Severe acute respiratory syndrome coronavirus (SARS-CoV) encodes eight accessory proteins, the functions of which are not yet fully understood. SARS-CoV protein 6 (P6) is one of the previously studied accessory proteins that have been documented to enhance viral replication and suppress host interferon (IFN) signaling pathways. Through yeast two-hybrid screening, we identified eight potential cellular P6-interacting proteins from a human spleen cDNA library. For further investigation, we targeted the IFN signaling pathway-mediating protein, N-Myc (and STAT) interactor (Nmi). Its interaction with P6 was confirmed within cells. The results showed that P6 can promote the ubiquitin-dependent proteosomal degradation of Nmi. This study revealed a new mechanism of SARS-CoV P6 in limiting the IFN signaling to promote SARS-CoV survival in host cells.
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The authors contributed equally to this work.
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Cheng, W., Chen, S., Li, R. et al. Severe acute respiratory syndrome coronavirus protein 6 mediates ubiquitin-dependent proteosomal degradation of N-Myc (and STAT) interactor. Virol. Sin. 30, 153–161 (2015). https://doi.org/10.1007/s12250-015-3581-8
- severe acute respiratory syndrome coronavirus (SARS-CoV)
- N-Myc (and STAT) interactor (Nmi)
- interferon (IFN) signaling pathway
- proteosomal degradation