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SRP043159
Mus musculus
6 Downloadable Samples
Illumina HiSeq 2500
Description
Analysis of gene-probe expression data (FPKM) for mouse skin using single-end read RNA-seq Overall design: RNA was collected and analyzed for 2 biological replicates each from 3 developmental stages (E18.5, P3, 10 weeks)
Publication Title
RNA-seq studies reveal new insights into p63 and the transcriptomic landscape of the mouse skin.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 4 Downloadable Samples
Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
We developed a Tet-inducible system to express deltaNp63alpha isoform under the control of keratin 5 promoter. Transgenic mice, which were Bigenic (BG) developed a severe skin phenotype with abnormal keratinocyte differentiation and defects in hair follicle development and cycling. Skin samples from transgenic animals and wild type animals were analyzed for global transcriptome changes.
Publication Title
Abnormal hair follicle development and altered cell fate of follicular keratinocytes in transgenic mice expressing DeltaNp63alpha.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 2 Downloadable Samples
- Illumina MouseRef-8 v2.0 expression beadchip
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
MAFG is a transcriptional repressor of bile acid synthesis and metabolism.
Sample Metadata Fields
Treatment
View Samples- Mus musculus
- 2 Downloadable Samples
- Illumina MouseRef-8 v2.0 expression beadchip
Description
Specific bile acids are potent signaling molecules that modulate metabolic pathways affecting lipid, glucose and bile acid homeostasis, and the microbiota. Bile acids are synthesized from cholesterol in the liver, and the key enzymes involved in bile acid synthesis (Cyp7a1, Cyp8b1) are regulated transcriptionally by the nuclear receptor FXR. We have identified an FXR-regulated pathway upstream of a transcriptional repressor that controls multiple bile acid metabolism genes. We identify MafG as an FXR target gene and show that hepatic MAFG overexpression represses genes of the bile acid synthetic pathway and modifies the biliary bile acid composition. In contrast, loss-of-function studies using MafG(+/-) mice causes de-repression of the same genes with concordant changes in biliary bile acid levels. Finally, we identify functional MafG response elements in bile acid metabolism genes using ChIP-seq analysis. Our studies identify a molecular mechanism for the complex feedback regulation of bile acid synthesis controlled by FXR
Publication Title
MAFG is a transcriptional repressor of bile acid synthesis and metabolism.
Sample Metadata Fields
Treatment
View Samples- Mus musculus
- 13 Downloadable Samples
- Illumina HiSeq 2500
Description
Analysis of gene expression changes during mouse salivary gland development using RNA-Seq Overall design: RNA was collected and analyzed for at least two biological replicates each from six developmental timepoints (E14.5, E16.5, E18.5, P5, 4 weeks, 12 weeks)
Publication Title
RNA-seq based transcriptomic map reveals new insights into mouse salivary gland development and maturation.
Sample Metadata Fields
Age, Specimen part, Cell line, Subject
View Samples- Homo sapiens
- 382 Downloadable Samples
- Affymetrix HT Human Genome U133A Array (hthgu133a)
Description
Oxidized phospoholipids are a pro-inflammatory component of minimally modified lipoproteins that get trapped in the subendothelial space of atherosclerotic plaques of large arteries. To model the response of endothelial cells in a pro-atherosclerotic enviroment we measured the expression in primary endothelial cells with and without treatment with oxidized phsopolipids from 96 genetically identical donors of anonymous origin.
Publication Title
Systems genetics analysis of gene-by-environment interactions in human cells.
Sample Metadata Fields
Sex, Subject
View Samples- Homo sapiens
- 8 Downloadable Samples
- IlluminaHiSeq2500
Description
Analysis of gene-probe expression data (FPKM) for HNSCC cell-lines using single-end RNA-Seq Overall design: RNA was collected and analyzed from 6 HNSCC cell-lines ( SCC15, SCC4, SCC71, UMSCC103, UMSCC29, SCC351)
Publication Title
A global analysis of the complex landscape of isoforms and regulatory networks of p63 in human cells and tissues.
