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机构地区:[1]军事医学科学院生物工程研究所 [2]安徽大学生命科学学院,安徽合肥230039 [3]安徽大学生命科学学院
出 处:《生物技术通讯》2008年第5期734-736,共3页Letters in Biotechnology
摘 要:病毒感染启动宿主先天免疫反应是通过激活转录因子NF-κB和干扰素调节因子3(IRF-3),它们协同调控Ⅰ型干扰素的表达。病毒在复制过程中产生的复制中间体双链RNA作为一个病原相关分子模式,被细胞内具有RNA解旋酶活性的维甲酸诱导基因Ⅰ(RIG-1)编码蛋白检测到。线粒体抗病毒蛋白(MAVS)作为一个接头蛋白,在RIG-1信号通路的下游和NF-κB、IRF-3信号通路的上游扮演着重要的角色。MAVS通过其疏水跨膜结构域定位在线粒体外膜上,是线粒体中发现的第一个与先天免疫相关的蛋白质,将线粒体和先天免疫联系在一起。Viral infection triggers host innate immune responses through activation of the transcription factors NF-κB and interferon regulation factor 3(IRF-3), which coordinately regulate the expression of type-Ⅰ interferon. Viruses can form double-strand RNA duplication intermediates in the process of virus replication, which are regarded as an pathogen-associated molecular pattern(PAMP). PAMP can be detected by RIG-1(protein encoded by retinoic acid-induced geneⅠ) intraeellularly, RIG-1 contains a RNA helicase domain and 2 caspase recruitment domain. Mitochondrial antiviral signaling protein (MAVS), as an adaptor molecule, provides a link between RIG-1 sensing to incoming viral RNA and downstream activation events. MAVS is a mitochondral membrane protein which located on the mitochondrail extra-membrane through its transmenbrane domain, thus links mitochondrail with innate immune.
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