Replication vesicles are load- and choke-points in the hepatitis C virus lifecycle. - Wikidata - wikimedia - TriplyDB

Replication vesicles are load- and choke-points in the hepatitis C virus lifecycle.

Replication vesicles are load- and choke-points in the hepatitis C virus lifecycle.

http://www.wikidata.org/entity/Q31129723

about

HCV Kinetic Models and Their Implications in Drug Development Modelling hepatitis C therapy--predicting effects of treatment Live Cell Analysis and Mathematical Modeling Identify Determinants of Attenuation of Dengue Virus 2'-O-Methylation Mutant Spatiotemporal analysis of hepatitis C virus infection ZIKA virus reveals broad tissue and cell tropism during the first trimester of pregnancy Oxidative stress, a trigger of hepatitis C and B virus-induced liver carcinogenesis A new stochastic model for subgenomic hepatitis C virus replication considers drug resistant mutants Distinct Roles for Intracellular and Extracellular Lipids in Hepatitis C Virus Infection.Stearoyl-CoA desaturase inhibition blocks formation of hepatitis C virus-induced specialized membranes NS5A inhibitors unmask differences in functional replicase complex half-life between different hepatitis C virus strains.Hepatitis C virus capsid protein and intracellular lipids interplay and its association with hepatic steatosis Hepatitis C NS5A protein: two drug targets within the same protein with different mechanisms of resistance.Identification of HNRNPK as regulator of hepatitis C virus particle production.Serine phosphorylation of the hepatitis C virus NS5A protein controls the establishment of replication complexes.Quantification of Hepatitis C Virus Cell-to-Cell Spread Using a Stochastic Modeling Approach.Viral RNA Degradation and Diffusion Act as a Bottleneck for the Influenza A Virus Infection Efficiency.Viral genome imaging of hepatitis C virus to probe heterogeneous viral infection and responses to antiviral therapies.An integrative approach for a network based meta-analysis of viral RNAi screens Multiscale modeling of virus replication and spread.Modeling Viral Spread.Highly heterogeneous mutation rates in the hepatitis C virus genome.Modeling Suggests a Mechanism of Synergy Between Hepatitis C Virus Entry Inhibitors and Drugs of Other Classes Modeling and analysis of innate immune responses induced by the host cells against hepatitis C virus infection.Mathematical modeling of multi-drugs therapy: a challenge for determining the optimal combinations of antiviral drugs.3D Spatially Resolved Models of the Intracellular Dynamics of the Hepatitis C Genome Replication Cycle.Quantitative Analysis of Hepatitis C NS5A Viral Protein Dynamics on the ER Surface.A New Age-Structured Multiscale Model of the Hepatitis C Virus Life-Cycle During Infection and Therapy With Direct-Acting Antiviral Agents.Intracellular hepatitis C modeling predicts infection dynamics and viral protein mechanisms.Mathematical Analysis of Viral Replication Dynamics and Antiviral Treatment Strategies: From Basic Models to Age-Based Multi-Scale Modeling

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Replication vesicles are load- and choke-points in the hepatitis C virus lifecycle.

http://www.wikidata.org/entity/Q31129723

description

2013 nî lūn-bûn

@nan

2013 թուականի Օգոստոսին հրատարակուած գիտական յօդուած

@hyw

2013 թվականի օգոստոսին հրատարակված գիտական հոդված

@hy

2013年の論文

@ja

2013年論文

@yue

2013年論文

@zh-hant

2013年論文

@zh-hk

2013年論文

@zh-mo

2013年論文

@zh-tw

2013年论文

@wuu

name

Replication vesicles are load- and choke-points in the hepatitis C virus lifecycle.

@ast

Replication vesicles are load- and choke-points in the hepatitis C virus lifecycle.

@en

type

label

Replication vesicles are load- and choke-points in the hepatitis C virus lifecycle.

@ast

Replication vesicles are load- and choke-points in the hepatitis C virus lifecycle.

@en

prefLabel

Replication vesicles are load- and choke-points in the hepatitis C virus lifecycle.

@ast

Replication vesicles are load- and choke-points in the hepatitis C virus lifecycle.

@en

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JOURNAL.PPAT.1003561

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P1476

Replication vesicles are load- and choke-points in the hepatitis C virus lifecycle.

@en

P2093

Christian M Hüber

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

Diana Clausznitzer

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

Johannes P Schlöder

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

Manuel Schulze

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

Martin Trippler

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

Nurgazy Sulaimanov

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

Simon M Lenz

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

P2860

Universally sloppy parameter sensitivities in systems biology models

Hepatitis C virus NS3 serine protease interacts with the serpin C1 inhibitor

Hepatitis C virus infection protein network

The hepatitis C virus core protein contains a BH3 domain that regulates apoptosis through specific interaction with human Mcl-1

Hepatitis C virus nonstructural proteins inhibit apolipoprotein B100 secretion

Expression of hepatitis C virus proteins induces distinct membrane alterations including a candidate viral replication complex

Alpha interferon induces distinct translational control programs to suppress hepatitis C virus RNA replication

A diverse range of gene products are effectors of the type I interferon antiviral response

An update on treatment of genotype 1 chronic hepatitis C virus infection: 2011 practice guideline by the American Association for the Study of Liver Diseases

VirHostNet: a knowledge base for the management and the analysis of proteome-wide virus-host interaction networks

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e1003561

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scholarly article

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10.1371/JOURNAL.PPAT.1003561

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8

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9

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Ralf Bartenschlager

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2013-08-22T00:00:00Z

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256291585

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23990783

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3749965

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