gene expression profiles of leukocytes from blood (WBCs) and spleen harvested at an early (two hours) time point after injury or sham injury in mice subjected to trauma-hemorrhage, burn injury or lipopolysaccharide (LPS)-infusion at three experimental sites
Commonality and differences in leukocyte gene expression patterns among three models of inflammation and injury.
No sample metadata fields
View SamplesMolecular pathways activated in MALT lymphoma are not well defined.
Gene expression profiling of pulmonary mucosa-associated lymphoid tissue lymphoma identifies new biologic insights with potential diagnostic and therapeutic applications.
Sex
View SamplesHepatitis C Virus is a leading cause of chronic liver disease. The identification and characterisation of key host cellular factors that play a role in the HCV replication cycle is important for the understanding of disease pathogenesis and the identification of novel anti-viral therapeutic targets. Gene expression profiling of HCV infected Huh7 cells by microarray analysis was performed to identify host cellular genes that are transcriptionally regulated by infection. The expression of host genes involved in cellular defence mechanisms (apoptosis, proliferation and anti-oxidant responses), cellular metabolism (lipid and protein metabolism) and intracellular transport (vesicle trafficking and cytoskeleton regulation) was significantly altered by HCV infection. The gene expression patterns identified provide insight into the potential mechanisms that contribute to HCV associated pathogenesis. These include an increase in pro-inflammatory and pro-apoptotic signalling and a decrease in the anti-oxidant response pathways of the infected cell.
Gene expression profiling indicates the roles of host oxidative stress, apoptosis, lipid metabolism, and intracellular transport genes in the replication of hepatitis C virus.
Specimen part, Cell line
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GENE REGULATION. Discrete functions of nuclear receptor Rev-erbα couple metabolism to the clock.
Specimen part, Time
View SamplesCircadian and metabolic physiology are intricately intertwined, as illustrated by Rev-erb , a transcription factor (TF) that functions both as a core repressive component of the cell autonomous clock and as a regulator of metabolic genes. Here we show that Rev-erb modulates the clock and metabolism by different genomic mechanisms. Clock control requires Rev-erb to bind directly to the genome at its cognate sites, where it competes with activating ROR TFs. By contrast, Rev-erb regulates metabolic genes primarily by recruiting the HDAC3 corepressor to sites to which it is tethered by cell type-specific transcription factors. Thus, direct competition between Rev-erb and ROR TFs provides a universal mechanism for self-sustained control of molecular clock across all tissues, whereas Rev-erb utilizes lineage-determining factors to convey a tissue-specific epigenomic rhythm that regulates metabolism tailored to the specific need of that tissue.
GENE REGULATION. Discrete functions of nuclear receptor Rev-erbα couple metabolism to the clock.
Specimen part, Time
View SamplesAbstract: Immune subversion represents a hallmark of persistent infection, but microbial suppression of B cell responses remains mechanistically ill-defined. Adoptive transfer experiments in a chronic viral infection model evidenced the rapid and profound decimation of B cells that responded to virus or to concomitantly administered protein. Decimation affected naïve and memory B cells and resulted from biased differentiation into short-lived antibody-secreting cells. It was driven by type I interferon (IFN-I) signaling to several cell types including dendritic cells, T cells and myeloid cells. Durable B cell responses were restored upon IFN-I receptor blockade or, partially, when depleting myeloid cells or key IFN-I-induced cytokines. B cell decimation represents a molecular mechanism of humoral immune subversion and reflects an unsustainable “all-in” response of B cells in IFN-I-driven inflammation. Overall design: We adoptively transferred naïve KL25HL cells (LCMV-WE-GP-specific B cells) to aIFNAR- or isotype control-treated syngeneic recipient mice, followed by rLCMV-Cl13/WE-GP. On day 3 of infection, spleen were harvested and proliferated KL25HL B cell progeny (CD45.1+B220+CFSElo) were FACS-sorted and total RNA was processed for RNAseq. n=4
Interferon-driven deletion of antiviral B cells at the onset of chronic infection.
Age, Specimen part, Cell line, Subject
View SamplesGrowing evidence indicates that PPAR agonists, such as rosiglitazone (RSG,), induce adipose mitochondrial biogenesis. Using microarrays, we systematically analyzed nucleus-encoded mitochondrial gene expression in two common murine adipocyte models, 3T3 L1 and C3H/10T1/2 adipocytes, and aimed to further establish the direct role of RSG, and capture the temporal changes in mitochondrial gene transcription during this process.
Rosiglitazone Induces Mitochondrial Biogenesis in Differentiated Murine 3T3-L1 and C3H/10T1/2 Adipocytes.
Specimen part
View SamplesTo understand the age-dependent response to burn injury, blood samples from pediatric and adult patients were collected at different times after severe burn injury.
Analysis of factorial time-course microarrays with application to a clinical study of burn injury.
Sex, Disease
View SamplesThis SuperSeries is composed of the SubSeries listed below.
MicroRNAs are transported in plasma and delivered to recipient cells by high-density lipoproteins.
Sex, Age, Cell line, Treatment
View SamplesWe have used primary MEFs derived from wild type and E2F4 null mice growing asynchrounously in serum to generate a signature for E2F4 pathway activation. 10 wild type and 10 E2F4 null samples were each assayed using the Affymetrics Mouse Genome 430A 2.0 array.
Patterns of cell signaling pathway activation that characterize mammary development.
No sample metadata fields
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