Journal
SCIENCE SIGNALING
Volume 11, Issue 535, Pages -Publisher
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/scisignal.aas9332
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Funding
- Chinese Academy of Medical Sciences (CAMS) Initiative for Innovative Medicine [2016-I2M-1-005]
- National Science and Technology Major Project for Significant New Drugs Innovation and Development [2015ZX09102023]
- National Natural Science Foundation of China (NSFC) [91542201, 81590765]
- NIH [R01AI069120, AI056154, AI078389]
- Non-profit Central Research Institute Fund of CAMS [2016ZX310194, 2017NL31002]
- Ministry of Science and Technology (China) [2016YFD0500304]
- State Key Laboratory of Pathogen and Biosecurity [SKLPBS1601]
- NSFC Excellent Young Scientist Award [81522025]
- Innovative Research Group [81621005]
- Newton Advanced Fellowship from the UK Academy of Medical Sciences [NAF003/1003]
- NSFC [81661130162]
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Zika virus infection stimulates a type I interferon (IFN) response in host cells, which suppresses viral replication. Type I IFNs exert antiviral effects by inducing the expression of hundreds of IFN-stimulated genes (ISGs). To screen for antiviral ISGs that restricted Zika virus replication, we individually knocked out 21 ISGs in A549 lung cancer cells and identified PARP12 as a strong inhibitor of Zika virus replication. Our findings suggest that PARP12 mediated the ADP-ribosylation of NS1 and NS3, nonstructural viral proteins that are involved in viral replication and modulating host defense responses. This modification of NS1 and NS3 triggered their proteasome-mediated degradation. These data increase our understanding of the antiviral activity of PARP12 and suggest a molecular basis for the potential development of therapeutics against Zika virus.
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