Key result
The TMEV L protein blocks cellular mRNA export from the nucleus, correlating with Nup98 phosphorylation, and inhibits transcription of cytokine genes by preventing IRF-3 dimerization.
Population
BHK-21, BALB/3T3, and L929 cell lines; 3-4-week-old 129/Sv type I IFN receptor-deficient and wild-type mice.
Comparison
Theiler's murine encephalomyelitis virus… vs Mock infection, uninfected cells, or TMEV…
Design
Preclinical
Authors
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Highlights dual antiviral suppression by TMEV L protein in mice; leaves open relevance to human picornavirus pathogenesis.
The TMEV L protein antagonizes host antiviral responses through dual mechanisms: blocking mRNA export via Nup98 phosphorylation and inhibiting IRF-3 dimerization to suppress interferon transcription.
Ricour et al. (2008) studied Theiler's murine encephalomyelitis virus (TMEV) infection. TMEV L protein vs. Mutant L protein (Lcys or L deletion) or mock infection was evaluated on Inhibition of mRNA export and IRF-3 dimerization. The TMEV L protein blocks cellular mRNA export from the nucleus, correlating with Nup98 phosphorylation, and inhibits transcription of cytokine genes by preventing IRF-3 dimerization.
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