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GSE25096
Mus musculus
12 Downloadable Samples
mouse-6 v1.1 (Illumina), Agilent-014868 Whole Mouse Genome Microarray 4x44K G4122F (Feature Number version)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
HoxA3 is an apical regulator of haemogenic endothelium.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 12 Downloadable Samples
mouse-6 v1.1 (Illumina)
Description
We used a murine ES cell line in which HoxA3 expression is under control of a tetracycline-responsive element and differentiated these cells as embryoid bodies (EBs). Endothelial (Flk-1 VE-cadherin double positive, FV) and hematopoieitc progenitors (c-Kit CD41 double positive, K41) were isolated from differentiated EBs that had been induced for 6 hours by doxycycline (Dox) treatment.
Publication Title
HoxA3 is an apical regulator of haemogenic endothelium.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 18 Downloadable Samples
- Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
Controlled decay of cytokine and chemokine mRNAs restrains the time and amplitude of inflammatory responses. Tristetraprolin (TTP) binds to AU-rich elements in 3 untranslated regions of mRNA and targets the bound mRNA for degradation. We have addressed here the function of TTP in balancing the macrophage activation state by a comprehensive analysis of TTP-dependent mRNA decay in LPS-stimulated macrophages from WT and TTP-deficient mice.
Publication Title
Tristetraprolin-driven regulatory circuit controls quality and timing of mRNA decay in inflammation.
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens
- 21 Downloadable Samples
- Affymetrix HT Human Genome U133A Array (hthgu133a)
Description
Microarrays were used to determine relative global gene expression changes upon introduction of EMT-inducing or control vectors.
Publication Title
Core epithelial-to-mesenchymal transition interactome gene-expression signature is associated with claudin-low and metaplastic breast cancer subtypes.
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens
- 24 Downloadable Samples
- Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
Muscle contraction during exercise is the major stimulus for the release of peptides and proteins (myokines) that are supposed to take part in the benefical adaptation to exercise. We hypothesize that application of an in vitro exercise stimulus as electric pulse stimulation (EPS) to human myotubes enables the investigation of the human muscle secretome in a clearly defined model. We applied EPS for 24 h to primary human myotubes and studied the whole genome-wide transcriptional response and as well as the release of candidate myokines. We observed 183 differentially regulated transcripts with fold-changes > 1.3. The transcriptional response resembles several properties of the in vivo situation in the skeletal muscle after endurance exercise, namely significant enrichment of pathways associated with interleukin and chemokine signaling, lipid metabolism, and anti-oxidant defense; notably without increased release of creatin kinase.
Publication Title
Cytokine response of primary human myotubes in an in vitro exercise model.
Sample Metadata Fields
Sex, Specimen part, Subject
View Samples- Mus musculus
- 24 Downloadable Samples
- Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
The key lipid metabolism transcription factor sterol regulatory element-binding protein (SREBP)-1a integrates gene regulatory effects of hormones, cytokines, nutrition and metabolites as lipids, glucose or cholesterol via stimuli specific phosphorylation by different MAPK cascades. We have formerly reported the systemic impact of phosphorylation in transgenic mouse models with liver-specific overexpression of the N-terminal transcriptional active domain of SREBP-1a (alb-SREBP-1a) or a MAPK kinase phosphorylation sites deficient variant (alb-SREBP-1aP; (S63A, S117A, T426V)), respectively. Here we investigated the molecular basis of the systemic observation in holistic hepatic gene expression analyses and lipid degrading organelles involved in the pathogenesis of metabolic syndrome, i.e. peroxisomes, by 2D-DIGE and mass spectrometry analyses. Although alb-SREBP-1a mice develop a severe phenotype with visceral adipositas and hepatic lipid accumulation featuring a fatty liver, the hepatic differential gene expression and alterations in peroxisomal protein patterns compared to control mice were surprisingly relative low. In contrast, phosphorylation site deficient alb-SREBP-1aP mice, protected from hepatic lipid accumulation phenotype, showed gross alteration in hepatic gene expression and peroxisomal proteome. Further knowledge based analyzes revealed that overexpression of SREBP-1a favored mainly acceleration in lipid metabolism and indicated a regular insulin signaling, whereas disruption of SREBP-1a phosphorylation resulted in massive alteration of cellular processes including signs for loss of lipid metabolic targets. These results could be the link to a disturbed lipid metabolism that overall resembles a state of insulin resistance.
