ArticleJournal of virology2001
Y2, the smallest of the Sendai virus C proteins, is fully capable of both counteracting the antiviral action of interferons and inhibiting viral RNA synthesis.
Article in Journal of virology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 95 citations in OpenAlex.
- Developmental candidate GHP-88310/EIDD-3608 with high tolerability and oral efficacy in measles and respiratory paramyxovirus models.Science advances · 2026Article
- C Proteins: Controllers of Orderly Paramyxovirus Replication and of the Innate Immune Response.Viruses · 2022Review
- C Protein is Essential for Canine Distemper Virus Virulence and Pathogenicity in Ferrets.Journal of virology · 2021Article
- An Insight into DNA-free Reprogramming Approaches to Generate Integration-free Induced Pluripotent Stem Cells for Prospective Biomedical Applications.Stem cell reviews and reports · 2019Review
- Efficient Delivery of Human Cytomegalovirus T Cell Antigens by Attenuated Sendai Virus Vectors.Journal of virology · 2018Article
- Paramyxovirus Glycoproteins and the Membrane Fusion Process.Current clinical microbiology reports · 2016Article
- An RNA Molecule Derived From Sendai Virus DI Particles Induces Antitumor Immunity and Cancer Cell-selective Apoptosis.Molecular therapy : the journal of the American Society of Gene Therapy · 2016Article
- Structural Basis of the Inhibition of STAT1 Activity by Sendai Virus C Protein.Journal of virology · 2015Article
- The RIG-I/MAVS signaling pathway in cancer cell-selective apoptosis.Oncoimmunology · 2013Article
- Clustered basic amino acids of the small sendai virus C protein Y1 are critical to its RAN GTPase-mediated nuclear localization.PloS one · 2013Article
- Expression of the Sendai (murine parainfluenza) virus C protein alleviates restriction of measles virus growth in mouse cells.Proceedings of the National Academy of Sciences of the United States of America · 2011Article
- Conserved charged amino acids within Sendai virus C protein play multiple roles in the evasion of innate immune responses.PloS one · 2010Article
- Complete genome sequence and pathogenicity of two swine parainfluenzavirus 3 isolates from pigs in the United States.Journal of virology · 2010Article
- Article
- N-terminally truncated C protein, CNDelta25, of human parainfluenza virus type 3 is a potent inhibitor of viral replication.Virology · 2009Article
- The matrix protein of measles virus regulates viral RNA synthesis and assembly by interacting with the nucleocapsid protein.Journal of virology · 2009Article
- Measles virus circumvents the host interferon response by different actions of the C and V proteins.Journal of virology · 2008Article
- Human parainfluenza virus type 2 V protein inhibits genome replication by binding to the L protein: possible role in promoting viral fitness.Journal of virology · 2008Article
- Studies on the paramyxovirus accessory genes by reverse genetics in the Sendai virus-mouse system.Proceedings of the Japan Academy. Series B, Physical and biological sciences · 2008Review
- Importance of the anti-interferon capacity of Sendai virus C protein for pathogenicity in mice.Journal of virology · 2007Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
An open reading frame (ORF) overlapping the amino-terminal portion of the Sendai virus (SeV) P ORF in the +1 frame produces a nested set of carboxy-coterminal proteins, C', C, Y1, and Y2, which are referred to collectively as the C proteins. The C proteins are extremely versatile triple-role players; they counteract the antiviral action of interferons (IFNs), inhibit viral RNA synthesis, and are involved in virus assembly. In this study, we established HeLa cell lines stably expressing the C, Y1, and Y2 proteins individually and examined the capacities of these cells to circumvent the antiviral action of alpha/beta IFN (IFN-alpha/beta) and IFN-gamma and to inhibit viral transcription. The assay protocols included monitoring of IFN-alpha/beta-mediated signaling by interferon-stimulated response element-driven reporter gene expression and of the antiviral state induced by IFN-alpha/beta and IFN-gamma and measurement of reporter gene expression from an SeV minigenome, as well as quantification of SeV primary transcripts. When necessary, the activities measured were carefully normalized to the expression levels of the respective C proteins in cells. The data obtained clearly indicate that the smallest protein, Y2, was as active as the C and Y1 proteins in both counteracting the antiviral action of IFNs and inhibiting viral transcription. The data further show that intracellular transexpression of either C, Y1, or Y2 rendered HeLa cells moderately or only poorly permissive for not only wild-type SeV but also 4C(-) SeV, which expressed none of the four C proteins. On the basis of these findings, the roles of SeV C proteins in the natural life cycle are discussed.
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