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Hepatitis C virus hijacks P-body and stress granule components around lipid droplets

Hepatitis C virus hijacks P-body and stress granule components around lipid droplets

http://www.wikidata.org/entity/Q30155561

about

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 MicroRNAs, hepatitis C virus, and HCV/HIV-1 co-infection: new insights in pathogenesis and therapy N6-Methyladenosine in Flaviviridae Viral RNA Genomes Regulates Infection Hepatitis C Virus Exploitation of Processing Bodies Use of Cellular Decapping Activators by Positive-Strand RNA Viruses Nuclear proteins hijacked by mammalian cytoplasmic plus strand RNA viruses Characterization of RyDEN (C19orf66) as an Interferon-Stimulated Cellular Inhibitor against Dengue Virus Replication Zika virus disrupts molecular fingerprinting of human neurospheres Production of a dominant-negative fragment due to G3BP1 cleavage contributes to the disruption of mitochondria-associated protective stress granules during CVB3 infection Hepatitis C virus (HCV) induces formation of stress granules whose proteins regulate HCV RNA replication and virus assembly and egress.Herpes simplex virus 2 infection impacts stress granule accumulation How do viruses interact with stress-associated RNA granules?Hepatitis C virus genetics affects miR-122 requirements and response to miR-122 inhibitors.Modulation of hepatitis C virus RNA accumulation and translation by DDX6 and miR-122 are mediated by separate mechanisms The stress granule protein G3BP1 recruits protein kinase R to promote multiple innate immune antiviral responses.Cytoplasmic hGle1A regulates stress granules by modulation of translation.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 Regulation of Hepatitis C Virus Genome Replication by Xrn1 and MicroRNA-122 Binding to Individual Sites in the 5' Untranslated Region.IFN-β-inducing, unusual viral RNA species produced by paramyxovirus infection accumulated into distinct cytoplasmic structures in an RNA-type-dependent manner Heterologous Expression Screens in Nicotiana benthamiana Identify a Candidate Effector of the Wheat Yellow Rust Pathogen that Associates with Processing Bodies.Hepatitis C virus infection alters P-body composition but is independent of P-body granules.Doubly Spliced RNA of Hepatitis B Virus Suppresses Viral Transcription via TATA-Binding Protein and Induces Stress Granule Assembly.Emerging roles of interferon-stimulated genes in the innate immune response to hepatitis C virus infection Modulation of hepatitis C virus RNA abundance and virus release by dispersion of processing bodies and enrichment of stress granules.Japanese encephalitis virus core protein inhibits stress granule formation through an interaction with Caprin-1 and facilitates viral propagation Competing and noncompeting activities of miR-122 and the 5' exonuclease Xrn1 in regulation of hepatitis C virus replication.Movements of HIV-1 genomic RNA-APOBEC3F complexes and PKR reveal cytoplasmic and nuclear PKR defenses and HIV-1 evasion strategies.Methyl-Arginine Profile of Brain from Aged PINK1-KO+A53T-SNCA Mice Suggests Altered Mitochondrial Biogenesis.Diversion of stress granules and P-bodies during viral infection.Interaction of host cell microRNAs with the HCV RNA genome during infection of liver cells.Regulation of stress granules and P-bodies during RNA virus infection.Cytoplasmic RNA Granules and Viral Infection.Poliovirus infection induces the co-localization of cellular protein SRp20 with TIA-1, a cytoplasmic stress granule protein.Dynamic oscillation of translation and stress granule formation mark the cellular response to virus infection.mRNA decapping enzyme 1a (Dcp1a)-induced translational arrest through protein kinase R (PKR) activation requires the N-terminal enabled vasodilator-stimulated protein homology 1 (EVH1) domain.Regulation of stress granules in virus systems

P2860

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P2860

Hepatitis C virus hijacks P-body and stress granule components around lipid droplets

http://www.wikidata.org/entity/Q30155561

description

2011 nî lūn-bûn

@nan

2011 թուականի Մայիսին հրատարակուած գիտական յօդուած

@hyw

2011 թվականի մայիսին հրատարակված գիտական հոդված

@hy

2011年の論文

@ja

2011年論文

@yue

2011年論文

@zh-hant

2011年論文

@zh-hk

2011年論文

@zh-mo

2011年論文

@zh-tw

2011年论文

@wuu

name

Hepatitis C virus hijacks P-body and stress granule components around lipid droplets

@ast

Hepatitis C virus hijacks P-body and stress granule components around lipid droplets

@en

type

label

Hepatitis C virus hijacks P-body and stress granule components around lipid droplets

@ast

Hepatitis C virus hijacks P-body and stress granule components around lipid droplets

@en

prefLabel

Hepatitis C virus hijacks P-body and stress granule components around lipid droplets

@ast

Hepatitis C virus hijacks P-body and stress granule components around lipid droplets

@en

P1433

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P1433

Journal of Virology

P1476

Hepatitis C virus hijacks P-body and stress granule components around lipid droplets

@en

P2093

Kanae Osugi

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

Makoto Hijikata

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

Masanori Ikeda

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

Masatoshi Maki

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

Misao Kuroki

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

Nobuyuki Kato

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

Yasuo Ariumi

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

Yukihiro Kushima

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

P2860

Hepatitis C virus core protein interacts with cellular putative RNA helicase.

Hepatitis C virus core protein interacts with a human DEAD box protein DDX3

Hepatitis C virus core protein binds to a DEAD box RNA helicase

DDX3 DEAD-box RNA helicase is required for hepatitis C virus RNA replication

Ataxin-2 interacts with the DEAD/H-box RNA helicase DDX6 and interferes with P-bodies and stress granules

Subproteomic study of hepatitis C virus replicon reveals Ras-GTPase-activating protein binding protein 1 as potential HCV RC component

Cellular cofactors affecting hepatitis C virus infection and replication

The DNA damage sensors ataxia-telangiectasia mutated kinase and checkpoint kinase 2 are required for hepatitis C virus RNA replication

DDX6 (Rck/p54) is required for efficient hepatitis C virus replication but not for internal ribosome entry site-directed translation

Regulation of hepatitis C virus translation and infectious virus production by the microRNA miR-122

P304

6882-6892

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P31

scholarly article

P356

10.1128/JVI.02418-10

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P433

14

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P478

85

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

P577

2011-05-04T00:00:00Z

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

P698

21543503

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P932

3126564

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