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SRP145098
Rattus norvegicus
9 Downloadable Samples
Illumina HiSeq 4000
Description
RNA seq analyses were performed in granulosa cells (GCs) collected from gonadotropin treated ESR2 mutant rats. Data obtained from a null mutant with Esr2 exon 3 deletion (?3) and another DNA binding domain (DBD) mutant with exon 4 deletion (?4) were compared to that of wildtype (WT) rats. The raw data were analyzed using CLC genomics workbench. High quality RNA-sequencing reads were aligned to the Rattus norvegicus genome. Differentially expressed genes in ?3 or ?4 Esr2-mutant GCs were identified based on the following criteria: FDR p-Value =0.05 and an absolute fold change of 2. Fewer differentially expressed genes were identified in ?3 compared to the ?4 mutant group. As both of the mutant groups demonstrated a common phenotype of ovulation failure, differentially expressed genes common to both in ?3 and ?4 mutant rats were emphasized and further analyzed in the companion article “ESR2 regulates granulosa cell genes essential for follicle maturation and ovulation” (Khristi et al., 2018).
Publication Title
ESR2 regulates granulosa cell genes essential for follicle maturation and ovulation.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 24 Downloadable Samples
- Illumina HiSeq 2000
Description
Background: Arrhythmogenic cardiomyopathy (ACM) is a genetic autosomal disease characterized by abnormal cell-cell adhesion, cardiomyocyte death, progressive fibro-adipose replacement of the myocardium, arrhythmias and sudden death. Several different cell types contribute to the pathogenesis of ACM, including, as recently described, cardiac stromal cells (CStCs). In the present study, we aim to identify ACM-specific expression profiles of human CStCs derived from endomyocardial biopsies of ACM patients and healthy individuals employing TaqMan Low Density Arrays for miRNA expression profiling, and high throughput sequencing for gene expression quantification. Results: We identified 5 miRNAs and 272 genes as significantly differentially expressed. Both the differentially expressed genes as well as the target genes of the ACM-specific miRNAs were found to be enriched in cell adhesion related biological processes. Functional similarity and protein interaction based network analyses performed on the identified deregulated genes, miRNA targets and known ACM-causative genes revealed clusters of highly related genes involved in cell adhesion, extracellular matrix organization, lipid transport and ephrin receptor signaling. Conclusions: We determined for the first time the coding and non-coding transcriptome characteristic of ACM cardiac stromal cells, finding evidence for a potential contribution of miRNAs to ACM pathogenesis or phenotype maintenance. Besides known pathways, we identified also deregulation of genes encoding ephrin receptors and ephrins, thus suggesting a potential involvement of Eph-ephrin signaling in CStCs from ACM hearts. Overall design: Expression profiles of cardiac stromal cells from 3 ACM patients were compared against those of cardiac stromal cells from 3 healthy individuals.
Publication Title
The arrhythmogenic cardiomyopathy-specific coding and non-coding transcriptome in human cardiac stromal cells.
Sample Metadata Fields
Sex, Disease, Subject
View Samples- Mus musculus
- 15 Downloadable Samples
Affymetrix Mouse Gene 2.0 ST Array (mogene20st)
Description
Uremic media calcification is not only driven by systemic factors such as hyperphosphatemia, but also crticially dependent on vascular smooth muscle cells per se. We hypothesized that the different developmental origins of vscular smooth muscle cells might lead to a heterogeneous susceptibility to develop media calcification.
Publication Title
Heterogeneous susceptibility for uraemic media calcification and concomitant inflammation within the arterial tree.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 78 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
Proper cortical development relies on the balance of neuronal migration and proliferation. We investigated the gene expression differences of mouse knock-outs for Lissencephaly in humans.
Publication Title
Global developmental gene expression and pathway analysis of normal brain development and mouse models of human neuronal migration defects.
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens
- 147 Downloadable Samples
- Illumina HumanHT-12 V4.0 expression beadchip
Description
The disrupted genetic mechanisms underlying neural abnormalities in Autism Spectrum Disorder remain mostly unknown and speculative. No biological marker nor genetic signature is currently available to assist with early diagnosis.
Publication Title
Prediction of autism by translation and immune/inflammation coexpressed genes in toddlers from pediatric community practices.
