We aimed to identify gene expression profiles/differences between spontaneously hypertensive rat(SHR) and normotensive rat (BN) in a set of recombinant inbred (RI) strains.
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Sex, Age, Specimen part
View SamplesAnalysis of genes regulated by Gab1 mediated signaling in hair cycle initiation
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Age, Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
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Age, Specimen part
View SamplesAnalysis of genes regulated by Gab1 mediated signaling in hair cycle initiation
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Age, Specimen part
View SamplesAnalysis of genes regulated by Shp2 mediated signaling in hair cycle initiation which are rescued by overactivation of Mek1
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Age, Specimen part
View SamplesIn this study we showed that rat XEN cells grown in the presence of a GSK3 inhibitor exhibited enhanced formation of cell contacts and decreased motility. In contrast, treatment with forskolin induced the PE formation and epithelial-mesenchymal transition (EMT) in rat XEN cells. Using microarray and real-time PCR assays, we found that VE versus PE formation of rat XEN cells was correlated with change in expression levels of VE or PE marker genes. Similar to forskolin, EMT was prompted upon treatment of rat XEN cells with recombinant parathyroid hormone related peptide (PTHRP), an activator of the cAMP pathway in vivo. Taken together, our data suggest that rat XEN cells are PrE-like cells. The activation of Wnt pathway in rat XEN cells leads to the acquisition of VE characteristics, whereas the activation of the PTHRP/cAMP pathway leads to EMT and the formation of PE.
Activation of the PTHRP/adenylate cyclase pathway promotes differentiation of rat XEN cells into parietal endoderm, whereas Wnt/β-catenin signaling promotes differentiation into visceral endoderm.
Specimen part
View SamplesDysferlin is expressed in skeletal and cardiac muscle. However, dysferlin deficiency, namely limb girdle muscular dystrophy 2B (LGMD2B) and Myoshi myopathy, results in skeletal muscle weakness and spares the heart. This dichotomy could be caused by differential regulation of protective mechanisms. Therefore, we compared intraindividual mRNA expression profiles between cardiac and skeletal muscle in dysferlin-deficient SJL/J mice and normal C57BL/6 mice.
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View SamplesAim was to identify novel targets of protoporphyrin-IX (PpIX) after silencing Ferrochelatase (FECH) enzyme. PpIX is a light sensitive metabolite of heme synthesis. Generation of PpIX is increased if FECH activity is suppressed. Here, silencing of FECH leads to down-regulation of PpIX, measured by a decrease of PpIX-specific fluorescence.
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Specimen part, Cell line, Treatment
View SamplesGene expression analysis of whole heart samples obtained from CAR wild type and knockout mouse E10.5 embryos.
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Specimen part
View SamplesGene expression analyis of two neonatal fibroblasts (BJ and HFF1), one adult dermal fibroblasts (NFH2), two BJ-derived human iPSCs (iB4 and iB5), two HFF1-derived iPSCs (iPS 2 and iPS4), four NFH2-derived iPSCs (OiPS3, OiPS6, OiPS8, OiPS16), one amniotic fluid cells and three derived iPSCs (lines 4, 5, 6, 10, and 41), two human ES cells (H1 and H9), neonatal fibroblasts transduced with the four retroviral factors (OKSM) after 24h, 48h, and 72h, neonatal fibroblasts treated with EDHB for 24h, 48h, and 72h, neonatal fibroblasts transduced with four factors and treated with EDHB for 24h, 48h, and 72h, neonatal fibroblasts knocked down for HIF1A (HIF1-KD) and for a scrambled sequence (SCR-KD)
HIF1α modulates cell fate reprogramming through early glycolytic shift and upregulation of PDK1-3 and PKM2.
Age, Specimen part, Cell line
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