Mechanism of inflammasome activation by SARS
coronavirus 3a protein: abridged secondary publication
DY Jin, BJ Zheng, HMV Tang
School of Biomedical Sciences and Department of Microbiology, The University of Hong Kong
1. SARS-CoV and its ORF3a protein sufficiently
activate pro-IL-1β transcription and IL-1β
secretion, which are the two signals required for
full activation of NLRP3 inflammasomes.
2. Activation of pro-IL-1β transcription by ORF3a is mediated through NF-κB, and it requires ubiquitin ligase TRAF3.
3. ORF3a interacts with TRAF3 and an adaptor protein ASC required for NLRP3 inflammasome activation.
4. ORF3a activates NLRP3 inflammasomes by promoting TRAF3-mediated ubiquitination of ASC.
2. Activation of pro-IL-1β transcription by ORF3a is mediated through NF-κB, and it requires ubiquitin ligase TRAF3.
3. ORF3a interacts with TRAF3 and an adaptor protein ASC required for NLRP3 inflammasome activation.
4. ORF3a activates NLRP3 inflammasomes by promoting TRAF3-mediated ubiquitination of ASC.