Host shutoff is a conserved phenotype of gammaherpesvirus infection and is orchestrated exclusively from the cytoplasm.
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A Tale of Two RNAs during Viral Infection: How Viruses Antagonize mRNAs and Small Non-Coding RNAs in The Host CellShutoff of Host Gene Expression in Influenza A Virus and Herpesviruses: Similar Mechanisms and Common ThemesAlphaherpesvirus Subversion of Stress-Induced Translational ArrestThe KSHV RNA regulator ORF57: target specificity and its role in the viral life cycleA ribonucleoprotein complex protects the interleukin-6 mRNA from degradation by distinct herpesviral endonucleasesInfluenza a virus host shutoff disables antiviral stress-induced translation arrestA gammaherpesvirus complement regulatory protein promotes initiation of infection by activation of protein kinase Akt/PKB.Deep sequencing reveals direct targets of gammaherpesvirus-induced mRNA decay and suggests that multiple mechanisms govern cellular transcript escape.Global mRNA degradation during lytic gammaherpesvirus infection contributes to establishment of viral latency.A viral nuclear noncoding RNA binds re-localized poly(A) binding protein and is required for late KSHV gene expression.Coordinated destruction of cellular messages in translation complexes by the gammaherpesvirus host shutoff factor and the mammalian exonuclease Xrn1.Nuclear import of cytoplasmic poly(A) binding protein restricts gene expression via hyperadenylation and nuclear retention of mRNA.Immune escape of γ-herpesviruses from adaptive immunityHistone demethylase JMJD2A regulates Kaposi's sarcoma-associated herpesvirus replication and is targeted by a viral transcriptional factor.Importin alpha-mediated nuclear import of cytoplasmic poly(A) binding protein occurs as a direct consequence of cytoplasmic mRNA depletionNuclear translocation and regulation of intranuclear distribution of cytoplasmic poly(A)-binding protein are distinct processes mediated by two Epstein Barr virus proteins.Murine Gammaherpesvirus 68 Pathogenesis Is Independent of Caspase-1 and Caspase-11 in Mice and Impairs Interleukin-1β Production upon Extrinsic Stimulation in Culture.ORF45-Mediated Prolonged c-Fos Accumulation Accelerates Viral Transcription during the Late Stage of Lytic Replication of Kaposi's Sarcoma-Associated Herpesvirus.Transcriptome-Wide Cleavage Site Mapping on Cellular mRNAs Reveals Features Underlying Sequence-Specific Cleavage by the Viral Ribonuclease SOX.Tiled microarray identification of novel viral transcript structures and distinct transcriptional profiles during two modes of productive murine gammaherpesvirus 68 infection.Murine gammaherpesvirus 68 infection protects lupus-prone mice from the development of autoimmunity.The "Bridge" in the Epstein-Barr virus alkaline exonuclease protein BGLF5 contributes to shutoff activity during productive infection.The Epstein-Barr virus miR-BHRF1-1 targets RNF4 during productive infection to promote the accumulation of SUMO conjugates and the release of infectious virusCyclin D1 overexpression supports stable EBV infection in nasopharyngeal epithelial cellsInterplay between polyadenylate-binding protein 1 and Kaposi's sarcoma-associated herpesvirus ORF57 in accumulation of polyadenylated nuclear RNA, a viral long noncoding RNA.Murine Gammaherpesvirus 68 LANA and SOX Homologs Counteract ATM-Driven p53 Activity during Lytic Viral ReplicationImmune regulation and evasion of Mammalian host cell immunity during viral infection.Critical Role of the PA-X C-Terminal Domain of Influenza A Virus in Its Subcellular Localization and Shutoff ActivityGammaherpesviral gene expression and virion composition are broadly controlled by accelerated mRNA degradation.Immune responses to Epstein-Barr virus: molecular interactions in the virus evasion of CD8+ T cell immunityPoly(A)-binding protein (PABP): a common viral target.Tinkering with translation: protein synthesis in virus-infected cells.Virus-encoded endonucleases: expected and novel functions.Emerging roles for RNA degradation in viral replication and antiviral defense.Viral Nucleases Induce an mRNA Degradation-Transcription Feedback Loop in Mammalian Cells.Diverse mechanisms evolved by DNA viruses to inhibit early host defenses.An RNA element in human interleukin 6 confers escape from degradation by the gammaherpesvirus SOX protein.Nuclease escape elements protect messenger RNA against cleavage by multiple viral endonucleases.Genome-wide mapping of infection-induced SINE RNAs reveals a role in selective mRNA export.A common strategy for host RNA degradation by divergent viruses
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Host shutoff is a conserved phenotype of gammaherpesvirus infection and is orchestrated exclusively from the cytoplasm.
description
article científic
@ca
article scientifique
@fr
articolo scientifico
@it
artigo científico
@pt
bilimsel makale
@tr
scientific article published on 08 July 2009
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vedecký článok
@sk
vetenskaplig artikel
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videnskabelig artikel
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vědecký článek
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name
Host shutoff is a conserved ph ...... xclusively from the cytoplasm.
@en
Host shutoff is a conserved ph ...... xclusively from the cytoplasm.
@nl
type
label
Host shutoff is a conserved ph ...... xclusively from the cytoplasm.
@en
Host shutoff is a conserved ph ...... xclusively from the cytoplasm.
@nl
prefLabel
Host shutoff is a conserved ph ...... xclusively from the cytoplasm.
@en
Host shutoff is a conserved ph ...... xclusively from the cytoplasm.
@nl
P2093
P2860
P356
P1433
P1476
Host shutoff is a conserved ph ...... xclusively from the cytoplasm.
@en
P2093
Britt A Glaunsinger
Karen Clyde
Sergio Covarrubias
Yeon J Lee
P2860
P304
P356
10.1128/JVI.01051-09
P407
P577
2009-07-08T00:00:00Z