Harada H, Fujita T, Miyamoto M, Kimura Y, Maruyama M, Furia A, Miyata T, Taniguchi T
Institute for Molecular and Cellular Biology, Osaka University, Japan.
Cell. 1989 Aug 25;58(4):729-39. doi: 10.1016/0092-8674(89)90107-4.
Viral infections commonly induce expression of type I interferon (IFN) genes. The induction is transient and involves transcriptional activation wherein a positive factor, IRF-1, binds to upstream regulatory cis elements. In the present study we report the isolation of a cDNA encoding a novel factor, termed IRF-2, that interacts with the same nucleotide sequence elements as IRF-1. Both genes are inducible not only by virus but also by IFN. Unlike IRF-1, IRF-2 does not function as an activator; rather, it suppresses the function of IRF-1 under certain circumstances. Our results suggest that transcription of the IFN and IFN-inducible genes is regulated by two similar trans-acting factors that apparently compete for the same cis-acting recognition sequences, but which have opposite effects.
病毒感染通常会诱导I型干扰素（IFN）基因的表达。这种诱导是短暂的，涉及转录激活，其中一个正向因子IRF-1与上游调控顺式元件结合。在本研究中，我们报告了一个编码新型因子（称为IRF-2）的cDNA的分离，该因子与IRF-1结合相同的核苷酸序列元件。这两个基因不仅可被病毒诱导，也可被IFN诱导。与IRF-1不同，IRF-2不具有激活剂的功能；相反，在某些情况下它会抑制IRF-1的功能。我们的结果表明，IFN和IFN诱导基因的转录受两个相似的反式作用因子调控，这两个因子显然竞争相同的顺式作用识别序列，但作用相反。