Sample Metadata Fields
No sample metadata fields
View Samples- Saccharomyces cerevisiae
- 40 Downloadable Samples
- Affymetrix Yeast Genome 2.0 Array (yeast2)
Description
We conducted a set of lab-evolution experiments in yeast and followed the long-term dynamics of aneuploidy under diverse conditions including heat shock and high PH.
Publication Title
Chromosomal duplication is a transient evolutionary solution to stress.
Sample Metadata Fields
No sample metadata fields
View Samples- Drosophila melanogaster
- 18 Downloadable Samples
- Illumina HiSeq 2500
Description
Cancer cells have abnormal gene expression profiles, however, the transcription factors and the architecture of the regulatory network that drive cancer specific gene expression is often not known. Here we studied a model of Ras-driven invasive tumorigenesis in Drosophila epithelial tissues and combined in vivo genetics with high-throughput sequencing and computational modeling to decipher the regulatory logic of tumor cells. Surprisingly, we discovered that the bulk of the tumor specific gene expression is driven by an ectopic network of a few transcription factors that are overexpressed and/or hyperactivated in tumor cells. These factors are Stat, AP-1, the bHLH proteins Myc and AP-4, the nuclear hormone receptor Ftz-f1, the nuclear receptor coactivator Taiman/AIB1, and Mef2. Notably, many of these transcription factors are also hyperactivated in human tumors. Bioinformatics analysis predicted that these factors directly regulate the majority of the tumor specific gene expression, that they are interconnected by extensive cross-regulation, and that they show a high degree of co-regulation of target genes. Indeed, the factors of this network were required in multiple epithelia for tumor growth and invasiveness and knock-down of individual factors caused a reversion of the tumor specific expression profile, but had no observable effect on normal tissues. We further found that the Hippo pathway effector Yki/Sd was strongly activated in tumor cells and initiated cellular reprogramming by activating several transcription factors of this network. Thus, modeling regulatory networks identified an ectopic yet highly ordered network of master regulators that control tumor cell specific gene expression. Overall design: RNA-seq gene expression profiling across Drosophila 3rd instar larval wild type wing discs and genetic perturbations of wts.
Publication Title
An Ectopic Network of Transcription Factors Regulated by Hippo Signaling Drives Growth and Invasion of a Malignant Tumor Model.
Sample Metadata Fields
Subject, Time
View Samples- Mus musculus
- 11 Downloadable Samples
- Illumina HiSeq 2500
Description
Mononuclear phagocytes are a diverse cell family that occupy all tissues and assume numerous functions to support tissue and systemic homeostasis. Our ability to investigate the roles of individual subsets is limited by an absence of approaches to ablate gene function within specific sub-populations. Using Nr4a1-dependent Ly6Clow monocytes as a representative cell type we show that enhancer deletion addresses these limitations. Combining ChIP-Seq and molecular approaches we identify a single, conserved, sub-domain within the Nr4a1 enhancer that is essential for Ly6Clow monocyte development. Mice lacking this enhancer lack Ly6Clow monocytes but retain Nr4a1 gene expression in macrophages during steady state and in response to LPS. Nr4a1 is a key negative regulator of inflammatory gene expression and decoupling these processes allows Ly6Clow monocytes to be studied without confounding influences. Enhancer targeting possesses greater specificity than cre recombinase-mediated gene deletion, providing a route to generate loss-of-function models in closely related cell types. Overall design: Paired End mRNA sequencing of FACS purified primary murine MDP, cMoP, Ly6Chi and Ly6Clow monocytes from the bone marrow and Ly6Chi and Ly6Clow monocytes from the peripheral blood
Publication Title
Deleting an Nr4a1 Super-Enhancer Subdomain Ablates Ly6C<sup>low</sup> Monocytes while Preserving Macrophage Gene Function.
Sample Metadata Fields
Specimen part, Cell line, Subject
View Samples