Hepatitis C virus (HCV) induces formation of stress granules whose proteins regulate HCV RNA replication and virus assembly and egress. - Wikidata - wikimedia - TriplyDB

Hepatitis C virus (HCV) induces formation of stress granules whose proteins regulate HCV RNA replication and virus assembly and egress.

Hepatitis C virus (HCV) induces formation of stress granules whose proteins regulate HCV RNA replication and virus assembly and egress.

http://www.wikidata.org/entity/Q30010035

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A host YB-1 ribonucleoprotein complex is hijacked by hepatitis C virus for the control of NS3-dependent particle production Who Regulates Whom? An Overview of RNA Granules and Viral Infections Regulation of antiviral innate immune signaling by stress-induced RNA granules Interplay between Inflammation and Cellular Stress Triggered by Flaviviridae Viruses Spatiotemporal analysis of hepatitis C virus infection T-cell intracellular antigens in health and disease Mumps Virus Induces Protein-Kinase-R-Dependent Stress Granules, Partly Suppressing Type III Interferon Production.Viral and cellular proteins containing FGDF motifs bind G3BP to block stress granule formation Hepatic interferon-stimulated genes are differentially regulated in the liver of chronic hepatitis C patients with different interleukin-28B genotypes.Induction of stress granules by interferon and down-regulation by the cellular RNA adenosine deaminase ADAR1.Picornavirus morphogenesis.HIV-2 genomic RNA accumulates in stress granules in the absence of active translation.Impairment of type I but not type III IFN signaling by hepatitis C virus infection influences antiviral responses in primary human hepatocytes Hepatitis C Virus. Strategies to Evade Antiviral Responses Dynamic Interaction of Stress Granules, DDX3X, and IKK-α Mediates Multiple Functions in Hepatitis C Virus Infection Supporting Role for GTPase Rab27a in Hepatitis C Virus RNA Replication through a Novel miR-122-Mediated Effect IFN-β-inducing, unusual viral RNA species produced by paramyxovirus infection accumulated into distinct cytoplasmic structures in an RNA-type-dependent manner dsRNA-dependent protein kinase PKR and its role in stress, signaling and HCV infection.Emerging roles of interferon-stimulated genes in the innate immune response to hepatitis C virus infection Movements of HIV-1 genomic RNA-APOBEC3F complexes and PKR reveal cytoplasmic and nuclear PKR defenses and HIV-1 evasion strategies.Diversion of stress granules and P-bodies during viral infection.Interplay between viruses and host mRNA degradation Regulation of stress granules and P-bodies during RNA virus infection.A genetic screen identifies interferon-α effector genes required to suppress hepatitis C virus replication Cytoplasmic RNA Granules and Viral Infection.RNA-dependent protein kinase PKR and the Z-DNA binding orthologue PKZ differ in their capacity to mediate initiation factor eIF2α-dependent inhibition of protein synthesis and virus-induced stress granule formation.Porcine Reproductive and Respiratory Syndrome Virus Infection Induces Stress Granule Formation Depending on Protein Kinase R-like Endoplasmic Reticulum Kinase (PERK) in MARC-145 Cells.Virion assembly and release.Zika virus inhibits eIF2α-dependent stress granule assembly.The amazing innate immune response to influenza A virus infection.The influence of viral RNA secondary structure on interactions with innate host cell defences.RNA helicase DDX3: at the crossroad of viral replication and antiviral immunity.Innate detection of hepatitis B and C virus and viral inhibition of the response.The cis-acting replication element of the Hepatitis C virus genome recruits host factors that influence viral replication and translation Protein kinase R (PKR) plays a pro-viral role in porcine reproductive and respiratory syndrome virus (PRRSV) replication by modulating viral gene transcription.Amino acids 78 and 79 of Mammalian Orthoreovirus protein µNS are necessary for stress granule localization, core protein λ2 interaction, and de novo virus replication.Ultrastructural and biochemical basis for hepatitis C virus morphogenesis.The spliceosome factor SART1 exerts its anti-HCV action through mRNA splicing.Zika virus hijacks stress granule proteins and modulates the host stress response.Hepatitis C virus plays with fire and yet avoids getting burned. A review for clinicians on processing bodies and stress granules.

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P2860

Hepatitis C virus (HCV) induces formation of stress granules whose proteins regulate HCV RNA replication and virus assembly and egress.

http://www.wikidata.org/entity/Q30010035

description

2012 nî lūn-bûn

@nan

2012 թուականի Օգոստոսին հրատարակուած գիտական յօդուած

@hyw

2012 թվականի օգոստոսին հրատարակված գիտական հոդված

@hy

2012年の論文

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2012年論文

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2012年論文

@zh-hant

2012年論文

@zh-hk

2012年論文

@zh-mo

2012年論文

@zh-tw

2012年论文

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name

Hepatitis C virus (HCV) induce ...... and virus assembly and egress.

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Hepatitis C virus (HCV) induce ...... and virus assembly and egress.

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type

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Hepatitis C virus (HCV) induce ...... and virus assembly and egress.

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Hepatitis C virus (HCV) induce ...... and virus assembly and egress.

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Hepatitis C virus (HCV) induce ...... and virus assembly and egress.

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Hepatitis C virus (HCV) induce ...... and virus assembly and egress.

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P1433

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P3181

P356

P1433

Journal of Virology

P1476

Hepatitis C virus (HCV) induce ...... and virus assembly and egress.

@en

P2093

Bryan Boyd

http://www.w3.org/2001/XMLSchema#string

Stefan Wieland

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P2860

PKR protein kinase is activated by hepatitis C virus and inhibits viral replication through translational control

Cell proteins TIA-1 and TIAR interact with the 3' stem-loop of the West Nile virus complementary minus-strand RNA and facilitate virus replication.

A phylogenetically conserved stem-loop structure at the 5' border of the internal ribosome entry site of hepatitis C virus is required for cap-independent viral translation.

Sequences in the 5' nontranslated region of hepatitis C virus required for RNA replication.

Robust hepatitis C virus infection in vitro.

Initiation of Protein Synthesis by Hepatitis C Virus Is Refractory to Reduced eIF2 {middle dot} GTP {middle dot} Met-tRNAiMet Ternary Complex Availability

Differential Biophysical Properties of Infectious Intracellular and Secreted Hepatitis C Virus Particles

Persistent Hepatitis C Virus Infection In Vitro: Coevolution of Virus and Host

Interaction of TIA-1/TIAR with West Nile and dengue virus products in infected cells interferes with stress granule formation and processing body assembly

P304

11043-11056

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scholarly article

P3181

1730586

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P356

10.1128/JVI.07101-11

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P433

20

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P478

86

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P50

Francis V. Chisari

Urtzi Garaigorta

P577

2012-08-01T00:00:00Z

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P698

22855484

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P932

3457181

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