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SRP167832
Mus musculus
12 Downloadable Samples
Illumina HiSeq 2500
Description
Phospho-ribosome associated RNAs were immunopurified using the antibodies against phospho-S6. The purified RNAs were converted to cDNAs, which were sequenced in Illumina HiSeq platform. Vomeronasal organs were extracted from male CD-1 animals exposed to either pup cues or fresh bedding. Overall design: Total of 6 samples, 2 conditions and 3 replicates
Publication Title
Multisensory Logic of Infant-Directed Aggression by Males.
Sample Metadata Fields
Sex, Specimen part, Cell line, Subject
View Samples- Rattus norvegicus
- 8 Downloadable Samples
Affymetrix Rat Genome 230 2.0 Array (rat2302)
Description
A high phosphorus (HP) diet causes disorders of renal function, bone metabolism, and vascular function. We previously demonstrated that DNA microarray analysis is an appropriate method to comprehensively evaluate the effects of a HP diet on kidney dysfunction such as calcification, fibrillization, and inflammation. We reported that type IIb sodium-dependent phosphate transporter is significantly up-regulated in this context. In the present study, we performed DNA microarray analysis to investigate the effects of a HP diet on the liver, which plays a pivotal role in energy metabolism. DNA microarray analysis was performed with total RNA isolated from the livers of rats fed a control diet (containing 0.3% phosphorus) or a HP diet (containing 1.2% phosphorus). Gene Ontology analysis of differentially expressed genes (DEGs) revealed that the HP diet induced down-regulation of genes involved in hepatic amino acid catabolism and lipogenesis, while genes related to fatty acid -oxidation process were up-regulated. Although genes related to fatty acid biosynthesis were down-regulated in HP diet-fed rats, genes important for the elongation and desaturation reactions of omega-3 and -6 fatty acids were up-regulated. Concentrations of hepatic arachidonic acid and eicosapentaenoic acid were increased in HP diet-fed rats. These essential fatty acids activate peroxisome proliferator-activated receptor alpha (PPAR), a transcription factor for fatty acid -oxidation. Evaluation of the upstream regulators of DEGs using Ingenuity Pathway Analysis indicated that PPAR was activated in the livers of HP diet-fed rats. Furthermore, the serum concentration of fibroblast growth factor 21, a hormone secreted from the liver that promotes fatty acid utilization in adipose tissue as a PPAR target gene, was higher (p = 0.054) in HP diet-fed rats than in control diet-fed rats. These data suggest that a HP diet enhances energy expenditure through the utilization of free fatty acids released via lipolysis of white adipose tissue.
Publication Title
A High Phosphorus Diet Affects Lipid Metabolism in Rat Liver: A DNA Microarray Analysis.
Sample Metadata Fields
Sex, Age, Specimen part
View Samples- Mus musculus
- 53 Downloadable Samples
- Affymetrix Murine Genome U74A Version 2 Array (mgu74av2)
Description
NIH-3T3 cells transduced with either EBF1-, PPARg2- or empty vector were stimulated with hormones to initiate adipocyte differentiation. RNA extraction was done using TriZol at d0, d2, d4 and d10 after stimulation. Samples were handled according to standard affymetrix protocols.
Publication Title
Gene expression analysis suggests that EBF-1 and PPARgamma2 induce adipogenesis of NIH-3T3 cells with similar efficiency and kinetics.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 15 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
To elucidate the bioactive property of the dietary antioxidant curcumin, we examined tissue distribution and the gene expression- and lipidomic-profiles in epididymal white adipose tissue (eWAT) of the diet-induced obese mice. Dietary intake of curcumin (0.1% W/W) didnt affect the eWAT weight and the plasma lipid levels but reduced the levels of lipid peroxidation marker in eWAT. Curcumin was a slightly accumulated in eWAT and altered the gene expression associated with eukaryotic translation initiation factor 2 (EIF2) signaling. Curcumin suppressed the endoplasmic reticulum (ER) stress-related eIF2 phospholyration, the accumulation of macrophages and the expression of oxidative stress-sensitive transcription factor NF-B p65 and leptin, whereas anti-inflammatory effect wasnt enough to reduce the TNF- and IFN- levels. Lipidomic- and gene expression analysis suggests that curcumin reduced the contents of some diacylglyverols (DAGs) and DAG derived glycerophospholipids by suppressing the expressions of lipogenesis-related glycerol-3-phosphate acyltransferase 1 and lipolysis-related adipose triglyceride lipase.
