We compared the Galpha13 knockout and wild type mouse embryonic stem cells (cell line CJ7) to analyse the gene expression levels using Affymatrix mouse MGU_74Av2 array
Gene Expression Analysis of Galpha13-/- Knockout Mouse Embryos Reveals Perturbations in Galpha13 Signaling Related to Angiogenesis and Hypoxia
Specimen part, Cell line, Time
View SamplesWT cells and mutants during growth on low phosphate levels and recovery
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Specimen part, Disease, Cell line
View SamplesWT and mutants cells during growth in low phosphate levels and recovery into 20mM phosphate
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Specimen part, Disease, Cell line
View Samplesinvestigation of lncRNAs deregulated in oncogenic induced senescence.
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View SamplesThe neuronal ceroid lipofuscinoses (NCL) are a group of childhood inherited neurodegenerative disorders characterized by blindness, early dementia and pronounced cortical atrophy. The similar pathological and clinical profiles of different forms of NCL suggest that common disease mechanisms may be involved. Here, we have performed quantitative gene expression profiling of cortex from targeted knock out mice produced for Cln1 and Cln5 to explore NCL-associated molecular pathways. Combined microarray datasets from both mouse models exposed a common affected pathway: genes regulating cytoskeletal dynamics and neuronal growth cone stabilization display similar aberrations. We analyzed locus specific gene expression and showed regional clustering of Cln1 and three major genes of this pathway, further supporting a close functional relationship between the corresponding gene products, Cap1, Ptprf and Ptp4a2. The evidence from the gene expression data was substantiated by immunohistochemical staining data of Cln1-/- and Cln5-/- cortical neurons. These primary neurons displayed abnormalities in beta-tubulin and actin as well as abnormal intracellular distribution of growth cone associated proteins GAP-43, synapsin and Rab3. Our data provide the first evidence for a common molecular pathogenesis behind neuronal degeneration in CLN1 and CLN5. Since CLN1 and CLN5 code for proteins with distinct functional roles these data may have implications for other forms of NCL.
Brain gene expression profiles of Cln1 and Cln5 deficient mice unravels common molecular pathways underlying neuronal degeneration in NCL diseases.
Sex, Age, Specimen part, Disease
View SamplesWe carried out a genome-wide investigation of the primary transcriptional targets of 1a,25(OH)2D3 in breast epithelial cancer cells using RNA-Seq technology. We identified early transcriptional targets of 1a,25(OH)2D3 involved in adhesion, growth regulation, angiogenesis, actin cytoskeleton regulation, hexose transport, inflammation and immunomodulation, apoptosis, endocytosis and signaling. Furthermore, we found several transcription factors to be regulated by 1a,25(OH)2D3 that subsequently amplify and diversify the transcriptional output driven by 1a,25(OH)2D3 leading finally to a growth arrest of the cells. Moreover, we could show that 1a,25(OH)2D3 elevates the trimethylation of histone H3 lysine 4 at several target gene promoters. Our present transcriptomic analysis of differential expression after 1a,25(OH)2D3 treatment provides a resource of primary 1a,25(OH)2D3 targets that might drive the antiproliferative action in breast cancer epithelial cells.
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View SamplesMale broilers from two lines (n=10 per line) with different growth rate were raised at the same condition with free access to feed and drink. At day 6 and day 21, half samples of each broiler line were euthanized by cervical dislocation, and left ventricles were collected for RNA isolation. Gene expression in left ventricle was measured by RNA-seq and compared between different time points and chicken lines. The purpose of this study is to investigate gene expression change during broiler cardiac development and to compared gene expression between fast-growing modern broilers and slow-growing heritage broilers to find possible genes and pathways related to differential cardiac development and differential susceptibility to cardiac diseases between the two broiler lines.
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Sex, Specimen part, Disease
View Samplesbroilers heat stress.
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Sex, Age, Specimen part
View SamplesWe used isolated zygotene meiocytes, corresponding anthers and 2-week-old seedlings from the Zea mays inbred line Mo17 for RNA extraction and library construction for sequencing with Illumina technology to gain insight on gene expression during a key step in meiosis when recombination initiates.
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Age, Specimen part
View SamplesDengue virus (DENV) infection causes profound changes in the host cells and these changes underlie the immune response-based viral clearance and pathogenesis. There are several major cell/tissue types relevant for DENV pathogenesis in vivo, including immune cells, liver, and vascular endothelial cells. We applied a directed differentiation system that produces hepatocyte-like cells (HLCs) from pluripotent stem cells to investigate various aspects of DENV- hepatic cells interaction. Human embryonic stem cells were resistant to DENV infection while progeny hepatic cells were permissive. The transition to DENV permissiveness coincided with the upregulation of entry factors for the virus. Infection of HLCs by DENV was self-limiting due to the activation of the interferon (IFN) pathways, which protected by-stander cells from infection but failed to induce the same level of interferon-induced genes (ISGs) expression in the infected cells due to the subversion of IFN signaling by DENV. Innate immunity also protected the infected cells from virus-induced apoptosis. Furthermore, DENV infection activated the NF-?B pathway, increased production of reactive oxidative species (ROS), and led to production of inflammatory cytokines which may contribute to the cytokine storm implicated in dengue hemorrhagic fever (DHF). Finally, DENV infection of HLCs resulted several in vitro phenotypes that may have relevance for acute liver failure and vascular permeability during DHF. These include the disruption of adherens junctions and the downregulation of many liver specific genes such as albumin (ALB) and coagulation factor V (F5).
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Sex, Age, Specimen part, Disease, Cell line
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