ArticleJournal of virology2004
Characterization of the amino acid residues of sendai virus C protein that are critically involved in its interferon antagonism and RNA synthesis down-regulation.
Article in Journal of virology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 49 citations in OpenAlex.
- The human DEAD-box protein DDX3X regulates host and viral mRNA translation during Sendai Virus infection.bioRxiv : the preprint server for biology · 2026Article
- SeV C Protein Plays a Role in Restricting Macrophage Phagocytosis by Limiting the Generation of Intracellular Double-Stranded RNA.Frontiers in microbiology · 2022Article
- Structural analysis of the STAT1:STAT2 heterodimer revealed the mechanism of Sendai virus C protein-mediated blockade of type 1 interferon signaling.The Journal of biological chemistry · 2017Article
- Type I Interferon-Mediated Induction of Antiviral Genes and Proteins Fails to Protect Cells from the Cytopathic Effects of Sendai Virus Infection.Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research · 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
- Simian virus 40 large T antigen induces IFN-stimulated genes through ATR kinase.Journal of immunology (Baltimore, Md. : 1950) · 2014Article
- Attenuated and protease-profile modified sendai virus vectors as a new tool for virotherapy of solid tumors.PloS one · 2014Article
- Article
- Paramyxovirus activation and inhibition of innate immune responses.Journal of molecular biology · 2013Review
- Paramyxovirus evasion of innate immunity: Diverse strategies for common targets.World journal of virology · 2013Review
- Clustered basic amino acids of the small sendai virus C protein Y1 are critical to its RAN GTPase-mediated nuclear localization.PloS one · 2013Article
- Article
- 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
- Cytopathogenesis of Sendai virus in well-differentiated primary pediatric bronchial epithelial cells.Journal of virology · 2010Article
- Conserved charged amino acids within Sendai virus C protein play multiple roles in the evasion of innate immune responses.PloS one · 2010Article
- N-terminally truncated C protein, CNDelta25, of human parainfluenza virus type 3 is a potent inhibitor of viral replication.Virology · 2009Article
- Evidence for phosphorylation of human parainfluenza virus type 3 C protein: mutant C proteins exhibit variable inhibitory activities in vitro.Virus research · 2009Article
- Host specificity of the anti-interferon and anti-apoptosis activities of parainfluenza virus P/C gene products.The Journal of general virology · 2009Article
- The C proteins of human parainfluenza virus type 1 (HPIV1) control the transcription of a broad array of cellular genes that would otherwise respond to HPIV1 infection.Journal of virology · 2009Article
- Virus versus host cell translation love and hate stories.Advances in virus research · 2009Review
Corrections and comments
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Authors and funding
10 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sendai virus (SeV) encodes two accessory proteins, V and C, in the alternative reading frames in the P gene that are accessed transcriptionally (V) or translationally (C). The C protein is expressed as a nested set of four C-coterminal proteins, C', C, Y1, and Y2, that use different initiation codons. Using HeLa cell lines constitutively expressing the various C proteins, we previously found that the smallest (the 175-residue Y2) of the four C proteins was fully capable of counteracting the antiviral action of interferons (IFNs) and inhibiting viral RNA synthesis and that the C-terminal half of 106 residues was sufficient for both of these inhibitory functions (A. Kato et al., J. Virol. 75:3802-3810, 2001, and A. Kato et al., J. Virol. 76:7114-7124, 2002). Here, we further generated HeLa cell lines expressing the mutated C (Cm) proteins with charged amino acids substituted for alanine residues at either positions 77 and 80; 114 and 115; 139 and 142; 151, 153, and 154; 156; or 173, 175, and 176. We found that only the mutations at positions 151, 153, and 154 abolished IFN antagonism. All the Cm proteins lost the ability to bind with STAT1 under our assay conditions, regardless of their ability to inhibit IFN signaling. On the other hand, the Cm proteins that altered the tyrosine phosphorylation and dephosphorylation of STAT1 and STAT2 always retained IFN antagonism. Thus, the abnormality of phosphorylation or dephosphorylation appeared to be a cause of the IFN antagonism by SeV C. Regarding viral RNA synthesis inhibition, all mutants but the mutant with replacements at positions 114 and 115 greatly reduced the inhibitory activity, indicating that anti-RNA synthesis by the C protein is governed by amino acids scattered across its C-terminal half. Thus, amino acid sequence requirements differ greatly between IFN antagonism and RNA synthesis inhibition. In addition, we confirmed that another SeV accessory protein, V, does not antagonize IFN.
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