Sample Metadata Fields
Sex, Specimen part
View Samples- Homo sapiens
- 6 Downloadable Samples
- Affymetrix Human Exon 1.0 ST Array [probe set (exon) version (huex10st)
Description
Transcriptome analysis of control and MALAT1 lncRNA-depleted RNA samples from human diploid lung fibroblasts [WI38]
Publication Title
Long noncoding RNA MALAT1 controls cell cycle progression by regulating the expression of oncogenic transcription factor B-MYB.
Sample Metadata Fields
Specimen part, Cell line
View Samples- Mus musculus
- 6 Downloadable Samples
- Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
VAChT KDHOM mice have a 70% decrease in the vesicular acetylcholine transporter (VAChT) and this leads to a systemic decrease in ACh release and cardiac dysfunction.
Publication Title
An analysis of the myocardial transcriptome in a mouse model of cardiac dysfunction with decreased cholinergic neurotransmission.
Sample Metadata Fields
Sex, Age, Specimen part
View Samples- Mus musculus
- 6 Downloadable Samples
- Affymetrix Mouse Gene 1.1 ST Array (mogene11st)
Description
We have previously shown that total estrogen receptor alpha (ERalpha knockout (KO) mice exhibit hepatic insulin resistance. To investigate the contribution of hepatic ERalpha action for the observed phenotype, we established a liver-selective ERalphaKO mouse model, LERKO. We demonstrate that LERKO mice have efficient reduction of ERalpha selectively within the liver. However, LERKO and wild type control mice do not differ in body weight, and have a comparable hormone profile as well as insulin and glucose response, even when challenged with a high fat diet. Furthermore, LERKO mice display very minor changes in their hepatic transcript profile. Collectively, our findings indicate that hepatic ERalpha action may not be the initiating factor for the previously identified hepatic insulin resistance in ERalphaKO mice.
Publication Title
Estrogen signalling and the metabolic syndrome: targeting the hepatic estrogen receptor alpha action.
Sample Metadata Fields
Sex, Specimen part
View Samples- Homo sapiens
- 6 Downloadable Samples
- Illumina HumanHT-12 V4.0 expression beadchip
Description
Long non-coding RNAs (lncRNAs) regulate vital biological processes, including cell proliferation, differentiation and development. A subclass of lncRNAs is synthesized from microRNA host genes (MIRHGs) due to pre-miRNA processing, and is categorized as miRNA-host gene lncRNAs (lnc-miRHGs). Presently, it is not clear whether lnc-miRHG perform additional functions. We demonstrate a miRNA-independent role for a nuclear-enriched lnc-miRHG in cell cycle progression. MIR100HG produces spliced and stable lncRNAs (lnc-MIR100HG) that display elevated levels during the G1 phase of the cell cycle. Depletion of lnc-MIR100HG in human cells results in aberrant cell cycle progression with out altering the levels of miRNA encoded within MIR100HG. Notably, lnc-MIR100HG interacts with the HuR/Elav as well as with several of HuR-target mRNAs. Further, lnc-MIR100HG-depleted cells show reduced interaction between HuR and its target mRNAs, indicating that lnc-MIR100HG facilitates interaction between HuR and target mRNAs. Our studies have unearthed novel roles played by miRHG-encoded lncRNAs in regulating RNA binding protein activity, thereby underscoring the importance of determining the function of several hundreds of miRHG lncRNAs that are present in human genome.
Publication Title
MIR100 host gene-encoded lncRNAs regulate cell cycle by modulating the interaction between HuR and its target mRNAs.
Sample Metadata Fields
Cell line, Treatment
View Samples- Drosophila melanogaster
- 24 Downloadable Samples
- Illumina HiSeq 2500
Description
In order to study the transcriptional response of the fly brain to sugar and complete starvation, we first confirmed that 24 hours of sugar and complete starvation in flies is sufficient to elicit a homeostatic response. Subsequently, we used holidic medium to study effects of deficiency of a specfic macronutrient- cabohydrate in the food. To do so , we generated RNA- seq libraries from brains of 5 day old mated adult male flies maintained on different feeding regimes and used the sequencing data to identify diffrentially expressed genes in the brain under different feeding regimes. Overall design: For each condition, we used RNA prepared from 120-130 manually dissected adult fly brains maintained under complete starvation or sugar starvation regime for 24 hours.
Publication Title
Sugar Promotes Feeding in Flies via the Serine Protease Homolog scarface.
Sample Metadata Fields
Sex, Specimen part, Cell line, Subject
View Samples