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GSE36583
Mus musculus
2 Downloadable Samples
Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
The mammalian liver, the largest solid organ in the body, accomplishes multiple critical roles necessary to preserve homeostasis. Human liver diseases are debilitating, costly and very often result in death. Uncovering developmental mechanisms that establish the complex architecture of the liver or generate the cellular diversity of this organ is necessary to develop more adequate methods to prevent, diagnose and cure liver diseases. This study investigated the role of the homeobox gene Prox1 during mouse hepatogenesis.
Publication Title
Prox1 ablation in hepatic progenitors causes defective hepatocyte specification and increases biliary cell commitment.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 6 Downloadable Samples
- Affymetrix Mouse Gene 2.0 ST Array (mogene20st)
Description
Impact of mmu-miR-337-3p on the global gene expression in murine hepatoblasts.
Publication Title
MicroRNA-337-3p controls hepatobiliary gene expression and transcriptional dynamics during hepatic cell differentiation.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 73 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
The functioning of a specific tissue depends on the expression pattern of the different genes. We used microarrays to compare gene expression across different murine tissues, to get a better understanding in the expression pattern and functioning of the different tissues. With this analysis, we were not only able to identify genes that were specifically expressed in a spicific tissue but, as important, we also identified genes that were specifically repressed in a tissue, compared to al the other analysed tissues.
Publication Title
Tissue-specific disallowance of housekeeping genes: the other face of cell differentiation.
Sample Metadata Fields
Sex, Specimen part
View Samples- Mus musculus
- 40 Downloadable Samples
- Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
We used Affymetrix Gene Arrays (1.0 ST) to compare gene expression across different murine tissues.
Publication Title
Tissue-specific disallowance of housekeeping genes: the other face of cell differentiation.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 7 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
Glis3 mutant mice (Glis3zf/zf) die within the first week after birth due to overt diabetes, evidenced by hyperglycemia and hypoinsulinemia. Histopathological analysis showed that Glis3zf/zf mice develop a pancreatic phenotype with a dramatic loss of beta- (insulin) and delta- (somatostatin) cells contrasting a smaller relative loss of alpha- (glucagon), PP- (pancreatic polypeptide), and epsilon- (ghrelin) cells. Glis3zf/zf mice develop ductal cysts with decreased number of primary cilia, while the acini are not significantly affected. Gene expression profiling by microarray analysis demonstrated that the expression of terminal hormonal genes and several transcription factors important in endocrine development were significantly deregulated in Glis3zf/zf mice. During pancreatic development, Glis3 mRNA expression is induced during the secondary transition, a stage of cell lineage specification and extensive patterning. Changes in pancreatic development of Glis3zf/zf mice are noted during and after this stage. The population of pancreatic progenitors appears not to be greatly affected in Glis3zf/zf mice; however, the number of neurogenin 3 (Ngn3) positive, endocrine progenitors is significantly reduced. Our study indicates that Glis3 plays a key role in cell lineage specification, particularly the development of mature pancreatic beta-cells. In addition, we identified evidence that Glis3 regulates insulin gene expression through two Glis-binding sites in its proximal promoter indicating that Glis3 is a regulator of insulin gene expression.
Publication Title
Transcription factor Glis3, a novel critical player in the regulation of pancreatic beta-cell development and insulin gene expression.
Sample Metadata Fields
Specimen part
View Samples- Drosophila melanogaster
- 12 Downloadable Samples
Illumina HiSeq 2000, Illumina HiSeq 2500
Description
Spiroplasma (Mollicutes) is one of the heritable bacterial endosymbionts of Drosophila species. Several strains like S. poulsonii manipulate host reproduction in a selfish manner. When females of D. melanogaster are infected with natural S. poulsonii strain MSRO (melanogaster sex ratio organism), only male offspring are killed during embryogenesis, and this phenomenon is called male-killing. To understand the molecular mechanism of male-killing, we compared gene expression profiles between MSRO-infected and uninfected embryos of D. melanogaster by using RNA-sequencing (RNA-seq). For embryonic sexing, we employed a transgenic reporter strain Sex-lethal (Sxl)-Pe-EGFP, which expresses GFP only in females. We collected female and male embryos at stage 10-11, when abnormal apoptosis associated with male-killing starts to occur in male progenies. For each sample, we analyzed three biological replicates.
