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Homo sapiens
9 Downloadable Samples
Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Our data indicated that activation of the PPARg nuclear receptor induces a retinoid response in human dendritic cells. In order to assess the contribution of retinoid signaling to the PPARg response we decided to use a combination of pharmacological activators and inhibitors of these pathways. Cells were treated with the synthetic PPARg ligand rosiglitazone (RSG), or with RSG along with the RARa antagonist (AGN193109) to block RARa mediated gene expression, or the RARa specific agonists (AM580) alone. This design allows one to determine if retinoid signaling is a downstream event of PPARg activation and what portion of PPARg regulated genes are regulated via induced retinoid signaling.
Publication Title
PPARgamma controls CD1d expression by turning on retinoic acid synthesis in developing human dendritic cells.
Sample Metadata Fields
Sex, Specimen part
View Samples- Mus musculus
- 12 Downloadable Samples
Illumina HiSeq 2000
Description
Purpose: to identify the effects on the transcriptome of deleting ZFP36L1 in MZ B cells Overall design: Method (MZ B cells): RNAseq libraries were prepared from 5ng RNA isolated from sorted ex-vivo MZ B cells. Total RNA samples were sent to Aros Applied Biotechnology A/S and were prepared using the Clontech SMARTer kit. Libraries were sequenced (100bp paired end) on the Illumina Hiseq. Method (FO B cells): RNAseq libraries were prepared from RNA isolated from sorted ex-vivo FO B cells. Total RNA samples were sent to Aros Applied Biotechnology A/S and were prepared using the TruSeq Stranded mRNA Sample Prep Kit (Illumina). Libraries were sequenced (100bp single end) on the Illumina Hiseq.
Publication Title
Maintenance of the marginal-zone B cell compartment specifically requires the RNA-binding protein ZFP36L1.
Sample Metadata Fields
Specimen part, Cell line, Subject
View Samples- Homo sapiens
- 14 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Tuberculosis Immune Reconstitution Inflammatory Syndrome (TB-IRIS) frequently complicates combined anti-retroviral therapy (ART) and anti-tubercular therapy in HIV-1 co-infected tuberculosis (TB) patients. The immunopathological mechanism underlying TB-IRIS is incompletely defined.
Publication Title
Cytotoxic mediators in paradoxical HIV-tuberculosis immune reconstitution inflammatory syndrome.
Sample Metadata Fields
Specimen part, Subject
View Samples- Mus musculus
- 2 Downloadable Samples
- Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
Adipose tissue iNKT cells have different functions than iNKT cells in the blood and other organs.
Publication Title
Regulatory iNKT cells lack expression of the transcription factor PLZF and control the homeostasis of T(reg) cells and macrophages in adipose tissue.
Sample Metadata Fields
Age, Specimen part
View Samples- Mus musculus
- 4 Downloadable Samples
- Affymetrix Mouse Gene 1.1 ST Array (mogene11st)
Description
Lipid overload and adipocyte dysfunction are key to the development of insulin resistance and can be induced by a high-fat diet. CD1d-restricted invariant natural killer T (iNKT) cells have been proposed as mediators between lipid overload and insulin resistance, but recent studies found decreased iNKT cell numbers and marginal effects of iNKT cell depletion on insulin resistance under high-fat diet conditions. Here, we focused on the role of iNKT cells under normal conditions. We showed that iNKT celldeficient mice on a low-fat diet, considered a normal diet for mice, displayed a distinctive insulin resistance phenotype without overt adipose tissue inflammation. Insulin resistance was characterized by adipocyte dysfunction, including adipocyte hypertrophy, increased leptin, and decreased adiponectin levels. The lack of liver abnormalities in CD1d-null mice together with the enrichment of CD1d-restricted iNKT cells in both mouse and human adipose tissue indicated a specific role for adipose tissueresident iNKT cells in the development of insulin resistance. Strikingly, iNKT cell function was directly modulated by adipocytes, which acted as lipid antigen-presenting cells in a CD1d-mediated fashion. Based on these findings, we propose that, especially under low-fat diet conditions, adipose tissueresident iNKT cells maintain healthy adipose tissue through direct interplay with adipocytes and prevent insulin resistance.
