DNA识别受体在病原体入侵引发的固有免疫应答反应中具有关键作用，MITA（又名STING）是DNA识别受体信号通路中的关键蛋白，泛素化修饰是调控该信号通路的常见机制。E3泛素连接酶RNF144A在固有免疫应答反应中的功能尚不清楚。我们的初步研究提示，1）RNF144A与STING存在免疫共沉淀2）RNF144A促进STING的泛素化3）RNF144A促进STING介导的固有免疫信号通路。据此我们提出假说，RNF144A通过STING的泛素化修饰来调控固有免疫应答反应。我们拟通过免疫印迹、实时定量PCR、ELISA、免疫共沉淀、免疫荧光、荧光素酶报告基因检测、体外泛素化检测、空斑检测及RNAi等实验方法，利用RNF144A缺陷小鼠和细胞株，验证这一假说，揭示RNF144A在固有免疫应答反应中的功能及机制。该研究有助于深入理解机体内的固有免疫应答反应，并可能为临床上研制相关药物和疫苗提供线索。

DNA sensor is essential to pathogen-triggered innate immune responses. MITA, also called STING, is the central molecular in DNA sensor signaling pathways, and ubiquitination is one of the most well studied posttranslational modification regulating these pathways. RNF144A is a known E3 ubiquitin ligase and its role in innate immune responses is unknown. Our research indicated that RNF144A might interact with STING, promoting the ubiquitination of STING and STING-mediated innate immune responses. Therefore, we propose the hypothesis that RNF144A regulates innate immune responses by targeting STING for ubiquitination. We will prove this hypothesis by the methods of western blot, real-time PCR, ELISA, coimmunoprecipitation, immunofluorescence microscopy，luciferase reporter gene assay, in vitro ubiquitination assay, plague assay and RNAi silence. Furthermore, we will use RNF144A deficient cells and mice to illuminate the function and mechanism of RNF144A in innate immune responses. This research will contribute to our understanding of innate immune responses and may provide clues for drug and vaccine development against infectious diseases.