Neddylation of the EV71 VP2 protein at the K69 residue promotes its degradation and restricts viral replication, revealing a novel host defense mechanism.
Reveals a host restriction mechanism for EV71; leaves open whether neddylation can be targeted therapeutically.
Neddylation is a ubiquitin-like posttranslational modification by conjugation of neural precursor cell-expressed developmentally downregulated protein 8 (NEDD8) to specific proteins for regulation of their metabolism and biological activities. In this study, we demonstrated for the first time that EV71 VP2 protein is neddylated at K69 residue to promote viral protein degradation and consequentially suppress multiplication of the virus. Our findings advance knowledge related to the roles of VP2 in EV71 virulence and the neddylation pathway in the host restriction of EV71 infection.
No takes yet. Share an insight, caveat, or question.
Wang et al. (2022) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: