Hepatitis C virus infection reduces hepatocellular polarity in a vascular endothelial growth factor-dependent manner - Wikidata - awgldk - TriplyDB

Hepatitis C virus infection reduces hepatocellular polarity in a vascular endothelial growth factor-dependent manner

Hepatitis C virus infection reduces hepatocellular polarity in a vascular endothelial growth factor-dependent manner

http://www.wikidata.org/entity/Q36694938

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Hypoxia-inducible factors as molecular targets for liver diseases Viral Interactions with PDZ Domain-Containing Proteins-An Oncogenic Trait?Angiogenesis and liver fibrosis The novel immunosuppressive protein kinase C inhibitor sotrastaurin has no pro-viral effects on the replication cycle of hepatitis B or C virus The missing pieces of the HCV entry puzzle.Networks inferred from biochemical data reveal profound differences in toll-like receptor and inflammatory signaling between normal and transformed hepatocytes.The role of O-GlcNAc signaling in the pathogenesis of diabetic retinopathy.The SR-BI partner PDZK1 facilitates hepatitis C virus entry.HepG2 cells expressing microRNA miR-122 support the entire hepatitis C virus life cycle.HCV IRES-mediated core expression in zebrafish.New Methods in Tissue Engineering: Improved Models for Viral Infection Up-regulation of Hedgehog pathway is associated with cellular permissiveness for hepatitis C virus replication.Viral disruption of the blood-brain barrier.Structural and functional hepatocyte polarity and liver disease.Hepatitis C virus envelope glycoprotein fitness defines virus population composition following transmission to a new host Hepatitis C virus-related hepatocellular carcinoma: An insight into molecular mechanisms and therapeutic strategies Hepatitis C virus infection induces autocrine interferon signaling by human liver endothelial cells and release of exosomes, which inhibits viral replication Very-low-density lipoprotein (VLDL)-producing and hepatitis C virus-replicating HepG2 cells secrete no more lipoviroparticles than VLDL-deficient Huh7.5 cells.The anti-viral effect of sorafenib in hepatitis C-related hepatocellular carcinoma Hepatocyte polarity SHIP2 regulates epithelial cell polarity through its lipid product, which binds to Dlg1, a pathway subverted by hepatitis C virus core protein Mechanism of hepatitis C virus (HCV)-induced osteopontin and its role in epithelial to mesenchymal transition of hepatocytes Recent advances in hepatitis C virus cell entry.Hepatitis C virus entry: beyond receptors.Hypoxia inducible factors in hepatocellular carcinoma Paracrine signals from liver sinusoidal endothelium regulate hepatitis C virus replication.Clathrin mediates infectious hepatitis C virus particle egress.Signal transducer and activator of transcription 3 is a proviral host factor for hepatitis C virus.A dual role for hypoxia inducible factor-1α in the hepatitis C virus lifecycle and hepatoma migration.Impact of intra- and interspecies variation of occludin on its function as coreceptor for authentic hepatitis C virus particles.Human embryonic stem cell-derived hepatoblasts are an optimal lineage stage for hepatitis C virus infection.In vitro systems for the study of hepatitis C virus infection.Interplay among cellular polarization, lipoprotein metabolism and hepatitis C virus entry.Response of VEGF to activation of viral receptors and TNFα in human mesangial cells.A circuit of paracrine signals between liver sinusoid endothelial cells and hepatocytes regulates hepatitis C virus replication.Letter: The antiviral activity of sorafenib in patients with hepatitis C-related hepatocellular carcinoma.Alteration of the ERK5 pathway by hydroxysafflor yellow A blocks expression of MEF2C in activated hepatic stellate cells in vitro: Potential treatment for hepatic fibrogenesis.

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Hepatitis C virus infection reduces hepatocellular polarity in a vascular endothelial growth factor-dependent manner

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P2860

Hepatitis C virus proteins

Robust hepatitis C virus infection in vitro.

Hepatitis C virus glycoproteins mediate pH-dependent cell entry of pseudotyped retroviral particles

Hepatitis C Virus Stabilizes Hypoxia-Inducible Factor 1 and Stimulates the Synthesis of Vascular Endothelial Growth Factor

CD81 and Claudin 1 Coreceptor Association: Role in Hepatitis C Virus Entry

Hepatitis C Virus Core Protein Augments Androgen Receptor-Mediated Signaling

Polarization Restricts Hepatitis C Virus Entry into HepG2 Hepatoma Cells

Human occludin is a hepatitis C virus entry factor required for infection of mouse cells

Identification and Analysis of Occludin Phosphosites: A Combined Mass Spectrometry and Bioinformatics Approach

The biology of VEGF and its receptors

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