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Inducible processing of interferon regulatory factor-2.

机译：干扰素调节因子2的诱导加工。

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摘要

PRDI-BFc and PRDI-BFi are proteins that bind specifically to a regulatory element required for virus induction of the human beta interferon (IFN-beta). PRDI-BFc is a constitutive binding activity, while the PRDI-BFi binding activity is observed only after cells are treated with inducers such as virus or poly(I).poly(C) plus cycloheximide or in some cells by cycloheximide alone. In this paper we report that PRDI-BFc is interferon regulatory factor-2 (IRF-2), a known transcriptional repressor. In addition, we find that PRDI-BFi is a truncated form of IRF-2, lacking approximately 185 C-terminal amino acids. Thus, PRDI-BFi appears to be generated by inducible proteolysis. Although the affinity of PRDI-BFc/IRF-2 for the IFN-beta promoter does not appear to be affected by the removal of C-terminal amino acids, the ability of PRDI-BFi to function as a repressor in cotransfection experiments is significantly less than that of intact IRF-2. Studies have shown that IRF-2 can block the activity of the transcriptional activator IRF-1, which also binds specifically to the IFN-beta gene promoter. Thus, the inducible proteolysis of IRF-2 may be involved in the regulation of the IFN-beta gene or of other genes in which the ratio of IRF-1 to IRF-2 can affect the level of transcription.
机译：PRDI-BFc和PRDI-BFi是与病毒诱导人β干扰素（IFN-β）所需的调节元件特异性结合的蛋白质。 PRDI-BFc是组成性结合活性，而PRDI-BFi结合活性仅在用诱导剂如病毒或聚（I），聚（C）加环己酰亚胺处理细胞后或在某些细胞中仅通过环己酰亚胺观察到。在本文中，我们报告PRDI-BFc是干扰素调节因子2（IRF-2），一种已知的转录阻遏物。此外，我们发现PRDI-BFi是IRF-2的截短形式，缺少大约185个C端氨基酸。因此，PRDI-BFi似乎是由诱导蛋白水解产生的。尽管PRDI-BFc / IRF-2对IFN-β启动子的亲和力似乎不受C端氨基酸去除的影响，但PRDI-BFi在共转染实验中充当阻遏物的能力明显降低比完整的IRF-2好。研究表明，IRF-2可以阻断转录激活因子IRF-1的活性，后者也与IFN-β基因启动子特异性结合。因此，IRF-2的诱导蛋白水解可能参与IFN-β基因或其中IRF-1与IRF-2的比率可以影响转录水平的其他基因的调节。

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