ArticleJournal of virology2003
The amino-terminal extensions of the longer Sendai virus C proteins modulate pY701-Stat1 and bulk Stat1 levels independently of interferon signaling.
Article in Journal of virology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 56 citations in OpenAlex.
- RNase L Amplifies Interferon Signaling by Inducing Protein Kinase R-Mediated Antiviral Stress Granules.Journal of virology · 2020Article
- Interferons and viruses: an evolutionary arms race of molecular interactions.Trends in immunology · 2015Review
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- 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
- Regulation of STAT signaling in mouse bone marrow derived dendritic cells by respiratory syncytial virus.Virus research · 2011Article
- Functional analysis of Rousettus aegyptiacus "signal transducer and activator of transcription 1" (STAT1).Developmental and comparative immunology · 2010Article
- Article
- Article
- Host specificity of the anti-interferon and anti-apoptosis activities of parainfluenza virus P/C gene products.The Journal of general virology · 2009Article
- Human parainfluenza virus type 1 C proteins are nonessential proteins that inhibit the host interferon and apoptotic responses and are required for efficient replication in nonhuman primates.Journal of virology · 2008Article
- Role of interferon in the replication of human parainfluenza virus type 1 wild type and mutant viruses in human ciliated airway epithelium.Journal of virology · 2008Article
- Cytokine-independent upregulation of MDA5 in viral infection.Journal of virology · 2007Article
- Targeting of the Sendai virus C protein to the plasma membrane via a peptide-only membrane anchor.Journal of virology · 2007Article
- Importance of the anti-interferon capacity of Sendai virus C protein for pathogenicity in mice.Journal of virology · 2007Article
- Global suppression of the host antiviral response by Ebola- and Marburgviruses: increased antagonism of the type I interferon response is associated with enhanced virulence.Journal of virology · 2006Article
- A short peptide at the amino terminus of the Sendai virus C protein acts as an independent element that induces STAT1 instability.Journal of virology · 2004Article
- Characterization of the amino acid residues of sendai virus C protein that are critically involved in its interferon antagonism and RNA synthesis down-regulation.Journal of virology · 2004Article
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The Sendai virus (SeV) C proteins are known to interact with Stat1 to prevent interferon (IFN)-induced pY701-Stat1 formation and IFN signaling. Nevertheless, pY701-Stat1 levels paradoxically increase during SeV infection. The C proteins also induce bulk Stat1 instability in some cells, similar to rubulavirus V proteins. We have found that SeV infection increases pY701-Stat1 levels even in cells in which bulk Stat1 levels strongly decrease. Remarkably, both the decrease in bulk Stat1 levels and the increase in pY701-Stat1 levels were found to be independent of the IFN signaling system, i.e., these events occur in mutant cells in which various components of the IFN signaling system have been disabled. Consistent with this, the C-induced decrease in Stat1 levels does not require Y701 of Stat1. We present evidence that C interacts with Stat1 in two different ways, one that prevents IFN-induced pY701-Stat1 formation and IFN signaling that has already been documented, and another that induces pY701-Stat1 formation (while decreasing bulk Stat1 levels) in a manner that does not require IFN signaling. These two types of Stat1 interaction are also distinguishable by C gene mutations. In particular, the IFN signaling-independent Stat1 interactions specifically require the amino-terminal extensions of the longer C proteins. The actions of the SeV C proteins in counteracting the cellular antiviral response are clearly more extensive than previously appreciated.
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