Hardy Matthew P, McGGettrick Anne F, O'Neill Luke A J
Department of Biochemistry and Biotechnology Institute, Trinity College, University of Dublin, College Green, Dublin 2, Ireland.
Biochem J. 2004 May 15;380(Pt 1):83-93. doi: 10.1042/BJ20040030.
TRIF [TIR (Toll/interleukin-1 receptor) domain-containing adaptor protein inducing interferon beta; also known as TICAM-1 (TIR-containing adaptor molecule-1)] is a key adaptor for TLR3 (Toll-like receptor 3)- and TLR4-mediated signalling. We have performed a detailed annotation of the human TRIF gene and fine analysis of the basal and inducible promoter elements lying 5' to the site of initiation of transcription. Human TRIF maps to chromosome 19p13.3 and is flanked upstream by TIP47, which encodes the mannose 6-phosphate receptor binding protein, and downstream by a gene encoding FEM1a, a human homologue of the Caenorhabditis elegans Feminisation-1 gene. Using promoter-reporter deletion constructs, we identified a distal region with the ability to negatively regulate basal transcription and a proximal region containing an Sp1 (stimulating protein 1) site that confers approx. 75% of basal transcriptional activity. TRIF expression can be induced by multiple stimuli, such as the ligands for TLR2, TLR3 and TLR4, and by the pro-inflammatory cytokines tumour necrosis factor alpha and interleukin-1alpha. All of these stimuli act via an NF-kappaB (nuclear factor-kappaB) motif at position -127. In spite of the presence of a STAT1 (signal transduction and activators of transcription 1) motif at position -330, the addition of type I or type II interferon had no effect on TRIF activity. The human TRIF gene would therefore appear to be regulated primarily by NF-kappaB.
TRIF [含TIR(Toll样/白细胞介素-1受体)结构域的干扰素β诱导衔接蛋白;也称为TICAM-1(含TIR衔接分子-1)]是TLR3(Toll样受体3)和TLR4介导信号传导的关键衔接蛋白。我们对人类TRIF基因进行了详细注释,并对转录起始位点5'端的基础和诱导型启动子元件进行了精细分析。人类TRIF定位于19号染色体p13.3,其上游侧翼是编码甘露糖6-磷酸受体结合蛋白的TIP47,下游侧翼是编码FEM1a的基因,FEM1a是秀丽隐杆线虫雌性化-1基因的人类同源物。使用启动子-报告基因缺失构建体,我们鉴定出一个具有负调控基础转录能力的远端区域和一个包含Sp1(刺激蛋白1)位点的近端区域,该位点赋予约75%的基础转录活性。TRIF表达可由多种刺激诱导,如TLR2、TLR3和TLR4的配体,以及促炎细胞因子肿瘤坏死因子α和白细胞介素-1α。所有这些刺激均通过位于-127位的NF-κB(核因子κB)基序起作用。尽管在-330位存在STAT1(信号转导和转录激活因子1)基序,但添加I型或II型干扰素对TRIF活性没有影响。因此,人类TRIF基因似乎主要受NF-κB调控。