Analysis on molecular mechanisms of antiviral innate immune regulation via RNA sensors

2016 Fiscal Year Final Research Report

• Project/Area Number: 26293107
• Research Category: Grant-in-Aid for Scientific Research (B)
• Allocation Type: Partial Multi-year Fund
• Section: 一般
• Research Field: Immunology
• Research Institution: Nara Institute of Science and Technology
• Principal Investigator: Kawai Taro 奈良先端科学技術大学院大学, バイオサイエンス研究科, 教授 (50456935)
• Project Period (FY): 2014-04-01 – 2017-03-31
• Keywords: 自然免疫 / ウイルス感染 / シグナル伝達 / サイトカイン

Outline of Final Research Achievements

Virus infection is usually sensed by innate immune receptors for foreign RNAs such as RIG-I-like receptors (RLRs). In this research, we have identified Arl5b as a negative regulator for RLRs signaling. Moreover, we have discovered a lipid kinase PIKfyve as a positive regulator for RLRs. Moreover, we have identified RNA-binding protein HuR as a positive regulator for RLR signaling. We found that HuR binds to mRNA encoding the kinase Plk2 and it plays a critical roles in induction of type I interferon during RLR signaling. These findings demonstrate that HuR-mediated stabilization of Plk2 mRNA regulates antiviral innate immunity.

Free Research Field

自然免疫