干扰素诱导的小鼠p48（ISGF3γ）基因受原癌基因c-myc调控。
The interferon-inducible murine p48 (ISGF3gamma) gene is regulated by protooncogene c-myc.
作者信息
Weihua X, Lindner D J, Kalvakolanu D V
机构信息
Marlene and Stewart Greenebaum Cancer Center, University of Maryland School of Medicine, Baltimore, MD 21201, USA.
出版信息
Proc Natl Acad Sci U S A. 1997 Jul 8;94(14):7227-32. doi: 10.1073/pnas.94.14.7227.
Abstract
p48 protein is an integral component of the multimeric interferon (IFN)-regulated transcription factor, ISGF3. We have shown earlier that this gene is regulated by a novel IFN-gamma-regulated element. In addition to the IFN-regulated element, a myc-max binding site is also present in this promoter. In this investigation we have studied the role of this site in the regulation of the p48 gene. In serum-induced quiescent cells Myc up-regulated the expression of p48 mRNA. We show that the protooncogene Myc regulates the expression of p48 through the element CACGTG. Mutations in this motif abolish Myc-inducibility of the reporter genes carrying p48 promoter elements. Purified Myc and Max proteins interact with the Myc-stimulated element of the p48 promoter. We also show that cells lacking p48 expression are highly susceptible to the cytocidal action of anticancer drugs. Taken together these data suggest that p48 may function as an anti-stress cell survival factor.
摘要
p48蛋白是多聚体干扰素（IFN）调节转录因子ISGF3的一个组成部分。我们之前已经表明，该基因受一种新型的IFN-γ调节元件调控。除了IFN调节元件外，该启动子中还存在一个Myc-Max结合位点。在本研究中，我们探讨了该位点在p48基因调控中的作用。在血清诱导的静止细胞中，Myc上调了p48 mRNA的表达。我们发现原癌基因Myc通过元件CACGTG调节p48的表达。该基序中的突变消除了携带p48启动子元件的报告基因的Myc诱导性。纯化的Myc和Max蛋白与p48启动子的Myc刺激元件相互作用。我们还表明，缺乏p48表达的细胞对抗癌药物的杀细胞作用高度敏感。综合这些数据表明，p48可能作为一种抗应激细胞存活因子发挥作用。
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本文引用的文献
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Essential and non-redundant roles of p48 (ISGF3 gamma) and IRF-1 in both type I and type II interferon responses, as revealed by gene targeting studies.基因靶向研究揭示了p48（ISGF3γ）和IRF-1在I型和II型干扰素反应中的重要且非冗余作用。
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Interferon gamma-induced transcription of the murine ISGF3gamma (p48) gene is mediated by novel factors.干扰素γ诱导的小鼠ISGF3γ（p48）基因转录由新因子介导。
Proc Natl Acad Sci U S A. 1997 Jan 7;94(1):103-8. doi: 10.1073/pnas.94.1.103.
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