ArticleJournal of virology2006
The alpha isoform of protein kinase CKI is responsible for hepatitis C virus NS5A hyperphosphorylation.
Article in Journal of virology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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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.
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Who cites it
38 citing papers in PubMed, 73 citations in OpenAlex.
- CK1 and PP1 regulate Rift Valley fever virus genome replication through L protein phosphorylation.Antiviral research · 2024Article
- Targeting ER stress/PKA/GSK-3β/β-catenin pathway as a potential novel strategy for hepatitis C virus-infected patients.Cell communication and signaling : CCS · 2023Article
- Hepatitis C Viral Replication Complex.Viruses · 2021Review
- Hepatitis C Virus Replication.Cold Spring Harbor perspectives in medicine · 2020Review
- DEAD-box RNA Helicase DDX3: Functional Properties and Development of DDX3 Inhibitors as Antiviral and Anticancer Drugs.Molecules (Basel, Switzerland) · 2020Review
- Serine 229 Balances the Hepatitis C Virus Nonstructural Protein NS5A between Hypo- and Hyperphosphorylated States.Journal of virology · 2019Article
- Characterization of a Threonine-Rich Cluster in Hepatitis C Virus Nonstructural Protein 5A and Its Contribution to Hyperphosphorylation.Journal of virology · 2018Article
- Sequential S232/S235/S238 Phosphorylation of the Hepatitis C Virus Nonstructural Protein 5A.Journal of virology · 2018Article
- HCV NS5A dimer interface residues regulate HCV replication by controlling its self-interaction, hyperphosphorylation, subcellular localization and interaction with cyclophilin A.PLoS pathogens · 2018Article
- Casein kinase 1α: biological mechanisms and theranostic potential.Cell communication and signaling : CCS · 2018Review
- Cell culture-adaptive mutations in hepatitis C virus promote viral production by enhancing viral replication and release.World journal of gastroenterology · 2018Article
- Human single chain-transbodies that bound to domain-I of non-structural protein 5A (NS5A) of hepatitis C virus.Scientific reports · 2017Article
- Serine 235 Is the Primary NS5A Hyperphosphorylation Site Responsible for Hepatitis C Virus Replication.Journal of virology · 2017Article
- Phosphoproteomics Identified an NS5A Phosphorylation Site Involved in Hepatitis C Virus Replication.The Journal of biological chemistry · 2016Article
- Phosphorylation of Serine 235 of the Hepatitis C Virus Non-Structural Protein NS5A by Multiple Kinases.PloS one · 2016Article
- Involvement of FKBP6 in hepatitis C virus replication.Scientific reports · 2015Article
- Vinexin β Interacts with Hepatitis C Virus NS5A, Modulating Its Hyperphosphorylation To Regulate Viral Propagation.Journal of virology · 2015Article
- Should NS5A inhibitors serve as the scaffold for all-oral anti-HCV combination therapies?Hepatic medicine : evidence and research · 2015Review
- NS5A inhibitors impair NS5A-phosphatidylinositol 4-kinase IIIα complex formation and cause a decrease of phosphatidylinositol 4-phosphate and cholesterol levels in hepatitis C virus-associated membranes.Antimicrobial agents and chemotherapy · 2014Article
- Expanding the proteome of an RNA virus by phosphorylation of an intrinsically disordered viral protein.The Journal of biological chemistry · 2014Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hepatitis C virus (HCV) has been the subject of intensive studies for nearly two decades. Nevertheless, some aspects of the virus life cycle are still a mystery. The HCV nonstructural protein 5A (NS5A) has been shown to be a modulator of cellular processes possibly required for the establishment of viral persistence. NS5A is heavily phosphorylated, and a switch between a basally phosphorylated form of NS5A (p56) and a hyperphosphorylated form of NS5A (p58) seems to play a pivotal role in regulating HCV replication. Using kinase inhibitors that specifically inhibit the formation of NS5A-p58 in cells, we identified the CKI kinase family as a target. NS5A-p58 increased upon overexpression of CKI-alpha, CKI-delta, and CKI-epsilon, whereas the RNA interference of only CKI-alpha reduced NS5A hyperphosphorylation. Rescue of inhibition of NS5A-p58 was achieved by CKI-alpha overexpression, and we demonstrated that the CKI-alpha isoform is targeted by NS5A hyperphosphorylation inhibitors in living cells. Finally, we showed that down-regulation of CKI-alpha attenuates HCV RNA replication.
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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.