Publication Title
Male-killing symbiont damages host's dosage-compensated sex chromosome to induce embryonic apoptosis.
Sample Metadata Fields
No sample metadata fields
View Samples- Drosophila melanogaster
- 48 Downloadable Samples
- Illumina HiSeq 2000
Description
Organisms need to assess their nutritional state and adapt their digestive capacity to the demands for various nutrients. Modulation of digestive enzyme production represents a rational step to regulate nutriment uptake. However, the role of digestion in nutrient homeostasis has been largely neglected. In this study, we analyzed the mechanism underlying glucose repression of digestive enzymes in the adult Drosophila midgut. We demonstrate that glucose represses the expression of many carbohydrases and lipases. Our data reveal that the consumption of nutritious sugars stimulates the secretion of the transforming growth factor ß (TGF-ß) ligand, Dawdle, from the fat body. Dawdle then acts via circulation to activate TGF-ß/Activin signaling in the midgut, culminating in the repression of digestive enzymes that are highly expressed during starvation. Thus, our study not only identifies a mechanism that couples sugar sensing with digestive enzyme expression but points to an important role of TGF-ß/Activin signaling in sugar metabolism. Overall design: RNA-sequencing of whole guts from Drosophila melannogaster OregonR adult females was performed under three feeding conditions: Standard medium, glucose, and agar. Three biological repeats were performed for each condition.
Publication Title
Transforming growth factor β/activin signaling functions as a sugar-sensing feedback loop to regulate digestive enzyme expression.
Sample Metadata Fields
Specimen part, Cell line, Subject
View Samples- Mus musculus
- 7 Downloadable Samples
- Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
Using mouse lung resident conventional CD11b+ dendritic cells (CD11b+ cDCs) in the context of house-dust mite (HDM)-driven allergic airway sensitization as a model, we aimed here to identify transcriptional events regulating the pro-Th2 activity of cDCs.
Publication Title
Interferon response factor-3 promotes the pro-Th2 activity of mouse lung CD11b<sup>+</sup> conventional dendritic cells in response to house dust mite allergens.
Sample Metadata Fields
Sex, Specimen part
View Samples- Mus musculus
- 6 Downloadable Samples
- Illumina HiSeq 2000
Description
TSHZ3, which encodes a zinc-finger transcription factor, was recently positioned as a hub gene in a module of genes with the highest expression in the developing human neocortex, but its functions remained unknown. Here, we identify TSHZ3 as the critical region for a syndrome associated with heterozygous deletions at 19q12q13.11, which includes autism spectrum disorder (ASD). In Tshz3 null mice, differentially expressed genes include layer-specific markers of cerebral cortical projection neurons (CPNs) and their human orthologues are strongly associated with ASD. Furthermore, heterozygous Tshz3-deficient mice show functional changes at synapses established by CPNs and exhibit core ASD-like behavioral abnormalities. These findings reveal essential roles for Tshz3 in CPN development and function, whose alterations can account for ASD in the newly-defined TSHZ3 deletion syndrome. Overall design: Three independent replicates, each containing cortices from 3-4 embryos from multiple litters, were prepared from wild-type and Tshz3 mutant neocortex at E18.5. Caubit et al., TSHZ3 deletion causes an autism syndrome and defects in cortical projection neurons. Nat. Genet ###, xxx-yyy (2016).
Publication Title
TSHZ3 deletion causes an autism syndrome and defects in cortical projection neurons.
Sample Metadata Fields
Specimen part, Subject
View Samples- Homo sapiens
- 11 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Aberrant signal transduction contributes substantially to leukemogenesis. The Janus kinase 1 (JAK1) gene encodes a cytoplasmic tyrosine kinase that noncovalently associates with a variety of cytokine receptors and plays a nonredundant role in lymphoid cell precursor proliferation, survival, and differentiation. Somatic mutations in JAK1 occur in individuals with acute lymphoblastic leukemia (ALL). JAK1 mutations were more prevalent among adult subjects with the T cell precursor ALL, where they accounted for 18% of cases, and were associated with advanced age at diagnosis, poor response to therapy, and overall prognosis
Publication Title
ALL-associated JAK1 mutations confer hypersensitivity to the antiproliferative effect of type I interferon.
Sample Metadata Fields
Specimen part
View Samples