ArticleJournal of virology2011
Antagonistic effects of cellular poly(C) binding proteins on vesicular stomatitis virus gene expression.
Article in Journal of virology, 2011. 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.
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Who cites it
26 citing papers in PubMed, 38 citations in OpenAlex.
- Participation of host cell proteins in inclusion bodies of non-segmented RNA virus infected cells: a molecular insight.Virology journal · 2025Review
- HnRNPC triggers the degradation of MITA to suppress the interferon-mediated antiviral response.Veterinary research · 2025Article
- Sensing nucleotide composition in virus RNA.Bioscience reports · 2023Review
- Poly(C)-binding protein 2 positively regulates interferon downstream signaling.Acta biochimica et biophysica Sinica · 2022Article
- Article
- Multiple functions of heterogeneous nuclear ribonucleoproteins in the positive single-stranded RNA virus life cycle.Frontiers in immunology · 2022Review
- Cellular poly(C) binding protein 2 interacts with porcine epidemic diarrhea virus papain-like protease 1 and supports viral replication.Veterinary microbiology · 2020Article
- Identification of protein inhibitor of activated STAT 4, a novel host interacting partner that involved in bovine viral diarrhea virus growth.Virology journal · 2020Article
- Nucleocapsid Interacts with NPM1 and Protects it from Proteolytic Cleavage, Enhancing Cell Survival, and is Involved in PEDV Growth.Scientific reports · 2017Article
- Cellular STAT3 functions via PCBP2 to restrain Epstein-Barr Virus lytic activation in B lymphocytes.Journal of virology · 2015Article
- Interferon-inducible protein IFI35 negatively regulates RIG-I antiviral signaling and supports vesicular stomatitis virus replication.Journal of virology · 2014Article
- Norovirus genome circularization and efficient replication are facilitated by binding of PCBP2 and hnRNP A1.Journal of virology · 2013Article
- Understanding and altering cell tropism of vesicular stomatitis virus.Virus research · 2013Review
- Heterogeneous nuclear ribonucleoprotein K supports vesicular stomatitis virus replication by regulating cell survival and cellular gene expression.Journal of virology · 2013Article
- Mapping the LINE1 ORF1 protein interactome reveals associated inhibitors of human retrotransposition.Nucleic acids research · 2013Article
- Manipulation of cellular processing bodies and their constituents by viruses.DNA and cell biology · 2013Article
- Hemoglobin subunit beta interacts with the capsid protein and antagonizes the growth of classical swine fever virus.Journal of virology · 2013Article
- Poly(C)-binding protein 1, a novel N(pro)-interacting protein involved in classical swine fever virus growth.Journal of virology · 2013Article
- Article
- Induction of stress granule-like structures in vesicular stomatitis virus-infected cells.Journal of virology · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Immunoprecipitation and subsequent mass spectrometry analysis of the cellular proteins from cells expressing the vesicular stomatitis virus (VSV) P protein identified the poly(C) binding protein 2 (PCBP2) as one of the P protein-interacting proteins. To investigate the role of PCBP2 in the viral life cycle, we examined the effects of depletion or overexpression of this protein on VSV growth. Small interfering RNA-mediated silencing of PCBP2 promoted VSV replication. Conversely, overexpression of PCBP2 in transfected cells suppressed VSV growth. Further studies revealed that PCBP2 negatively regulates overall viral mRNA accumulation and subsequent genome replication. Coimmunoprecipitation and immunofluorescence microscopic studies showed that PCBP2 interacts and colocalizes with VSV P protein in virus-infected cells. The P-PCBP2 interaction did not result in reduced levels of protein complex formation with the viral N and L proteins, nor did it induce degradation of the P protein. In addition, PCBP1, another member of the poly(C) binding protein family with homology to PCBP2, was also found to interact with the P protein and inhibit the viral mRNA synthesis at the level of primary transcription without affecting secondary transcription or genome replication. The inhibitory effects of PCBP1 on VSV replication were less pronounced than those of PCBP2. Overall, the results presented here suggest that cellular PCBP2 and PCBP1 antagonize VSV growth by affecting viral gene expression and highlight the importance of these two cellular proteins in restricting virus infections.
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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.