北大翟中和院士Nature子刊文章

2008年8月19日，北大生科院翟中和院士，特聘****舒红兵（通讯作者）Nature子刊Cell Research发表最新细胞信号转导文章。

　　

原文摘要：

Cell Research advance online publication 19 August 2008; doi: 10.1038/cr.2008.277

Negative feedback regulation of cellular antiviral signaling by RBCK1-mediated degradation of IRF3

Min Zhang¹, Yang Tian¹, Rui-Peng Wang¹, Dong Gao¹, Yan Zhang¹, Fei-Ci Diao¹, Dan-Ying Chen¹, Zhong-He Zhai¹ and Hong-Bing Shu²

1.                               ¹College of Life Sciences, Peking University, Beijing 100871, China

2.                               ²College of Life Sciences, Wuhan University, Wuhan 430072, China

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.

(生物通 张欢)