ArticleVirology2009
Formation and function of hepatitis C virus replication complexes require residues in the carboxy-terminal domain of NS4B protein.
Article in Virology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
26 citing papers in PubMed, 41 citations in OpenAlex.
- Porcine alveolar macrophages host proteins interacting with African swine fever virus p72.Frontiers in microbiology · 2024Article
- The Implication of Sphingolipids in Viral Infections.International journal of molecular sciences · 2023Review
- The bZIP Proteins of Oncogenic Viruses.Viruses · 2020Review
- Review
- Rab5 Enhances Classical Swine Fever Virus Proliferation and Interacts with Viral NS4B Protein to Facilitate Formation of NS4B Related Complex.Frontiers in microbiology · 2017Article
- Interaction between Nonstructural Proteins NS4B and NS5A Is Essential for Proper NS5A Localization and Hepatitis C Virus RNA Replication.Journal of virology · 2016Article
- Preclinical Characterization and In Vivo Efficacy of GSK8853, a Small-Molecule Inhibitor of the Hepatitis C Virus NS4B Protein.Antimicrobial agents and chemotherapy · 2015Article
- The interaction between the hepatitis C proteins NS4B and NS5A is involved in viral replication.Virology · 2015Article
- Article
- Lipids and RNA virus replication.Current opinion in virology · 2014Review
- Stearoyl coenzyme A desaturase 1 is associated with hepatitis C virus replication complex and regulates viral replication.Journal of virology · 2014Article
- Modulation of hepatitis C virus genome replication by glycosphingolipids and four-phosphate adaptor protein 2.Journal of virology · 2014Article
- Modulation of hepatitis C virus genome encapsidation by nonstructural protein 4B.Journal of virology · 2013Article
- Hepatitis C virus NS4B targets lipid droplets through hydrophobic residues in the amphipathic helices.Journal of lipid research · 2013Article
- Hepatitis C virus RNA replication.Current topics in microbiology and immunology · 2013Review
- Cytosolic phospholipase A2 gamma is involved in hepatitis C virus replication and assembly.Journal of virology · 2012Article
- Hepatitis C virus activates Bcl-2 and MMP-2 expression through multiple cellular signaling pathways.Journal of virology · 2012Article
- Proline-serine-threonine phosphatase-interacting protein 2 (PSTPIP2), a host membrane-deforming protein, is critical for membranous web formation in hepatitis C virus replication.Journal of virology · 2012Article
- Rab5 and class III phosphoinositide 3-kinase Vps34 are involved in hepatitis C virus NS4B-induced autophagy.Journal of virology · 2011Article
- TARGETING THE NS5A PROTEIN OF HCV: AN EMERGING OPTION.Drugs of the future · 2011Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
During replication, hepatitis C virus (HCV) NS4B protein rearranges intracellular membranes to form foci, or the web, the putative site for HCV replication. To understand the role of the C-terminal domain (CTD) in NS4B function, mutations were introduced into NS4B alone or in the context of HCV polyprotein. First, we show that the CTD is required for NS4B-induced web structure, but it is not sufficient to form the web nor is it required for NS4B membrane association. Interestingly, all the mutations introduced into the CTD impeded HCV genome replication, but only two resulted in a disruption of NS4B foci. Further, we found that NS4B interacts with NS3 and NS5A, and that mutations causing NS4B mislocalization have a similar effect on these proteins. Finally, we show that the redistribution of Rab5 to NS4B foci requires an intact CTD, suggesting that Rab5 facilitates NS4B foci formation through interaction with the CTD.
Indexed as
Identifiers
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.