ArticleAntimicrobial agents and chemotherapy2010
Inhibition of hepatitis C virus replication by a specific inhibitor of serine-arginine-rich protein kinase.
Article in Antimicrobial agents and chemotherapy, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 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.
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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
36 citing papers in PubMed, 59 citations in OpenAlex.
- CMGC Kinases in Viral Infection and Human Disease.Pathogens (Basel, Switzerland) · 2026Review
- Viral Modulation of Host Splicing.Annual review of virology · 2025Review
- The splicing factor kinase, SR protein kinase 1 (SRPK1) is essential for late events in the human papillomavirus life cycle.PLoS pathogens · 2025Article
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- Prognostic alternative splicing and multi-omics characteristics reveal FTCD is a potential target of hepatocellular carcinoma.Discover oncology · 2024Article
- NMR analysis, cytotoxic activity and theoretical study of a complex between SRPIN340 andFuture medicinal chemistry · 2024Article
- Serine-arginine protein kinases and their targets in viral infection and their inhibition.Cellular and molecular life sciences : CMLS · 2023Review
- Liquid-liquid phase separation of nucleocapsid proteins during SARS-CoV-2 and HIV-1 replication.Cell reports · 2023Review
- The SARS-CoV-2 nucleocapsid protein: its role in the viral life cycle, structure and functions, and use as a potential target in the development of vaccines and diagnostics.Virology journal · 2023Review
- Host protein kinases required for SARS-CoV-2 nucleocapsid phosphorylation and viral replication.Science signaling · 2022Article
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- Host proviral and antiviral factors for SARS-CoV-2.Virus genes · 2021Review
- Inhibition of Long Noncoding RNA Linc-Pint by Hepatitis C Virus in Infected Hepatocytes Enhances Lipogenesis.Hepatology (Baltimore, Md.) · 2021Observational
- Protein-Protein Interaction Inhibitor of SRPKs Alters the Splicing Isoforms of VEGF and Inhibits Angiogenesis.iScience · 2021Article
- Lithium and Therapeutic Targeting of GSK-3.Cells · 2021Review
- Interplay Between CMGC Kinases Targeting SR Proteins and Viral Replication: Splicing and Beyond.Frontiers in microbiology · 2021Review
- Potential for Protein Kinase Pharmacological Regulation inInternational journal of molecular sciences · 2020Review
- A proposed role for the SARS-CoV-2 nucleocapsid protein in the formation and regulation of biomolecular condensates.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
Corrections and comments
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Authors and funding
13 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Splicing of messenger RNAs is regulated by site-specific binding of members of the serine-arginine-rich (SR) protein family, and SR protein kinases (SRPK) 1 and 2 regulate overall activity of the SR proteins by phosphorylation of their RS domains. We have reported that specifically designed SRPK inhibitors suppressed effectively several DNA and RNA viruses in vitro and in vivo. Here, we show that an SRPK inhibitor, SRPIN340, suppressed in a dose-dependent fashion expression of a hepatitis C virus (HCV) subgenomic replicon and replication of the HCV-JFH1 clone in vitro. The inhibitory effects were not associated with antiproliferative or nonspecific cytotoxic effects on the host cells. Overexpression of SRPK1 or SRPK2 resulted in augmentation of HCV replication, while small interfering RNA (siRNA) knockdown of the SRPKs suppressed HCV replication significantly. Immunocytochemistry showed that SRPKs and the HCV core and NS5A proteins colocalized to some extent in the perinuclear area. Our results demonstrate that SRPKs are host factors essential for HCV replication and that functional inhibitors of these kinases may constitute a new class of antiviral agents against HCV infection.
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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.