Key result
PKR deficiency largely abolished the rapid phosphorylation and nuclear accumulation of IRF-3 induced by infection with E3L deletion mutant vaccinia virus in HeLa cells.
Population
HeLa cells made stably deficient in PKR using an RNA interference strategy compared with PKR-sufficient cells
Comparison
Infection with E3L deletion mutant virus or… vs PKR-sufficient cells vs PKR-deficient cells
Design
Preclinical
Authors
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PKR mediates IRF-3 antiviral signaling in cell models; leaves open in vivo relevance and clinical translation.
PKR facilitates the host innate immune response and apoptosis in virus-infected cells by mediating IRF-3 activation through the mitochondrial IPS-1 signal transduction pathway.
Zhang et al. (2008) studied Vaccinia virus infection. PKR deficiency via RNA interference vs. PKR-sufficient cells was evaluated on IRF-3 phosphorylation and nuclear accumulation. PKR deficiency largely abolished the rapid phosphorylation and nuclear accumulation of IRF-3 induced by infection with E3L deletion mutant vaccinia virus in HeLa cells.
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