Publication Title
Natural killer T cells in adipose tissue prevent insulin resistance.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 16 Downloadable Samples
- Illumina HiSeq 2000
Description
The FBXL10 protein (also known as KDM2B, JHDM1B, CXXC2, and NDY1) is bound to essentially all CpG-rich promoters in the mammalian genome. FBXL10 is expressed as two isoforms: FBXL10-1, a longer form that contains an N-terminal JmjC domain with C- terminal F-box, CXXC, PHD, RING, and leucine rich repeat (LRR) domains, and FBXL10-2, a shorter form that initiates at an alternative internal exon and which lacks the JmjC domain but retains the other domains. Selective deletion of Fbxl10-1 had been reported to produce a minor and variable phenotype, and most mutant animals were essentially normal. We show here that deletion of Fbxl10-2 (in a manner that does not perturb expression of Fbxl10-1) resulted in a very different phenotype with craniofacial abnormalities, greatly increased lethality, and female sterility in surviving homozygous mutants. The phenotype of the Fbxl10-2 deletion was more severe in female mutants. We found that mutants that lacked both FBXL10-1 and -2 showed embryonic lethality and even more extreme sexual dimorphism, with more severe gene dysregulation in mutant female embryos. X-linked genes were most severely dysregulated, and there was marked overexpression of Xist in mutant females although genes that encode factors that bind to Xist RNA were globally down-regulated in mutant female as compared to male embryos. FBXL10 is the first factor shown to be required both for the normal expression and function of the Xist gene. Overall design: Expression analysis using RNA-seq was performed on WT and Fbxl10T/T male and female embryos.
Publication Title
Abnormal X chromosome inactivation and sex-specific gene dysregulation after ablation of FBXL10.
Sample Metadata Fields
Sex, Specimen part, Cell line, Subject
View Samples- Saccharomyces cerevisiae
- 12 Downloadable Samples
- Affymetrix Yeast Genome 2.0 Array (yeast2)
Description
Effect of either FLO8 or MSS11 deletion and -overexpression on yeast transcript profiles compared to wild type in laboratory yeast strains 1278b and S288c - also the effect of FLO11 (MUC1) overexpression in the 1278b genetic background
Publication Title
Many Saccharomyces cerevisiae Cell Wall Protein Encoding Genes Are Coregulated by Mss11, but Cellular Adhesion Phenotypes Appear Only Flo Protein Dependent.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 12 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
In this study, we have investigated the role of secondhand smoke (SHS) in the development of metabolic liver disease by characterizing the global regulation of genes and molecular pathways in SHS-exposed mice after termination of exposure (SHS 4M) and following one-month recovery in clean air (SHS 4M +1M RECOVERY).
Publication Title
Secondhand Smoke Induces Liver Steatosis through Deregulation of Genes Involved in Hepatic Lipid Metabolism.
Sample Metadata Fields
Sex
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GSE24071- Mus musculus
- 8 Downloadable Samples
- Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
Overexpression of high mobility group AT-hook 2 (HMGA2) associated with truncations of its 3 untranslated region (UTR) with let-7 micro RNA-complementary sequences have been identified in patients with paroxysmal nocturnal hemoglobinuria (PNH). Here, we generated transgenic mice (Hmga2 mice) with a 3UTR-trncated Hmga2 cDNA that overexpress Hmga2 mRNA and protein in hematopoietic organs. Hmga2 mice showed proliferative hematopoiesis that mimicked a myeloproliferative neoplasm (MPN)-like phenotype with increased numbers of all lineages of peripheral blood cells, hypercellular bone marrow (BM), splenomegaly with extramedullary erythropoiesis, and erythropoietin-independent erythroid colony formation compared to wild-type mice. Hmga2 BM-derived cells took over most of hematopoiesis in competitive repopulations during serial BM transplants. When we bred mice with circulating PNH cells (Piga- mice) with Hmga2 mice, the lack of GPI-linked proteins did not add an additional clonal advantage to the Hmga2+ cells. In summary, our results showed that the overexpression of a 3UTR-truncated Hmga2 leads to a proliferative hematopoiesis with clonal advantage, which may explain clonal expansion in PNH or MPN at the level of HSC.
Publication Title
3'UTR-truncated Hmga2 cDNA causes MPN-like hematopoiesis by conferring a clonal growth advantage at the level of HSC in mice.
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens
- 72 Downloadable Samples
- Illumina HiSeq 2500
Description
We report RNA-sequencing data of 80 tumor-educated blood platelet (TEP) samples isolated from 39 patients with lower-grade glioma (LGG) and 41 healthy donors (HD). This dataset can be employed as input for the thromboSeq source code (available via GitHub: https://github.com/MyronBest/) to reproduce the thromboSeq drylab pipeline. Overall design: Blood platelets were isolated from whole blood in purple-cap BD Vacutainers containing EDTA anti-coagulant by standard centrifugation. Total RNA was extracted from the platelet pellet, subjected to cDNA synthesis and SMARTer amplification, fragmented by Covaris shearing, and prepared for sequencing using the Truseq Nano DNA Sample Preparation Kit. Subsequently, pooled sample libraries were sequenced on the Illumina Hiseq 2500 platform. All steps were quality-controlled using Bioanalyzer 2100 with RNA 6000 Picochip, DNA 7500 and DNA High Sensitivity chips measurements. For further downstream analyses, reads were quality-controlled using Trimmomatic, mapped to the humane reference genome using STAR, and intron-spanning reads were summarized using HTSeq.
Publication Title
RNA sequencing and swarm intelligence-enhanced classification algorithm development for blood-based disease diagnostics using spliced blood platelet RNA.
Sample Metadata Fields
Specimen part, Disease stage, Subject
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