Background: Gq-coupled G protein-coupled receptors (GPCR) mediate the actions of a variety of messengers that are key regulators of cardiovascular function. Enhanced Gaq-mediated signaling plays an important role in cardiac hypertrophy and in the transition to heart failure. We have recently described that Gaq acts as an adaptor protein that facilitates PKCz-mediated activation of ERK5 in epithelial cells. Since the ERK5 cascade is known to be involved in cardiac hypertrophy, we have investigated the potential relevance of this pathway in Gq-dependent signaling in cardiac cells.
Protein kinase C (PKC)ζ-mediated Gαq stimulation of ERK5 protein pathway in cardiomyocytes and cardiac fibroblasts.
Sex, Age, Specimen part
View SamplesTranscriptional response to virus infection in mice lacking type I and type III signaling
Transcription factor redundancy ensures induction of the antiviral state.
Specimen part, Cell line, Treatment
View SamplesWT and Ikbke-/- EF cells were stimulated with recombinant interferon beta for 6 hours. Cells lacking IKKe kinase show a defect in a subset of interferon stimulated gene transcription
Multiple functions of the IKK-related kinase IKKepsilon in interferon-mediated antiviral immunity.
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View SamplesCompare the behaviour of two populations of non-hematopoetic stem cells (MSC and MAPC) isolated from human bone marrow. The effect of culture conditions on the behaviour of MSC was also characterised by isolating MSC and then culturing the cells for 96h in MAPC growth conditions
Validation of COL11A1/procollagen 11A1 expression in TGF-β1-activated immortalised human mesenchymal cells and in stromal cells of human colon adenocarcinoma.
Age, Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Integrative analysis of DNA copy number, DNA methylation and gene expression in multiple myeloma reveals alterations related to relapse.
Sex, Age, Specimen part
View SamplesMultiple myeloma (MM) remains incurable despite the introduction of novel agents and a relapsing course is observed in the majority of patients. Although the development of genomic technologies has greatly improved our understanding of MM pathogenesis, the mechanisms underlying relapse have been less investigated. In this study, an integrative analysis of DNA copy number, DNA methylation and gene expression was conducted in matched diagnosis and relapse samples from 17 MM patients. Overall, the acquisition of abnormalities at relapse was much more frequent than the lost of lesions present at diagnosis, and DNA losses were significantly more frequent at relapse than in diagnosis samples. Interestingly, copy number abnormalities involving more than 100 Mb of DNA at relapse significantly impact the gene expression of these samples, provoking a particular deregulation of IL-8 pathway. On the contrary, no relevant modifications of gene expression were observed in those samples with less than 100 Mb affected by chromosomal changes. Although different statistical approaches were used to uncover genes whose abnormal expression at relapse was regulated by DNA methylation, only two genes significantly deregulated in relapse samples (SORL1 and GLT1D1) showed a negative methylation-expression correlation. A deeper analysis demonstrated that DNA methylation was involved in regulation of SORL1 expression in MM. Finally, relevant changes in gene expression observed in relapse samples, such us downregulation of CD27 and P2RY8, were not apparently preceded by alterations in corresponding DNA. Taken together, these results showed that genomic heterogeneity, both at the DNA and RNA level, is a hallmark of MM transition from diagnosis to relapse.
Integrative analysis of DNA copy number, DNA methylation and gene expression in multiple myeloma reveals alterations related to relapse.
Sex, Specimen part
View SamplesSarm-deficient mice are protected from VSV encephalitis and death. Microarray was done to examine genes contributing to this phenotype
SARM is required for neuronal injury and cytokine production in response to central nervous system viral infection.
Age, Specimen part
View SamplesDNA microarray technology is a powerfull tool for genome-wide gene expression analysis of biological samples. Here we review the methodology for expression profiling analysis of skin tissue or purified keratinocytes from mice. We explained the methodology and protocols for RNA preservation and purification, RNA quality and integrity tests, and DNA microarray technology types that can be used. Furthermore, using a dataset of mice samples, we explained how to perform chip raw data preprocessing and normalization, differential expression analysis, as well as gene-clustering and funcional analysis of gene deregulation.
Gene expression profiling of mouse epidermal keratinocytes.
Age, Specimen part
View SamplesA GFP-expressing recombinant A/Puerto Rico/8/1934 influenza virus was used to infect C57BL/6 wild type mice and on day 3 post infection, lung alveolar epithelial cells (AEC) were isolated and sorted based on GFP expression. GFP+ AEC represent the infected AEC and GFP- AEC represent the bystander AEC. AEC were also sorted from uninfected mice to serve as controls. Overall design: AEC from infected mice were pooled to make three (3) infected GFP+ AEC replicates for sequencing. Five (5) bystander GFP- replicates and five (5) uninfected AEC replicates were also isolated for sequencing
Transcriptome Analysis of Infected and Bystander Type 2 Alveolar Epithelial Cells during Influenza A Virus Infection Reveals <i>In Vivo</i> Wnt Pathway Downregulation.
Specimen part, Subject, Time
View SamplesThe weaning period consist of a critical postnatal window for structural and physiologic maturation of rat beta cells. To investigate transcriptome changes involved in the maturation of beta cells neighboring this period we performed microarray analysis in FACS beta cell enriched populations to detail the global programme of gene expression to identify its changes during this process.
Transcriptome landmarks of the functional maturity of rat beta-cells, from lactation to adulthood.
Sex
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