Key result
Downregulation of DHX30 with shRNAs reduced the antiviral activity of the zinc-finger antiviral protein (ZAP), indicating DHX30 is required for optimal ZAP function.
Population
In vitro cell models (implied by pull-down, co-immunoprecipitation, and shRNA assays)
Design
Preclinical
Authors
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Suggests DHX30 as antiviral cofactor target; leaves open translation to human infections or therapies.
DHX30 is identified as a cellular factor required for the optimal antiviral function of ZAP.
Ye et al. (2010) studied this question. Downregulation of DHX30 with shRNAs was evaluated on ZAP's antiviral activity. Downregulation of DHX30 with shRNAs reduced the antiviral activity of the zinc-finger antiviral protein (ZAP), indicating DHX30 is required for optimal ZAP function.
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