The effect of dietary calcium and dairy proteins on adipose tissue gene expression profile in diet induced obesity
Effect of dietary calcium and dairy proteins on the adipose tissue gene expression profile in diet-induced obesity.
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View SamplesAnalysis of human primary macrophages after live Lactobacillus rhamnosus GG (LGG) or LC705 stimulation for 6h and 24h. The results reveal novel mechanisms for probiotics-induced activation of the healthy human innate immune system.
Nonpathogenic Lactobacillus rhamnosus activates the inflammasome and antiviral responses in human macrophages.
Specimen part, Time
View SamplesAsbestos has been shown to cause chromosomal damage and DNA aberrations. The fiber is associated with many different lung diseases such as asbestosis, malignant mesothelioma, and lung cancer, but the disease-related processes are still largely unknown. Our aim was to identify specific gene expression profiles by using Affymetrix arrays, in human cell lines A549, Beas-2B, and MeT5A exposed to asbestos in a time-dependent manner. The hybridization data was analyzed using an algorithm specifically designed for clustering short time series expression data, a canonical correlation analysis (CCA) for identifying correlations between the cell lines, and a Gene Ontology (GO) analysis method for the identification of enriched differentially expressed biological processes.
Gene expression profiles in asbestos-exposed epithelial and mesothelial lung cell lines.
No sample metadata fields
View SamplesProgressive myoclonus epilepsy of Unverricht-Lundborg type (EPM1) is an inherited neurodegenerative disease with myoclonus, seizures and ataxia, caused by the mutations in cystatin B (CSTB) gene. In an approach towards understanding the molecular basis of pathogenic events in EPM1 we have utilized the cystatin B deficient mice (Cstb-/-), a model for the disease. We have characterized the gene expression changes from the cerebellum of Cstb-/- mouse at postnatal day 7 (P7) and P30 as well as in cultured cerebellar granule cells using a pathway-based approach. A marked upregulation of immune response genes was seen at P30, reflecting the ongoing neuropathology, however, the observed alterations in complement cascade genes could also imply defects in synaptic plasticity. Differentially expressed genes in pre-symptomatic Cstb-/- animals at P7 were connected to synaptic function and plasticity and in cultured cerebellar granule cells to cellular biogenesis, cytoskeleton and intracellular transport. Especially GABAergic pathways were affected.
Gene expression alterations in the cerebellum and granule neurons of Cstb(-/-) mouse are associated with early synaptic changes and inflammation.
Sex, Specimen part
View SamplesMutations in the genes encoding isocitrate dehydrogenase 1 and 2 (IDH1/2) occur in a variety of tumor types, resulting in production of the proposed oncometabolite, 2-hydroxyglutarate (2-HG). How mutant IDH and 2-HG alter signaling pathways to promote cancer, though, remains unclear. Additionally, there exist relatively few cell lines with IDH mutations. To examine the effect of endogenous IDH mutations and 2-HG, we created a panel of isogenic epithelial cell lines with either wild-type IDH1/2 or clinically relevant IDH1/2 mutations. Differences were noted in the ability of IDH mutations to cause robust 2-HG accumulation. IDH1/2 mutants that produce high levels of 2-HG cause an epithelial-mesenchymal transition (EMT)-like phenotype, characterized by changes in EMT-related gene expression and cellular morphology. 2-HG is sufficient to recapitulate aspects of this phenotype in the absence of an IDH mutation. In the cells types examined, mutant IDH-induced EMT is dependent on upregulation of the transcription factor ZEB1 and downregulation of the mir-200 family of microRNAs. Furthermore, sustained knockdown of IDH1 in IDH1 R132H mutant cells is sufficient to reverse many characteristics of EMT, demonstrating that continued expression of mutant IDH is required to maintain this phenotype. These results suggest mutant IDH proteins can reversibly deregulate discrete signaling pathways that contribute to tumorigenesis
Isocitrate dehydrogenase (IDH) mutations promote a reversible ZEB1/microRNA (miR)-200-dependent epithelial-mesenchymal transition (EMT).
Cell line
View SamplesWe used microarrays to detail the global changes in gene expression resulting from miR-95 overexpression
miRNA-95 mediates radioresistance in tumors by targeting the sphingolipid phosphatase SGPP1.
Cell line, Treatment
View SamplesVCaP cells expressing inducible shRNAs for either ERG or a non-targeting control were treated with Doxycycline for 1, 3, 7 and 10 days prior to collection
TMPRSS2:ERG blocks neuroendocrine and luminal cell differentiation to maintain prostate cancer proliferation.
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View SamplesA transgenic TMPRSS2:ERG mouse model was engineered in FVB background and compared to its wildtype counterpart in the absence of any treatment This experiment is designed to look at ERG-dependent changes in phenotype and gene expression Overall design: A loxP-GFP-loxP-hERG exon 4-11 cassette was inserted into a BAC clone containing the TMPRSS2 locus using a recombineering kit. This modified BAC was used for pronuclear injection and generation of germline-transmitting mice. One line expressing high GFP was used for pronuclear injection of Cre protein and one sub-line that transmitted the TMPRSS2:ERG transgene into the germline was subsequently bred to homozygosity.
TMPRSS2:ERG blocks neuroendocrine and luminal cell differentiation to maintain prostate cancer proliferation.
No sample metadata fields
View SamplesLNCaP-derived MDV3100-resistant clones were treated with MDV3100 for 24h prior to collection
An F876L mutation in androgen receptor confers genetic and phenotypic resistance to MDV3100 (enzalutamide).
Cell line
View SamplesGenetically engineered LNCaPs overexpressing various AR alleles were treated with 0.1% DMSO or 10uM MDV3100 for 24h prior to collection
An F876L mutation in androgen receptor confers genetic and phenotypic resistance to MDV3100 (enzalutamide).
Cell line
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