干扰素γ诱导的小鼠ISGF3γ（p48）基因转录由新因子介导。
Interferon gamma-induced transcription of the murine ISGF3gamma (p48) gene is mediated by novel factors.
作者信息
Weihua X, Kolla V, Kalvakolanu D V
机构信息
University of Maryland Cancer Center, Department of Microbiology and Immunology, University of Maryland School of Medicine, Baltimore 21201, USA.
出版信息
Proc Natl Acad Sci U S A. 1997 Jan 7;94(1):103-8. doi: 10.1073/pnas.94.1.103.
Abstract
In this investigation, we show that the gene encoding p48, a subunit of transcription factor ISGF3, is transcriptionally induced by interferon gamma (IFN-gamma). We have identified a novel IFN-gamma-activated response element in the p48 gene promoter. This motif, notated as gamma-activated transcriptional element (GATE), has no significant resemblance to either pIRE (palindromic IFN-response element) or GAS (the IFN-gamma-activated sequence) but has partial homology to ISRE (IFN-stimulated response element). When fused to a neutral promoter, GATE, a 24-bp element, induced the expression of reporter genes following IFN-gamma treatment. In murine RAW cells, two IFN-gamma-inducible factors (GIF) bind to GATE. Binding of these factors to GATE is inhibited by cycloheximide and staurosporine. Although p48 gene induction is dependent on STAT1 and JAK1, activated STAT1 does not bind to GATE. Thus, GIFs appear to be novel trans-acting factors in the IFN-signaling pathway.
摘要
在本研究中，我们发现编码转录因子ISGF3的一个亚基p48的基因可被干扰素γ（IFN-γ）转录诱导。我们在p48基因启动子中鉴定出一个新的IFN-γ激活反应元件。这个基序，记为γ激活转录元件（GATE），与回文IFN反应元件（pIRE）或IFN-γ激活序列（GAS）均无显著相似性，但与IFN刺激反应元件（ISRE）有部分同源性。当与中性启动子融合时，一个24bp的元件GATE在IFN-γ处理后可诱导报告基因的表达。在小鼠RAW细胞中，两个IFN-γ诱导因子（GIF）与GATE结合。这些因子与GATE的结合可被放线菌酮和星形孢菌素抑制。虽然p48基因的诱导依赖于STAT1和JAK1，但活化的STAT1并不与GATE结合。因此，GIF似乎是IFN信号通路中的新型反式作用因子。
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本文引用的文献
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