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Mus musculus
168 Downloadable Samples
NextSeq 500
Description
Increased miR-135a levels are observed in human patients with temporal lobe Epilepsy (TLE) and in experimental animal models. Upon targeting the increased miR-135a levels in vivo using antagomirs in kainic acid induced status epilepticus mouse model of TLE, we observed a strong reduction of spontaneous recurrent seizures. To understand this further and to find target mRNAs that potentially mediate the seizure suppressive function of miR-135a, we performed immunoprecipitation using biotin tagged miRNA mimics, followed by RNAsequencing (RNAseq). We found several novel neuronal targets of miRNA-135a and identified Mef2a as a key target in this study. Here we report the total RNAseq data. Overall design: N2A cells were transfected with biotin tagged miRNA mimics for miR-135a and negative control and immunoprecipitations were performed. N = 3 replicates of IP and input samples for each condition were generated and sequenced on illumina platform for total RNA for identification of novel targets of miR-135a.
Publication Title
Antagonizing Increased <i>miR-135a</i> Levels at the Chronic Stage of Experimental TLE Reduces Spontaneous Recurrent Seizures.
Sample Metadata Fields
Cell line, Subject
View Samples- Homo sapiens
- 6 Downloadable Samples
- Illumina HiSeq 4000
Description
Human T-lymphotropic virus type 1 (HTLV-1) is associated with the development of Adult T-cell Leukemia, an aggressive CD4+ T-cells malignancy. Here, we have developed a new procedure to infect humanized mice with proviruses displaying specific mutations, such as one leading to the loss of the PDZ domain-binding motif (PBM) of Tax. In order to specifically analyze the in vivo role of the PBM of Tax, a comparative study of infected hu-mice was performed. We used next-generation sequencing to perform genome-wide transcriptomic analysis of T-cells infected with wild-type HTLV-1 virus or with virus bearing a mutated form of Tax lacking the PBM. Our results suggest that Tax PBM might be involved in the regulation of genes implicated in proliferation, apoptosis and cytoskeleton organization. Overall design: mRNA profiles of T-cells obtained from hu-Mice infected with wild-type or Tax-PBM HTLV-1 were generated by deep-sequencing in triplicates using Illumina's Hiseq3000 platform.
Publication Title
PDZ domain-binding motif of Tax sustains T-cell proliferation in HTLV-1-infected humanized mice.
Sample Metadata Fields
Specimen part, Subject
View Samples- Mus musculus
- 3 Downloadable Samples
- Illumina HiSeq 2000
Description
We infected Mouse Embryonic Fibroblast and cultured them in anchorage independent conditions to study tranformation induced by the bacterium. We cultured these transformed cells multiple rounds in the presence of Ciprofloxacin to remove intracellular Salmonella after transformation occured. By doing RNA sequencing we indentified genes of which expression was altered upon infection. This helps us to understand how Salmonella alters the host cell, resulting in transformation Overall design: We Cultered two biological duplicates of infected MEF cells, which we compared to a non transformed MEF control sample
Publication Title
Salmonella Manipulation of Host Signaling Pathways Provokes Cellular Transformation Associated with Gallbladder Carcinoma.
Sample Metadata Fields
No sample metadata fields
View Samples- Saccharomyces cerevisiae
- 4 Downloadable Samples
- Illumina HiSeq 2500
Description
As a result of ancestral whole genome and small-scale duplication events, the genome of Saccharomyces cerevisiae's, and of many eukaryotes, still contain a substantial fraction of duplicated genes. In all investigated organisms, metabolic pathways, and more particularly glycolysis, are specifically enriched for functionally redundant paralogs. In ancestors of the Saccharomyces lineage, the duplication of glycolytic genes is purported to have played an important role leading to S. cerevisiae current lifestyle favoring fermentative metabolism even in the presence of oxygen and characterized by a high glycolytic capacity. In modern S. cerevisiae, the 12 glycolytic reactions leading to the biochemical conversion from glucose to ethanol are encoded by 27 paralogs. In order to experimentally explore the physiological role of this genetic redundancy, a yeast strain with a minimal set of 14 paralogs was constructed (MG strain). Remarkably, a combination of quantitative, systems approach and of semi-quantitative analysis in a wide array of growth environments revealed the absence of phenotypic response to the cumulative deletion of 13 glycolytic paralogs. This observation indicates that duplication of glycolytic genes is not a prerequisite for achieving the high glycolytic fluxes and fermentative capacities that are characteristic for S. cerevisiae and essential for many of its industrial applications and argues against gene dosage effects as a means for fixing minor glycolytic paralogs in the yeast genome. MG was carefully designed and constructed to provide a robust, prototrophic platform for quantitative studies, and is made available to the scientific community. Overall design: The goals of the present study are to experimentally explore genetic redundancy in yeast glycolysis by cumulative deletion of minor paralogs and to provide a new experimental platform for fundamental yeast research by constructing a yeast strain with a functional 'minimal glycolysis'. To this end, we deleted 13 minor paralogs, leaving only the 14 major paralogs for the S. cerevisiae glycolytic pathway. The cumulative impact of deleting all minor paralogs was investigated by two complementary approaches. A first, quantitative analysis focused on the impact on glycolytic flux under a number of controlled cultivation conditions that, in wild-type strains, result in different glycolytic fluxes. These quantitative growth studies were combined with transcriptome, enzyme-activity and intracellular metabolite assays to capture potential small phenotypic effects. A second, semi-quantitative characterization explored the phenotype of the 'minimal glycolysis' strain under a wide array of experimental conditions to identify potential context-dependent phenotypes
Publication Title
The Genetic Makeup and Expression of the Glycolytic and Fermentative Pathways Are Highly Conserved Within the <i>Saccharomyces</i> Genus.