Publication Title
Dietary Intake of Curcumin Improves eIF2 Signaling and Reduces Lipid Levels in the White Adipose Tissue of Obese Mice.
Sample Metadata Fields
Sex, Specimen part
View Samples- Homo sapiens
- 14 Downloadable Samples
- Illumina HiSeq 2500
Description
Difference in RNA content of different cell types introduces bias to gene expression deconvolution methods. If ERCC spike-ins are introduced into samples, predicted proportions of deconvolution methods can be corrected Overall design: Two cell types of distinctly different sizes and RNA per cell content: HEK cells and Jurkat cells were mixed in different proportions ensuring that each mixture contained total of one million cells. We sequenced RNA of the samples (including ERCC spike-in controls to 382 be able to control for the absolute RNA-concentration).
Publication Title
Complete deconvolution of cellular mixtures based on linearity of transcriptional signatures.
Sample Metadata Fields
Cell line, Subject
View Samples- Homo sapiens
- 5 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Idiopathic pulmonary fibrosis (IPF) is associated with the accumulation of collagen-secreting fibroblasts and myofibroblasts in the lung parenchyma. Many mechanisms contribute to their accumulation, including resistance to apoptosis. In previous work, we showed that exposure to the pro-inflammatory cytokines, TNF- and IFN- reverses fibroblast resistance to apoptosis. The goal of this study was to investigate the underlying mechanism. Based on an initial interrogation of the transcriptomes of unstimulated and TNF- and IFN--stimulated primary lung fibroblasts and the lung fibroblast cell line, MRC5, we show here that among Fas-signaling pathway molecules, Fas expression was increased ~6-fold in an NF-B and p38mapk-dependent fashion. Prevention of the increase in Fas expression using Fas siRNAs blocked the ability of TNF- and IFN- to sensitize fibroblasts to Fas ligation induced-apoptosis; while enforced adenovirus-mediated Fas overexpression was sufficient to overcome basal resistance to Fas-induced apoptosis. Examination of lung tissues from IPF patients revealed low to absent staining of Fas in fibroblastic cells of fibroblast foci. Collectively, these findings suggest that increased expression of Fas is necessary and sufficient to overcome the resistance of lung fibroblasts to Fas-induced apoptosis. They also suggest that approaches aimed at increasing Fas expression by lung fibroblasts and myofibroblasts may be therapeutically relevant.
Publication Title
Increased cell surface Fas expression is necessary and sufficient to sensitize lung fibroblasts to Fas ligation-induced apoptosis: implications for fibroblast accumulation in idiopathic pulmonary fibrosis.
Sample Metadata Fields
Specimen part, Treatment
View Samples- Homo sapiens
- 4 Downloadable Samples
Illumina HumanHT-12 V4.0 expression beadchip, Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
MEK inhibitors activate Wnt signalling and induce stem cell plasticity in colorectal cancer.
Sample Metadata Fields
Specimen part, Treatment
View Samples- Danio rerio
- 6 Downloadable Samples
- IlluminaHiSeq2000
Description
The goal of this study is to compare gene expression levels in the livers of larval Tg(fabp10:nls-mcherry) exposed to 1 mM inorganic arsenic from 4-120 hpf to the unexposed siblings. Samples were collected from Tg(fabp10:nls-mcherry) zebrafish larvae that were derived from incrossed parents of the same strain. The background of transgenic lines were typically from mixed outcrosses of the transgenics to AB, TAB5, and TAB14 strains when regenerating the lines as the working stocks aged. All samples were collected at approximately 120 hpf - natural spawning at 8:30-9:00AM EST on day zero, samples were collected at 8-10AM EST on day 5. Overall design: 10-20 livers from 5dpf embryos were pooled per sample of either control or 1 mM inorganic arsenic exposed Tg(fabp10:nls-mcherry) zebrafish larvae and RNA was extracted using the Zymo Quick-RNA Micro Kit with on-column DNase treatment. Libraries were prepared according to Illumina Truseq RNA sample prep kit, version 2, followed by Ribo-Zero Gold treatment.
