ArticleJournal of virology2000
Sendai virus blocks alpha interferon signaling to signal transducers and activators of transcription.
Article in Journal of virology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 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
40 citing papers in PubMed, 108 citations in OpenAlex.
- Double-edged sword of JAK/STAT signaling pathway in viral infections: novel insights into virotherapy.Cell communication and signaling : CCS · 2023Review
- SeV C Protein Plays a Role in Restricting Macrophage Phagocytosis by Limiting the Generation of Intracellular Double-Stranded RNA.Frontiers in microbiology · 2022Article
- High-Throughput Screening Identifies Mixed-Lineage Kinase 3 as a Key Host Regulatory Factor in Zika Virus Infection.Journal of virology · 2019Article
- Sendai virus C protein limits NO production in infected RAW264.7 macrophages.Innate immunity · 2018Article
- 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
- Virus Multiplicity of Infection Affects Type I Interferon Subtype Induction Profiles and Interferon-Stimulated Genes.Journal of virology · 2015Article
- STAT1 interaction with E3-14.7K in monocytes affects the efficacy of oncolytic adenovirus.Journal of virology · 2014Article
- Paramyxovirus evasion of innate immunity: Diverse strategies for common targets.World journal of virology · 2013Review
- Morbillivirus v proteins exhibit multiple mechanisms to block type 1 and type 2 interferon signalling pathways.PloS one · 2013Article
- Domain within the C protein of human parainfluenza virus type 3 that regulates interferon signaling.Gene expression · 2010Article
- Article
- Reovirus mu2 protein inhibits interferon signaling through a novel mechanism involving nuclear accumulation of interferon regulatory factor 9.Journal of virology · 2009Article
- 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
- Role for herpes simplex virus 1 ICP27 in the inhibition of type I interferon signaling.Virology · 2008Article
- Human parainfluenza virus type 4 is incapable of evading the interferon-induced antiviral effect.Journal of virology · 2005Article
- Inhibition of interferon-stimulated JAK-STAT signaling by a tick-borne flavivirus and identification of NS5 as an interferon antagonist.Journal of virology · 2005Article
- Respiratory syncytial virus nonstructural proteins NS1 and NS2 mediate inhibition of Stat2 expression and alpha/beta interferon responsiveness.Journal of virology · 2005Article
- Identification of paramyxovirus V protein residues essential for STAT protein degradation and promotion of virus replication.Journal of virology · 2005Article
- Synergistic inhibition of human cytomegalovirus replication by interferon-alpha/beta and interferon-gamma.Virology journal · 2005Article
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 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We demonstrate here that Sendai virus (SeV) blocks alpha interferon (IFN-alpha) signaling to signal transducers and activators of transcription (STATs) in HeLa cells. IFN-alpha-stimulated tyrosine phosphorylation of STATs and subsequent formation of the IFN-stimulated gene factor 3 transcription complex were inhibited in SeV-infected cells, resulting in inefficient induction of IFN-stimulated gene products. None of the components of the signaling pathway-type I IFN receptor subunits Jak1, Tyk2, Stat1, Stat2, and p48-was degraded. Moreover, tyrosine phosphorylation of Jak1 in response to IFN-alpha was unaffected at the early phase of infection, suggesting that oligomerization of the receptor subunits proceeded normally. In contrast to Jak1, IFN-alpha-stimulated tyrosine phosphorylation of Tyk2 was partially inhibited. Therefore, this partial inhibition of activation of Tyk2 probably contributes to the subsequent failure in the activation of STATs.
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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.