Uridine composition of the poly-U/UC tract of HCV RNA defines non-self recognition by RIG-I. - sprookjes - yvandenbroek - TriplyDB

Uridine composition of the poly-U/UC tract of HCV RNA defines non-self recognition by RIG-I.

Uridine composition of the poly-U/UC tract of HCV RNA defines non-self recognition by RIG-I.

http://www.wikidata.org/entity/Q34388463

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Comparative analysis of viral RNA signatures on different RIG-I-like receptors Targeting Innate Immunity for Antiviral Therapy through Small Molecule Agonists of the RLR Pathway Regulation of Retinoic Acid Inducible Gene-I (RIG-I) Activation by the Histone Deacetylase 6 Regulation of antiviral innate immune signaling by stress-induced RNA granules Recognition of human oncogenic viruses by host pattern-recognition receptors RNAs Containing Modified Nucleotides Fail To Trigger RIG-I Conformational Changes for Innate Immune Signaling RIG-I in RNA virus recognition HCV RNA Activates APCs via TLR7/TLR8 While Virus Selectively Stimulates Macrophages Without Inducing Antiviral Responses Zika Virus Antagonizes Type I Interferon Responses during Infection of Human Dendritic Cells Hepatitis C virus core protein inhibits interferon production by a human plasmacytoid dendritic cell line and dysregulates interferon regulatory factor-7 and signal transducer and activator of transcription (STAT) 1 protein expression.The favorable IFNL3 genotype escapes mRNA decay mediated by AU-rich elements and hepatitis C virus-induced microRNAs.IL-1β production through the NLRP3 inflammasome by hepatic macrophages links hepatitis C virus infection with liver inflammation and disease In vivo ligands of MDA5 and RIG-I in measles virus-infected cells.Identification, molecular cloning, and analysis of full-length hepatitis C virus transmitted/founder genotypes 1, 3, and 4 Hepatitis C virus and antiviral innate immunity: who wins at tug-of-war?Hepatitis C Virus. Strategies to Evade Antiviral Responses Activation and evasion of antiviral innate immunity by hepatitis C virus.Sequence-Specific Modifications Enhance the Broad-Spectrum Antiviral Response Activated by RIG-I Agonists Identification of a Natural Viral RNA Motif That Optimizes Sensing of Viral RNA by RIG-I.Pathogen-Associated Molecular Pattern Recognition of Hepatitis C Virus Transmitted/Founder Variants by RIG-I Is Dependent on U-Core Length.ATP hydrolysis by the viral RNA sensor RIG-I prevents unintentional recognition of self-RNA.Intracellular detection of viral nucleic acids.Direct, interferon-independent activation of the CXCL10 promoter by NF-κB and interferon regulatory factor 3 during hepatitis C virus infection.West Nile virus infection and immunity.cis-Acting RNA elements in the hepatitis C virus RNA genome.Emerging complexity and new roles for the RIG-I-like receptors in innate antiviral immunity.HCV genomic RNA activates the NLRP3 inflammasome in human myeloid cells.Restoration of the activated Rig-I pathway in hepatitis C virus (HCV) replicon cells by HCV protease, polymerase, and NS5A inhibitors in vitro at clinically relevant concentrations.Tumour viruses and innate immunity.Tylophorine Analogs Allosterically Regulates Heat Shock Cognate Protein 70 And Inhibits Hepatitis C Virus Replication.RNA PAMPs as Molecular Tools for Evaluating RIG-I Function in Innate Immunity.Pattern recognition receptor MDA5 modulates CD8+ T cell-dependent clearance of West Nile virus from the central nervous system.Laboratory of genetics and physiology 2 (LGP2) plays an essential role in hepatitis C virus infection-induced interferon responses.Innate and Adaptive Immune Responses in Chronic HCV Infection.NLRX1 mediates MAVS degradation to attenuate hepatitis C virus-induced innate immune response through PCBP2.Systematic editing of synthetic RIG-I ligands to produce effective antiviral and anti-tumor RNA immunotherapies.Hepatitis C virus NS4B induces the degradation of TRIF to inhibit TLR3-mediated interferon signaling pathway.Circular RNAs as Therapeutic Agents and Targets

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P2860

Uridine composition of the poly-U/UC tract of HCV RNA defines non-self recognition by RIG-I.

http://www.wikidata.org/entity/Q34388463

description

2012 nî lūn-bûn

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2012 թուականի Օգոստոսին հրատարակուած գիտական յօդուած

@hyw

2012 թվականի օգոստոսին հրատարակված գիտական հոդված

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2012年の論文

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2012年論文

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2012年論文

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2012年论文

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Uridine composition of the pol ...... non-self recognition by RIG-I.

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Uridine composition of the pol ...... non-self recognition by RIG-I.

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Uridine composition of the pol ...... non-self recognition by RIG-I.

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Uridine composition of the pol ...... non-self recognition by RIG-I.

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Uridine composition of the pol ...... non-self recognition by RIG-I.

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Uridine composition of the pol ...... non-self recognition by RIG-I.

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Uridine composition of the pol ...... non-self recognition by RIG-I.

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Uridine composition of the pol ...... non-self recognition by RIG-I.

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Uridine composition of the pol ...... non-self recognition by RIG-I.

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Uridine composition of the pol ...... non-self recognition by RIG-I.

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Gretja Schnell

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Joseph Marcotrigiano

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Yueh-Ming Loo

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P2860

Epidemiology of hepatitis C virus infection

Immune signaling by RIG-I-like receptors

The C-terminal regulatory domain is the RNA 5'-triphosphate sensor of RIG-I

Recognition of 5' triphosphate by RIG-I helicase requires short blunt double-stranded RNA as contained in panhandle of negative-strand virus.

IPS-1, an adaptor triggering RIG-I- and Mda5-mediated type I interferon induction

Cardif is an adaptor protein in the RIG-I antiviral pathway and is targeted by hepatitis C virus

Regulation of innate antiviral defenses through a shared repressor domain in RIG-I and LGP2

Viral and therapeutic control of IFN-beta promoter stimulator 1 during hepatitis C virus infection

3' nontranslated RNA signals required for replication of hepatitis C virus RNA

Regulating intracellular antiviral defense and permissiveness to hepatitis C virus RNA replication through a cellular RNA helicase, RIG-I

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