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Mus musculus
18 Downloadable Samples
Description
Cellular signal transduction is governed by multiple feedback mechanisms to elicit robust cellular decisions. We combined mathematical modeling and extensive time-resolved data sets in primary erythroid progenitor cells and dissected the roles of the two transcriptional feedback regulators of the SOCS family, CIS and SOCS3 in JAK2/STAT5 signaling. Our model revealed that both feedbacks are most effective at different ligand concentration ranges.
Publication Title
Division of labor by dual feedback regulators controls JAK2/STAT5 signaling over broad ligand range.
Sample Metadata Fields
Specimen part
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GSE21746- Mus musculus
- 2 Downloadable Samples
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
A tissue-specific landscape of sense/antisense transcription in the mouse intestine.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 2 Downloadable Samples
Description
Genome wide expression profiling to determine the overlap of Affymetrix-signals with SOLID sequencing
Publication Title
A tissue-specific landscape of sense/antisense transcription in the mouse intestine.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 6 Downloadable Samples
Description
Transcriptom analysis of stellate sympathetic ganglia after 8 weeks of cardiac pressure overload caused by transverse aortic constriction.
Publication Title
Sympathetic alpha(2)-adrenoceptors prevent cardiac hypertrophy and fibrosis in mice at baseline but not after chronic pressure overload.
Sample Metadata Fields
Sex
View Samples- Mus musculus
- 23 Downloadable Samples
Description
Studies investigating the causes of autism spectrum disorder (ASD) point to genetic as well as epigenetic mechanisms of the disease. Identification of epigenetic processes that contribute to ASD development and progression is of major importance and may lead to the development of novel therapeutic strategies. Here we identify the bromodomain and extra-terminal domain containing transcriptional regulators (BETs) as epigenetic drivers of an ASD-like disorder in mice. We found that the pharmacological suppression of the BET proteins by a novel, highly selective and brain-permeable inhibitor, I-BET858, leads to selective suppression of neuronal gene expression followed by the development of an autism-like syndrome in mice. Many of the I-BET858 affected genes have been linked to ASD in humans thus suggesting the key role of the BET-controlled gene network in ASD. Our studies also suggest that environmental factors controlling BET proteins or their target genes may contribute to the epigenetic mechanism of ASD.
Publication Title
Autism-like syndrome is induced by pharmacological suppression of BET proteins in young mice.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 7 Downloadable Samples
Description
JoMa1 cells are pluripotent precursor cells, derived from the neural crest of mice transgenic for tamoxifen-inducible c-Myc. Following transfection with a cDNA encoding for MYCN, cells become immortlized even in the absence of tamoxifen.
Publication Title
MYCN and ALKF1174L are sufficient to drive neuroblastoma development from neural crest progenitor cells.
Sample Metadata Fields
Specimen part, Cell line
View Samples- Mus musculus
- 2 Downloadable Samples
Description
Primary murine osteoblasts were isolated form the calvariae of newborn mice. 10 days after the addition of ascorbic acid (50 g/ml) and -glycerophosphate (10 mM), cells were serum-starved over night and then incubated for 6 hours with condtioned medium of MDA-PCa2b cells or conditioned medium of PC-3 cells
Publication Title
Osteolytic prostate cancer cells induce the expression of specific cytokines in bone-forming osteoblasts through a Stat3/5-dependent mechanism.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 8 Downloadable Samples
Description
Uniparental parthenotes are considered an unwanted byproduct of in vitro fertilization. In utero parthenote development is severely compromised by defective organogenesis and in particular by defective cardiogenesis. Although developmentally compromised, apparently pluripotent stem cells can be derived from parthenogenetic blastocysts. Here we hypothesized that nonembryonic parthenogenetic stem cells (PSCs) can be directed toward the cardiac lineage and applied to tissue-engineered heart repair. We first confirmed similar fundamental properties in murine PSCs and embryonic stem cells (ESCs), despite notable differences in genetic (allelic variability) and epigenetic (differential imprinting) characteristics. Haploidentity of major histocompatibility complexes (MHCs) in PSCs is particularly attractive for allogeneic cell-based therapies. Accordingly, we confirmed acceptance of PSCs in MHC-matched allotransplantation. Cardiomyocyte derivation from PSCs and ESCs was equally effective. The use of cardiomyocyte-restricted GFP enabled cell sorting and documentation of advanced structural and functional maturation in vitro and in vivo. This included seamless electrical integration of PSC-derived cardiomyocytes into recipient myocardium. Finally, we enriched cardiomyocytes to facilitate engineering of force-generating myocardium and demonstrated the utility of this technique in enhancing regional myocardial function after myocardial infarction. Collectively, our data demonstrate pluripotency, with unrestricted cardiogenicity in PSCs, and introduce this unique cell type as an attractive source for tissue-engineered heart repair.
Publication Title
Parthenogenetic stem cells for tissue-engineered heart repair.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 23 Downloadable Samples
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Polycomb repressive complex 2 (PRC2) silences genes responsible for neurodegeneration.
Sample Metadata Fields
Age, Specimen part
View Samples- Mus musculus
- 23 Downloadable Samples
Description
Normal brain function critically depends on the interaction between highly specialized neurons that operate within anatomically and functionally distinct brain regions. The fidelity of neuronal specification is contingent upon the robustness of the transcriptional program that supports the neuron type-specific patterns of gene expression. Changes in neuron type-specific gene expression are commonly associated with neurodegenerative disorders including Huntingtons and Alzheimers disease. The neuronal specification is driven by gene expression programs that are established during early stages of neuronal development and remain in place in the adult brain. Here we show that the Polycomb repressive complex 2 (PRC2), which supports neuron specification during early differentiation, contributes to the suppression of the transcription program that can be detrimental for the adult neuron function. We show that PRC2 deficiency in adult striatal neurons and in cerebellar Purkinje cells impairs the maintenance of neuron-type specific gene expression. The deficiency in PRC2 has a direct impact on a selected group of genes that is dominated by self-regulating transcription factors normally suppressed in these neurons. The age-dependent progressive transcriptional changes in PRC2-deficient neurons are associated with impaired neuronal function and survival and lead to the development of fatal neurodegenerative disorders in mice.
Publication Title
Polycomb repressive complex 2 (PRC2) silences genes responsible for neurodegeneration.
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