| Title | Negative feedback regulation of cellular antiviral signaling by RBCK1-mediated degradation of IRF3 |
| Authors | Zhang, Min Tian, Yang Wang, Rui-Peng Gao, Dong Zhang, Yan Diao, Fei-Ci Chen, Dan-Ying Zhai, Zhong-He Shu, Hong-Bing |
| Affiliation | Peking Univ, Coll Life Sci, Beijing 100871, Peoples R China. Wuhan Univ, Coll Life Sci, Wuhan 430072, Peoples R China. |
| Keywords | RBCK1 IRF3 antiviral response type I IFNs feedback regulation E3 ligase E3 UBIQUITIN LIGASE RNA HELICASE LGP2 INDUCIBLE GENE-I NF-KAPPA-B RIG-I TRANSCRIPTION FACTOR AUTOIMMUNE-DISEASES INTERFERON RESPONSE ADAPTER PROTEIN VIRUS |
| Issue Date | 2008 |
| Publisher | 细胞研究英文版 |
| Citation | CELL RESEARCH.2008,18,(11),1096-1104. |
| Abstract | Viral infection causes host cells to produce type I interferons (IFNs), which are critically involved in viral clearance. Previous studies have demonstrated that activation of the transcription factor interferon regulatory factor (IRF) 3 is essential for virus-triggered induction of type I IFNs. Here we show that the E3 ubiquitin ligase RBCC protein interacting with PKC1 (RBCK1) catalyzes the ubiquitination and degradation of IRF3. Overexpression of RBCK1 negatively regulates Sendai virus-triggered induction of type I IFNs, while knockdown of RBCK1 has the opposite effect. Plaque assays consistently demonstrate that RBCK1 negatively regulates the cellular antiviral response. Furthermore, viral infection leads to induction of RBCK1 and subsequent degradation of IRF3. These findings suggest that the cellular antiviral response is controlled by a negative feedback regulatory mechanism involving RBCK1-mediated ubiquitination and degradation of IRF3. |
| URI | http://hdl.handle.net/20.500.11897/320001 |
| ISSN | 1001-0602 |
| DOI | 10.1038/cr.2008.277 |
| Indexed | SCI(E) PubMed 中国科技核心期刊(ISTIC) 中国科学引文数据库(CSCD) |
| Appears in Collections: | 生命科学学院 |
