We used microarrays to identify the gene expression changes after SET knockdown in ESCs and 4 day RA differentiated ESCs
Alternative SET/TAFI Promoters Regulate Embryonic Stem Cell Differentiation.
Specimen part
View SamplesWe used microarrays to identify the gene expression changes after Smarcd1 knockdown in ESCs and 4 day RA differentiated ESCs
Differential association of chromatin proteins identifies BAF60a/SMARCD1 as a regulator of embryonic stem cell differentiation.
Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Heterochromatin Protein 1β (HP1β) has distinct functions and distinct nuclear distribution in pluripotent versus differentiated cells.
Specimen part, Cell line
View SamplesWe used microarrays to identify the gene expression changes in Cbx1-/- (HP1beta) knockout embryonic stem cells (ESCs) and Cbx5-/- (HP1alpha) knockout ESCs compared to WT ESCs and in embryoid bodies (EBs) differentiated from those three ESC types.
Heterochromatin Protein 1β (HP1β) has distinct functions and distinct nuclear distribution in pluripotent versus differentiated cells.
Specimen part, Cell line
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Chromatinized protein kinase C-θ directly regulates inducible genes in epithelial to mesenchymal transition and breast cancer stem cells.
Cell line, Treatment
View SamplesEpithelial to mesenchymal transition (EMT) is activated during cancer invasion and metastasis, enriches for cancer stem cells (CSCs), and contributes to therapeutic resistance and disease recurrence. The epithelial cell line MCF7, can be induced to undergo EMT with the induction of PKC by PMA. 5-10% of the resulting cells have a CSC phenotype. This study looks at the transcriptome of these cells and how it differs from cells with a non-CSC phenotype.
Chromatinized protein kinase C-θ directly regulates inducible genes in epithelial to mesenchymal transition and breast cancer stem cells.
Cell line, Treatment
View SamplesEpigenetic modifications have emerged as central players in the coordination of gene expression networks during cardiac development. While several studies have investigated the role of histone modifications during heart development, relatively little is known about the role of DNA methylation. The purpose of the current study was to determine whether DNA methylation plays an important role in guiding transcriptional changes during the neonatal period, which is an important developmental window for cardiac maturation and cardiomyocyte cell cycle arrest. We used methyl binding domain protein sequencing (MBD-seq) and mRNA-seq to profile DNA methyation and gene expression respectively in neonatal hearts at P1 and P14 stages. Thousands of differentially methylated regions (DMRs) were identified between P1 and P14, the vast majority of which were hypermethylated. Gene ontology analysis revealed that these hypermethylated genes were associated with transcriptional regulation of important developmental signaling pathways, including Hedgehog, BMP, TGF beta, FGF and Wnt/b-catenin signaling. A significant enrichment for myogenic transcription factors and Smad2/3/4 binding sites was also noted among differentially methylated peaks at P14. This study provides novel evidence for widespread alterations in DNA methylation during post-natal heart maturation and suggests that DNA methylation plays an important role in cardiomyocyte cell cycle arrest during the neonatal period. Overall design: mRNA-seq to profile gene expression in neonatal hearts at P1 and P14 stages (post-natal day 1 and 14 respectively) in three biological replicates.
Dynamic changes in the cardiac methylome during postnatal development.
No sample metadata fields
View SamplesDespite significant advances in our understanding of the biology determining systemic energy homeostasis, the treatment of obesity remains a medical challenge. Activation of AMP-activated protein kinase (AMPK) has been proposed as an attractive strategy for the treatment of obesity and its complications. AMPK is a conserved, ubiquitously expressed, heterotrimeric serine/threonine kinase whose short-term activation has multiple beneficial metabolic effects. Whether these translate into long-term benefits for obesity and its complications is unknown. Here, we observe that mice with chronic AMPK activation, resulting from mutation of the AMPK ?2 subunit, exhibit ghrelin signalling-dependent hyperphagia, obesity and impaired pancreatic islet insulin secretion. Humans bearing the homologous mutation manifest a congruent phenotype. Our studies highlight that long-term AMPK activation can have adverse metabolic consequences with implications for pharmacological strategies seeking to chronically activate AMPK systemically to treat metabolic disease. Overall design: Transcriptomic profiling of the hypothalamic arcuate nucleus from AMPK ?2 R299Q knock-in mice
Chronic Activation of γ2 AMPK Induces Obesity and Reduces β Cell Function.
Specimen part, Cell line, Subject
View SamplesExplore DNA methylation in focal amygdala stimulation model of epilepsy and its relationship to gene expression. Overall design: Examination of expression changes in stimulated rats compared to sham operated animals in focal amygdala stimulation model of epilpesy.
Etiology matters - Genomic DNA Methylation Patterns in Three Rat Models of Acquired Epilepsy.
No sample metadata fields
View SamplesThe fetal ovarian grafts under the kidney capsule of adult male mice undergo a partial sex-reversal showing ectopic SOX9-positive Sertoli cell-like cells around 15-20 days post-transplantation. However, the molecular bases of such masculinization of fetal ovaries in the paternal environment were unclear.
Molecular and genetic characterization of partial masculinization in embryonic ovaries grafted into male nude mice.
Specimen part
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