Tp80 is a novel antiviral compound. Antiviral mechanism of Tp80 is the inhibition of the viral genome replication through the recoverly of GPx2 expression downregulated by HCV infection.
Retinoid derivative Tp80 exhibits anti-hepatitis C virus activity through restoration of GI-GPx expression.
Specimen part, Cell line, Treatment
View SamplesWe used microarrays to evaluate the effect of SRPIN803 on gene expression in ARPE-19 cells.
Identification of a Dual Inhibitor of SRPK1 and CK2 That Attenuates Pathological Angiogenesis of Macular Degeneration in Mice.
Cell line
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Epigenetic silencing of antiviral genes renders clones of Huh-7 cells permissive for hepatitis C virus replication.
Specimen part
View SamplesMX1 is a well-characterized interferon-induced antiviral gene. MX1 is activated by viral infection due to interferon production in cells. We treated non-permissive Huh7 cells and permissive HRP4 cells with interferon. We compared the expression of genes induced by interferon to determine host factors affecting HCV replication.
Epigenetic silencing of antiviral genes renders clones of Huh-7 cells permissive for hepatitis C virus replication.
Specimen part
View SamplesOptic nerves are an accessible part of the CNS, providing a source of glia without the presence of neuronal cell bodies. Therefore, an analysis was carried out of gene expression in optic nerves at P4, before myelination begins and at P10, when myelination is very actively proceeding. The goal was to obtain a profile of the changing gene expression that accompanies this transition from unmyelinated CNS nerve to myelinated nerve.
Towards resolving the transcription factor network controlling myelin gene expression.
Specimen part
View SamplesThe intestinal immune system must elicit robust immunity against harmful pathogens but restrain immune responses directed against commensal microbes and dietary antigens. The mechanisms that maintain this dichotomy are poorly understood. Here we describe a population of CD11b+F4/80+CD11c macrophages in the lamina propria (LP) that express several anti-inflammatory molecules including interleukin 10 (IL-10), but little or no pro-inflammatory cytokines, even upon stimulation with Toll-like receptor (TLR) ligands. These macrophages induced, in a manner dependent on IL-10, retinoic acid and exogenous transforming growth factor-, differentiation of FoxP3+ regulatory T cells. In contrast, LP CD11b+ dendritic cells elicited IL-17 production. This IL-17 production was suppressed by LP macrophages, indicating that a dynamic interplay between these subsets may influence the balance between immune activation and tolerance.
Lamina propria macrophages and dendritic cells differentially induce regulatory and interleukin 17-producing T cell responses.
No sample metadata fields
View SamplesActivation of inflammatory pathways in human IBD
Activation of an IL-6:STAT3-dependent transcriptome in pediatric-onset inflammatory bowel disease.
No sample metadata fields
View SamplesDrugs directly targeting Hepatitis C (HCV) are often rendered useless by the high mutation rate of the virus. Thus, we deduce that targeting of host factor that affect HCV replication may provide enhanced therapy fort HCV infection. Hepatocyte cell line Huh7 is known to be non-permissive for Hepatits C (HCV) replication. Through a method developed by the Rice laboratory (Blight, K.J., et al., J Virol, 2002), selection of a small subset of permissive hepatocytes is possible. The Rice laboratory generated the first permissive cell line, Huh7.5, using this method. We generated another permissive cell line, HRP1, using the same method.
The membrane-bound transcription factor CREB3L1 is activated in response to virus infection to inhibit proliferation of virus-infected cells.
Specimen part, Cell line
View SamplesMembrane-bound transcription factor CREB3L1 undergoes Regulated Intramembrane Proteolysis (RIP) in response to Hepatitis C infection. RIP activates CREB3L1 so that it can prevent the growth of HCV infected cells through the action of downstream genes. We over-expressed a truncated form of CREB3L1 that does not require RIP to enter the nucleus. Cells over-expressing this truncated form were isolated by Fluorescence Activated Cell Sorting (FACS).
The membrane-bound transcription factor CREB3L1 is activated in response to virus infection to inhibit proliferation of virus-infected cells.
No sample metadata fields
View SamplesPathological bone changes differ considerably between inflammatory arthritic diseases, and most studies have focused on bone erosion. Collagen Induced Arthritis (CIA) is a model for Rheumatoid Arthritis, which, in addition to bone erosion, demonstrates bone formation at the time for clinical manifestations. The objective of this study was to use the CIA model to study bone remodelling by performing a gene expression profiling time-course study on the CIA model.
Kinetics of gene expression and bone remodelling in the clinical phase of collagen-induced arthritis.
Specimen part
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