Publication Title
Inorganic arsenic causes fatty liver and interacts with ethanol to cause alcoholic liver disease in zebrafish.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 22 Downloadable Samples
- Illumina HumanHT-12 V4.0 expression beadchip
Description
Short sleep duration is associated with adverse metabolic, cardiovascular, and inflammatory effects. Co-twin study methodologies account for familial (e.g., genetics and shared environmental) confounding, allowing assessment of subtle environmental effects, such as the effect of short habitual sleep duration on gene expression. Therefore, we sought to investigate gene expression in monozygotic twins discordant for actigraphically phenotyped habitual sleep duration. Eleven healthy monozygotic twin pairs (82% female; mean age 42.7 years; SD=18.1), selected based on subjective sleep duration discordance, were objectively phenotyped for habitual sleep duration with two-weeks of wrist actigraphy. Peripheral blood leukocyte (PBL) RNA from fasting blood samples was obtained on the final day of actigraphic measurement and hybridized to Illumina humanHT-12 microarrays. Differential gene expression was determined between paired samples and mapped to functional categories using Gene Ontology. Next, a more comprehensive gene set enrichment analysis was performed based on the entire PBL transcriptome. The mean 24 hour sleep duration of the total sample was 439.2 minutes (SD=46.8 minutes; range 325.4 to 521.6 minutes). Mean within-pair sleep duration difference per 24 hours was 64.4 minutes (SD=21.2; range 45.9 to 114.6 minutes). The twin cohort displayed distinctive pathway enrichment based on sleep duration differences. Short sleep was associated with up-regulation of genes involved in transcription, ribosome, translation and oxidative phosphorylation. Unexpectedly, genes down-regulated in short sleep twins were highly enriched in immuno-inflammatory pathways such interleukin signaling and leukocyte activation, as well as developmental programs, coagulation cascade, and cell adhesion. Objectively assessed habitual sleep duration in monozygotic twin pairs appears to be associated with distinct patterns of differential gene expression and pathway enrichment. By accounting for familial confounding and measuring real life sleep duration, our study shows the transcriptomic effects of short sleep on dysregulated immune response and provides a potential link between sleep deprivation and adverse metabolic, cardiovascular and inflammatory outcomes.
Publication Title
Transcriptional Signatures of Sleep Duration Discordance in Monozygotic Twins.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 14 Downloadable Samples
- Illumina HiSeq 2500
Description
The emergence of multidrug resistant (MDR) Mycobacterium tuberculosis (Mtb) strains, resistant to the frontline anti-tubercular drugs rifampicin and isoniazid, forces treatment with less effective and toxic second-line drugs and stands to derail TB control efforts. However, the immune response to MDR Mtb infection remains poorly understood. Here, we determined the RNA transcriptional profile of in vitro generated macrophages to infection with either drug susceptible Mtb HN878 or MDR Mtb W_7642 infection. Overall design: Bone marrow-derived macrophages (BMDMs) from WT and Il1r1–/– mice were derived in 7 days in GM-CSF supplemented complete DMEM. Cells were infected with either Mtb HN878 or Mtb W_7642 (multiplicity of infection = 1) and RNA samples collected after 6 days.
Publication Title
Mycobacterium tuberculosis carrying a rifampicin drug resistance mutation reprograms macrophage metabolism through cell wall lipid changes.
Sample Metadata Fields
Cell line, Subject
View Samples