Enoch T, Zinn K, Maniatis T
Mol Cell Biol. 1986 Mar;6(3):801-10. doi: 10.1128/mcb.6.3.801-810.1986.
beta-Interferon (beta-IFN) gene expression can be induced by poly(I)-poly(C) or virus, but there is considerable variation in the extent of induction between different cell lines. We characterized two poorly inducible human cell lines, HeLa and 143 thymidine kinase negative (143 tk-), to define cellular factors involved in the activation of the beta-IFN gene. We show that the deficiency in beta-IFN induction in these cells can be complemented by fusion to highly inducible mouse cells. We conclude that the human cells are deficient in a trans-acting factor required for B-IFN gene activation. The level of induction of the beta-IFN gene in HeLa and 143 tk- cells can also be increased by priming with IFN before induction. If IFN priming is carried out in the presence of cycloheximide, a approximately 200-fold increase in induction is observed. We conclude that activation of the beta-IFN gene requires an IFN-inducible factor that is only expressed at low levels in unprimed HeLa and 143 tk- cells.
β-干扰素（β-IFN）基因表达可由聚肌苷酸-聚胞苷酸（poly(I)-poly(C)）或病毒诱导，但不同细胞系之间诱导程度存在显著差异。我们对两种诱导性较差的人类细胞系——HeLa细胞和143胸苷激酶阴性（143 tk-）细胞进行了特性分析，以确定参与β-IFN基因激活的细胞因子。我们发现，这些细胞中β-IFN诱导缺陷可通过与高诱导性小鼠细胞融合来弥补。我们得出结论，人类细胞缺乏β-IFN基因激活所需的反式作用因子。在诱导前用IFN预处理，也可提高HeLa细胞和143 tk-细胞中β-IFN基因的诱导水平。如果在放线菌酮存在的情况下进行IFN预处理，则可观察到诱导增加约200倍。我们得出结论，β-IFN基因激活需要一种IFN诱导因子，该因子在未预处理的HeLa细胞和143 tk-细胞中仅低水平表达。
