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GSE32265
Mus musculus
5 Downloadable Samples
Description
We investigated the role of mTORC1 in murine hematopoiesis by conditionally deleting the Raptor gene in murine hematopoietic stem cells. We observed mutliple alterations evoked by Raptor loss in hematopoiesis and profiled gene-expression alterations induced by raptor loss in Flt3-Lin-Sca1+cKit+ hematopoietic stem and progenitor enriched cell populations, 5 weeks post Raptor deletion.
Publication Title
mTOR complex 1 plays critical roles in hematopoiesis and Pten-loss-evoked leukemogenesis.
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Specimen part
View Samples- Mus musculus
- 4 Downloadable Samples
Description
Epigenetically silenced Ink4a-Arf locus is activated by loss of H3K27me3 in cellular senescence, where secreted factor expression is also involved. Here we analyzed epigenome and transcriptome alteration during Ras-induced senescence using mouse embryonic fibroblast (MEF). Seventeen genes with H3K27me3 loss and H3K4me3 gain showed marked upregulation, including p16Ink4a and Bmp2, a secreted factor for BMP/SMAD signal. Smad6, specific BMP/SMAD pathway inhibitor, was identified as the only one gene showing de novo H3K27 trimethylation with H3K4me3, resulting in strong repression. Ras-activated cells senesced with SMAD1/5/8 phosphorylation, and they escaped from senescence with decreased SMAD1/5/8 phosphorylation when introducing Smad6 or knocking-down Bmp2.
Publication Title
Activation of Bmp2-Smad1 signal and its regulation by coordinated alteration of H3K27 trimethylation in Ras-induced senescence.
Alternate Accession IDs
Sample Metadata Fields
Specimen part, Treatment
View Samples- Mus musculus
- 6 Downloadable Samples
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
FAD-dependent lysine-specific demethylase-1 regulates cellular energy expenditure.
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Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 4 Downloadable Samples
Description
Adipogenic differentiation and metabolic adaptation are initiated through transcriptional and epigenetic reprogramming. In particular, dynamic changes in histone modifications may play central roles in the rearrangement of gene expression patterns. LSD1 (KDM1) protein, encoded by aof2 gene, is a histone demethylase, which is involved in transcriptional regulation. Since the enzymatic activity of LSD1 is FAD (flavin adenine dinucleotide)-dependent, its effects on gene expression may be influenced by FAD availability.
Publication Title
FAD-dependent lysine-specific demethylase-1 regulates cellular energy expenditure.
Alternate Accession IDs
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 2 Downloadable Samples
Description
Adipogenic differentiation and metabolic adaptation are initiated through transcriptional and epigenetic reprogramming. In particular, dynamic changes in histone modifications may play central roles in the rearrangement of gene expression patterns. BHC80 protein, encoded by phf21a gene, is a part of LSD1 histone demethylase complex and is essential for the demethylation activity.
Publication Title
FAD-dependent lysine-specific demethylase-1 regulates cellular energy expenditure.
Alternate Accession IDs
Sample Metadata Fields
Specimen part
View Samples- Mus musculus, Rattus norvegicus
- 26 Downloadable Samples
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
BET bromodomains mediate transcriptional pause release in heart failure.
Alternate Accession IDs
Sample Metadata Fields
Age, Specimen part, Treatment
View Samples- Mus musculus
- 4 Downloadable Samples
Description
Analysis of differentiating LSD1-KD C2C12 myoblasts. We found LSD1 is an important regulator of oxidative phenotypes in skeletal muscle cells.
Publication Title
LSD1 mediates metabolic reprogramming by glucocorticoids during myogenic differentiation.
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Sample Metadata Fields
Specimen part, Cell line
View Samples- Mus musculus
- 7 Downloadable Samples
Description
Objective Previous studies showed that genetic deletion or pharmacological blockade of the Receptor for Advanced Glycation Endproducts (RAGE) prevents the early structural changes in the glomerulus associated with diabetic nephropathy (DN). To overcome limitations of mouse models that lack the progressive glomerulosclerosis observed in humans, we studied the contribution of RAGE to DN in the OVE26 type 1 mouse, a model of progressive glomerulosclerosis and decline of renal function.
Publication Title
Deletion of the receptor for advanced glycation end products reduces glomerulosclerosis and preserves renal function in the diabetic OVE26 mouse.
Alternate Accession IDs
Sample Metadata Fields
Sex, Age, Specimen part, Disease, Disease stage
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