Sample Metadata Fields
Cell line, Subject
View Samples- Saccharomyces cerevisiae
- 161 Downloadable Samples
Affymetrix Yeast Genome S98 Array (ygs98)
Description
Background
Publication Title
Combinatorial effects of environmental parameters on transcriptional regulation in Saccharomyces cerevisiae: a quantitative analysis of a compendium of chemostat-based transcriptome data.
Sample Metadata Fields
No sample metadata fields
View Samples
SRP009275- Danio rerio
- 4 Downloadable Samples
- IlluminaGenomeAnalyzerII
Description
small RNA libraries from wild-type and Hen1 mutant testes were made with either polyA tailing (VASAGFPHen1minus/plus) or adapter ligation (Hen1Testis and WTTestis) and sequenced on an Illumina GAII platform. Overall design: RNA was isolated from total testis tissue of both Hen1 wildtype and Hen1 mutant animals. After size selection from gel, the small RNA libraries wre made.
Publication Title
Hen1 is required for oocyte development and piRNA stability in zebrafish.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 10 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Neuroblastoma is a pediatric tumor of the sympathetic nervous system. MYCN (V-myc myelocytomatosis viral-related oncogene, neuroblastoma derived [avian]) is amplified in 20% of neuroblastomas, and these tumors carry a poor prognosis. However, tumors without MYCN amplification also may have a poor outcome. Here, we identified downstream targets of MYCN by shRNA-mediated silencing MYCN in neuroblastoma cells. From these targets, 157 genes showed an expression profile correlating with MYCN mRNA levels in NB88, a series of 88 neuroblastoma tumors, and therefore represent in vivo relevant MYCN pathway genes. This 157-gene signature identified very poor prognosis tumors in NB88 and independent neuroblastoma cohorts and was more powerful than MYCN amplification or MYCN expression alone. Remarkably, this signature also identified poor outcome of a group of tumors without MYCN amplification. Most of these tumors have low MYCN mRNA levels but high nuclear MYCN protein levels, suggesting stabilization of MYCN at the protein level. One tumor has an MYC amplification and high MYC expression. Chip-on-chip analyses showed that most genes in this signature are directly regulated by MYCN. MYCN induces genes functioning in cell cycle and DNA repair while repressing neuronal differentiation genes. The functional MYCN-157 signature recognizes classical neuroblastoma with MYCN amplification, as well as a newly identified group marked by MYCN protein stabilization.
Publication Title
Functional MYCN signature predicts outcome of neuroblastoma irrespective of MYCN amplification.
Sample Metadata Fields
Specimen part, Cell line, Time
View Samples- Homo sapiens
- 18 Downloadable Samples
- Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
Analysis of estrogen receptor (ER)-positive MCF7 cell total RNA expression and polysome-assiciated RNA expression following treatment with estradiol (E2) and vehicle (etoh).
Publication Title
Estrogen coordinates translation and transcription, revealing a role for NRSF in human breast cancer cells.
Sample Metadata Fields
Cell line
View Samples- Homo sapiens
- 41 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Skeletal muscle mitochondrial dysfunction is secondary to T2DM and can be improved by long-term regular exercise training
Publication Title
Physical activity is the key determinant of skeletal muscle mitochondrial function in type 2 diabetes.
Sample Metadata Fields
Age
View Samples- Homo sapiens
- 41 Downloadable Samples
- Affymetrix Human Exon 1.0 ST Array [transcript (gene) version (huex10st)
Description
Expression profiles of anti-TNF responders were compared to profiles of anti-TNF non-responders in order to identify an expression signature for anti-TNF response
Publication Title
Validation study of existing gene expression signatures for anti-TNF treatment in patients with rheumatoid arthritis.
Sample Metadata Fields
Specimen part, Disease, Disease stage, Treatment
View Samples