Publication Title
Inactivation of SREBP-1a Phosphorylation Prevents Fatty Liver Disease in Mice: Identification of Related Signaling Pathways by Gene Expression Profiles in Liver and Proteomes of Peroxisomes.
Sample Metadata Fields
Sex, Age, Specimen part
View Samples- Homo sapiens
- 11 Downloadable Samples
- Affymetrix Human Exon 1.0 ST Array [probe set (exon) version (huex10st)
Description
In order to identify genes with different overall transcript levels or differential exon levels (alternative processing) between the groups Control and Tat-SF1KD, we studied 11 hybridizations on the HumanExon10ST array using mixed model analysis of variance. 526 genes with significant transcript level differences between the groups and 1397 genes with significant differential exon levels were found, including 99 genes with both transcript and exon level differences (p<0.01).
Publication Title
Identification of Tat-SF1 cellular targets by exon array analysis reveals dual roles in transcription and splicing.
Sample Metadata Fields
Cell line
View Samples- Drosophila melanogaster
- 2 Downloadable Samples
- Affymetrix Drosophila Genome 2.0 Array (drosophila2)
Description
Expression data from Kc167 cells under normal conditions. Used to assess expression levels of genes with ORC bound at promoter.
Publication Title
Drosophila ORC localizes to open chromatin and marks sites of cohesin complex loading.
Sample Metadata Fields
Cell line
View Samples- Homo sapiens
- 12 Downloadable Samples
IlluminaHiSeq2000
Description
In a fluorescence polarization screen for MYC-MAX interaction, we have identified a novel small molecule inhibitor of MYC, KJ-Pyr-9, from a Kröhnke pyridine library. The Kd of KJ-Pyr-9 for MYC in vitro is 6.5 ± 1.0 nM as determined by backscattering interferometry; KJ-Pyr-9 also interferes with MYC-MAX complex formation in the cell as shown in a protein fragment complementation assay. KJ-Pyr-9 specifically inhibits MYC-induced oncogenic transformation in cell culture; it has no or only weak effects on the oncogenic activity of several unrelated oncoproteins. KJ-Pyr-9 preferentially interferes with the proliferation of MYC-overexpressing human and avian cells and specifically reduces the MYC-driven transcriptional signature. In vivo, KJ-Pyr-9 effectively blocks the growth of a xenotransplant of MYC-overexpressing human cancer cells. Overall design: 4 treatment groups analyzed in triplicate: no treatment(control), 20uM KJ-Pyr-9, 0.1ug/mL doxycycline and KJ-Pyr-9 in combination with doxycycline
Publication Title
Inhibitor of MYC identified in a Kröhnke pyridine library.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 9 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
Major causes of lipid accumulation in liver are increased import, synthesis or decreased catabolism of fatty acids. The latter is caused by dysfunction of cellular organelle controlling energy homeostasis, i.e. mitochondria. However, peroxisomes appear to be an important organelle in lipid metabolism of hepatocytes, but little is known about their role in the development of non-alcoholic fatty liver disease (NAFLD). To investigate the role of peroxisomes next to mitochondria in excessive hepatic lipid accumulation we used the leptin resistant db/db mice on C57BLKS background, a mouse model that develops hyperphagia induced diabetes with obesity and NAFLD.
Publication Title
Peroxisomes compensate hepatic lipid overflow in mice with fatty liver.
Sample Metadata Fields
Sex, Age, Specimen part
View Samples