4月28日，美國《國家科學院院刊》(Proceedings of the National Academy of Sciences of the United States of America, 簡稱PNAS)發(fā)表了武漢大學生命科學學院舒紅兵研究組關于細胞抗病毒天然免疫負反饋調控機制的最新研究成果,，論文題目是“ISG56 is a negative-feedback regulator of virus-triggered signaling and cellular antiviral response”,。該文的第一作者是舒紅兵教授的研究生李穎，論文中蛋白質譜鑒定工作是其與中國科學院生物物理所楊福全研究組合作完成的,。
天然免疫是細胞和機體天然存在的非特異性或廣譜的抗病原微生物的功能，是機體抵抗病原微生物的第一道防線?？共《咎烊幻庖咦钪匾姆绞街皇峭ㄟ^I型干擾素（α/β干擾素）來介導的。在過去幾年中,，舒紅兵研究組發(fā)現了病毒感染誘導I型干擾素表達的信號轉導中兩個關鍵的接頭蛋白VISA和MITA,，論文分別在Molecular Cell和Immunity發(fā)表后，引起廣泛關注,，其中發(fā)表在Molecular Cell的論文在發(fā)表后三年多時間里已被SCI他引270多次,。舒紅兵研究組在近年中還發(fā)現了多種抗病毒天然免疫信號轉導的負調控機制，相關結果發(fā)表在Immunity, PNAS, EMBO J.等雜志,。
在這項最新研究中,，舒紅兵研究組發(fā)現病毒感染誘導的一個主要細胞蛋白ISG56通過打斷MITA相關信號轉導復合物的形成，抑制病毒誘導的I型干擾素表達,，從而揭示了一種新的抗病毒天然免疫信號轉導負反饋調控機制,。該項研究擴展了對ISG56功能機理的傳統(tǒng)認識，為了解抗病毒天然免疫的精細調控機制提供了新信息,。（生物谷Bioon.com）
生物谷推薦原始出處：
PNAS April 28, 2009, doi: 10.1073/pnas.0900818106
ISG56 is a negative-feedback regulator of virus-triggered signaling and cellular antiviral response
Ying Lia, Chao Lia, Peng Xueb, Bo Zhonga, Ai-Ping Maoa, Yong Rana, He Chena, Yan-Yi Wanga, Fuquan Yangb and Hong-Bing Shua,1
IFN-stimulated gene 56 (ISG56) is one of the first identified proteins induced by viruses and type I IFNs. In this study, we identified ISG56 as a virus-induced protein associated with MITA, an adapter protein involved in virus-triggered induction of type I IFNs. Overexpression of ISG56 inhibited Sendai virus-triggered activation of IRF3, NF-κB, and the IFN-β promoter, whereas knockdown of ISG56 had opposite effects. Consistently, overexpression of ISG56 reversed cytoplasmic poly(I:C)-induced inhibition of vesicular stomatitis virus (VSV) replication, whereas knockdown of ISG56 inhibited VSV replication. Competitive coimmunoprecipitation experiments indicated that ISG56 disrupted the interactions between MITA and VISA or TBK1, two components in the virus-triggered IFN signaling pathways. These results suggest that ISG56 is a mediator of negative-feedback regulation of virus-triggered induction of type I IFNs and cellular antiviral responses.
