inhibited NB metastasis in vivo. In addition, using gene expression profiling from the metastatic subpopulations, a gene signature (MET-75) was identified that predicts NB survival of patients with metastatic disease. This model therefore identifies genes regulating metastasis and candidate therapeutics for metastatic NB

Publication Title

A Metastatic Mouse Model Identifies Genes That Regulate Neuroblastoma Metastasis.

Sample Metadata Fields

Disease

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accession-icon SRP068592
STAT5 is a key transcription factor IL-3-mediated inhibition of RANKL-induced osteoclastogenesis
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Purpose: Among the diverse cytokines involved in osteoclast differentiation, IL-3 has been shown to inhibit RANKL-induced osteoclastogenesis. However, the mechanism underlying IL-3-mediated inhibition of osteoclast differentiation is not fully understood. In the present study, we demonstrate that IL-3 activation of STAT5 inhibits RANKL-induced osteoclastogenesis through the induction of Id genes. Methods: To investigate the effect of STAT5 on osteoclast differentiation and IL-3-mediated inhibition of osteoclast differentiation, bone marrow derived macrophages isolated from STAT5 wild-type (Stat5fl/fl) or STAT5 cKO (STAT5;MX1-Cre) were differentiated to osteoclast in the presence of M-CSF and RANKL with or without IL-3; and bone marrow derived macrophges from STAT5 wild-type and STAT5 cKO were overexpressed with PMX-FIG (control) or STAT5A1*6 (constitutively active form of STAT5A) and differentiated to osteoclast. To analyze bone phenotype, femurs and tibiae of 16 week-old STAT5 wild-type and STAT5 cKO were subjected to micro CT analysis and histomorphometry, respectively. Results: Overexpression of STAT5 inhibited RANKL-induced osteoclastogenesis. However, RANKL did not regulate either expression or activation of STAT5 during osteoclast differentiation. STAT5 deficiency prevented IL-3-mediated inhibition of osteoclastogenesis, suggesting that STAT5 plays an important role in IL-3-mediated inhibition of osteoclast differentiation. In addition, IL-3-induced STAT5 activation upregulated expression of the Id1 and Id2 genes, which are negative regulators of osteoclastogenesis. Overexpression of ID1 or ID2 in STAT5-deficient cells reversed osteoclast development recovered from IL-3-mediated inhibition. Moreover, micro-computed tomography and histomorphometric analysis revealed that STAT5 conditional knockout mice showed reduced bone mass, with an increased number of osteoclasts. Furthermore, IL-3 inhibited RANKL-induced osteoclast differentiation less effectively in STAT5 conditional knockout mice than in wild-type mice in a RANKL injection model. Conclusion: Taken together, our results suggest that STAT5 is a key transcription factor for IL-3-mediated inhibition of RANKL-induced osteoclastogenesis through Id gene expression. Overall design: Examination of 4 different combination of osteoclast differentiation condition of bone marrow derived macrophages.

Publication Title

STAT5 is a key transcription factor for IL-3-mediated inhibition of RANKL-induced osteoclastogenesis.

Sample Metadata Fields

Sex, Age, 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 SRP076543
mRNA profiling of liver-specific RORa KO mouse liver
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

The retinoic acid receptor-related orphan receptor a (RORa) is a member of the NR1 subfamily of orphan nuclear hormone receptors. RORa is an important regulator of various biological processes, including cerebellum development, cancer and circadian rhythm. To determine molecular mechanism by which hepatic deletion of RORa induces obesity and insulin resistance, we performed global transcriptome analysis from high-fat diet (HFD)-fed RORa f/f and RORa LKO mouse liver tissues. This analysis provides insight into molecular mechanisms for RORa in high-fat-diet condition. Overall design: mRNA expression profiles of RORa f/f and RORa LKO mice liver with control diet or high-fat-diet were examined by Illumina HiSeq 2500.

Publication Title

RORα controls hepatic lipid homeostasis via negative regulation of PPARγ transcriptional network.

Sample Metadata Fields

Specimen part, Treatment, Subject

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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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