Inclusion bodies are a site of ebolavirus replication - Wikidata - wikimedia - TriplyDB

Inclusion bodies are a site of ebolavirus replication

Inclusion bodies are a site of ebolavirus replication

http://www.wikidata.org/entity/Q36363434

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Viral suppression of innate immunity via spatial isolation of TBK1/IKKε from mitochondrial antiviral platform Interaction with Tsg101 is necessary for the efficient transport and release of nucleocapsids in marburg virus-infected cells Live-cell imaging of Marburg virus-infected cells uncovers actin-dependent transport of nucleocapsids over long distances.Virus nomenclature below the species level: a standardized nomenclature for filovirus strains and variants rescued from cDNA A novel life cycle modeling system for Ebola virus shows a genome length-dependent role of VP24 in virus infectivity Deep sequencing identifies noncanonical editing of Ebola and Marburg virus RNAs in infected cells.An upstream open reading frame modulates ebola virus polymerase translation and virus replication.Analysis of the highly diverse gene borders in Ebola virus reveals a distinct mechanism of transcriptional regulation.Colocalization of different influenza viral RNA segments in the cytoplasm before viral budding as shown by single-molecule sensitivity FISH analysis.Heat shock protein 70 regulates degradation of the mumps virus phosphoprotein via the ubiquitin-proteasome pathway.An Improved Reverse Genetics System to Overcome Cell-Type-Dependent Ebola Virus Genome Plasticity.Soluble Glycoprotein Is Not Required for Ebola Virus Virulence in Guinea Pigs Importin-α7 Is Involved in the Formation of Ebola Virus Inclusion Bodies but Is Not Essential for Pathogenicity in Mice.Actin-Modulating Protein Cofilin Is Involved in the Formation of Measles Virus Ribonucleoprotein Complex at the Perinuclear Region.Differential transcriptional responses to Ebola and Marburg virus infection in bat and human cells.The Ebola Virus VP30-NP Interaction Is a Regulator of Viral RNA Synthesis.Forty-five years of Marburg virus research.Modeling the lifecycle of Ebola virus under biosafety level 2 conditions with virus-like particles containing tetracistronic minigenomes.DNA topoisomerase 1 facilitates the transcription and replication of the Ebola virus genome.Ebola Virus Does Not Induce Stress Granule Formation during Infection and Sequesters Stress Granule Proteins within Viral Inclusions.A novel Ebola virus expressing luciferase allows for rapid and quantitative testing of antivirals Inclusion Body Fusion of Human Parainfluenza Virus Type 3 Regulated by Acetylated α-Tubulin Enhances Viral Replication.Development and application of reporter-expressing mononegaviruses: current challenges and perspectives.Conformational plasticity of the Ebola virus matrix protein.Reverse genetics systems as tools for the development of novel therapies against filoviruses.Ebolaviruses Associated with Differential Pathogenicity Induce Distinct Host Responses in Human Macrophages.A Polymorphism within the Internal Fusion Loop of the Ebola Virus Glycoprotein Modulates Host Cell Entry.Transport of Ebolavirus Nucleocapsids Is Dependent on Actin Polymerization: Live-Cell Imaging Analysis of Ebolavirus-Infected Cells.Putative domain-domain interactions in the vesicular stomatitis virus L polymerase protein appendage region.Forty Years of Ebolavirus Molecular Biology: Understanding a Novel Disease Agent Through the Development and Application of New Technologies.Host Factors Involved in Ebola Virus Replication.FAM134B, the Selective Autophagy Receptor for Endoplasmic Reticulum Turnover, Inhibits Replication of Ebola Virus Strains Makona and Mayinga.Generation of Recombinant Ebola Viruses Using Reverse Genetics.Reverse Genetics Systems for Filoviruses.Dynamic Phosphorylation of VP30 Is Essential for Ebola Virus Life Cycle.Negri bodies are viral factories with properties of liquid organelles.Inside the Cell: Assembly of Filoviruses.Live-Cell Imaging of Filoviruses.Functional organization of cytoplasmic inclusion bodies in cells infected by respiratory syncytial virus Intracellular Crosslinking of Filoviral Nucleoproteins with Xintrabodies Restricts Viral Packaging.

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P2860

Inclusion bodies are a site of ebolavirus replication

http://www.wikidata.org/entity/Q36363434

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2012 nî lūn-bûn

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2012年の論文

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2012年学术文章

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2012年学术文章

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2012年学术文章

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2012年学术文章

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2012年学术文章

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2012年學術文章

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2012年學術文章

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2012年學術文章

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Inclusion bodies are a site of ebolavirus replication

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Inclusion bodies are a site of ebolavirus replication

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Inclusion bodies are a site of ebolavirus replication

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Inclusion bodies are a site of ebolavirus replication

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Allison Groseth

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Astrid Herwig

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Christopher F Basler

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Gordian Schudt

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Michaela Weber

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Olga Dolnik

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Reed S Shabman

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P2860

The Ebola virus glycoprotein contributes to but is not sufficient for virulence in vivo

Intracellular events and cell fate in filovirus infection

Ebola haemorrhagic fever

The organisation of Ebola virus reveals a capacity for extensive, modular polyploidy

Ebolavirus is internalized into host cells via macropinocytosis in a viral glycoprotein-dependent manner

Protein expression redirects vesicular stomatitis virus RNA synthesis to cytoplasmic inclusions

Three-dimensional analysis of a viral RNA replication complex reveals a virus-induced mini-organelle

A PPxY motif within the VP40 protein of Ebola virus interacts physically and functionally with a ubiquitin ligase: implications for filovirus budding

Aggresomes, inclusion bodies and protein aggregation

Virus factories: associations of cell organelles for viral replication and morphogenesis

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10.1128/JVI.01525-12

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3486333

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