Key result
Expression of the mutant rZAPC88R acts as a dominant negative inhibitor of endogenous human ZAP, enhancing Sindbis virus replication and revealing that homotypic interactions are required for ZAP antiviral function.
Identification of a dominant negative inhibitor of human ZAP reveals an endogenous functional pool and demonstrates that homotypic interactions are essential for its antiviral activity against Sindbis virus.
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Provides dominant-negative tool to probe ZAP function; leaves open whether homotypic interactions can be targeted against Sindbis or related viruses.
Law et al. (2010) studied Sindbis virus infection (in vitro). rZAPC88R (mutant ZAP) expression vs. Wild-type ZAP or LacZ was evaluated on Sindbis virus replication and ZAP homotypic interactions. Expression of the mutant rZAPC88R acts as a dominant negative inhibitor of endogenous human ZAP, enhancing Sindbis virus replication and revealing that homotypic interactions are required for ZAP antiviral function.
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