ArticleThe Journal of general virology2020
Nucleolin (NCL) inhibits the growth of peste des petits ruminants virus.
Article in The Journal of general virology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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Who cites it
9 citing papers in PubMed, 18 citations in OpenAlex.
- Nucleolin a Central Player in Host Virus Interactions and its Role in Viral Progeny Production.Molecular biotechnology · 2026Review
- Japanese encephalitis virus NS5 protein interacts with nucleolin to enhance the virus replication.Journal of virology · 2024Article
- Ubiquitination-dependent degradation of nucleolin mediated by porcine circovirus type 3 capsid protein.Journal of virology · 2023Article
- Quantitative analysis of acetylation in peste des petits ruminants virus-infected Vero cells.Virology journal · 2023Article
- Interaction of Nucleolin with the Fusion Protein of Avian Metapneumovirus Subgroup C Contributes to Viral Replication.Viruses · 2022Article
- Seneca Valley Virus 3CMicrobiology spectrum · 2022Article
- Development of Nanobodies Targeting Peste des Petits Ruminants Virus: The Prospect in Disease Diagnosis and Therapy.Animals : an open access journal from MDPI · 2021Article
- Caprine MAVS Is a RIG-I Interacting Type I Interferon Inducer Downregulated by Peste des Petits Ruminants Virus Infection.Viruses · 2021Article
- Modification of Nuclear Compartments and the 3D Genome in the Course of a Viral Infection.Acta naturaeArticle
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Peste des petits ruminants (PPR) is a highly contagious disease of small ruminants that is caused by peste des petits ruminants virus (PPRV). To date, the molecular mechanism of PPRV infection is still unclear. It is well known that host proteins might be involved in the pathogenesis process for many viruses. In this study, we first proved that nucleolin (NCL), a highly conserved host factor, interacts with the core domain of PPRV N protein through its C terminus and co-locates with the N protein in the nucleus of cells. To investigate the role of NCL in PPRV infection, the expression level of NCL was inhibited with small interfering RNAs of NCL, and the results showed that PPRV growth was improved. However, the proliferation of PPRV was inhibited when the expression level of NCL was improved. Further analysis indicated that the inhibitory effect of NCL on the PPRV was caused by stimulating the interferon (IFN) pathways in host cells. In summary, our results will help us to understand the mechanism of PPRV 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.