Sundström S, Lundblad D, Lundgren E
Biochim Biophys Acta. 1987 Apr 29;908(3):275-84. doi: 10.1016/0167-4781(87)90108-4.
The putative role of inhibition of protein synthesis within the antiproliferative effect of interferon was analyzed in serum-stimulated Swiss 3T3 mouse fibroblasts. We observed an apparent coupling between protein-synthesis inhibition during G1 and a delayed entry into the S-phase. To reveal any specificity in the protein-synthesis inhibition, we measured the amounts of synthesis of 56 major individual proteins, by using isotope double-labelling and two-dimensional gel electrophoresis. Interferon inhibited preferentially the synthesis of proteins which were increased after serum stimulation, whereas proteins synthesized in constant or decreased amounts after serum stimulation were significantly more resistant. The effects of interferon were also compared to those of 5,6-dichloro-1-beta-ribofuranosylbenzimidazole (DRB), an inhibitor of transcription. All interferon-sensitive proteins studied were inhibited by DRB treatment, but in addition DRB also inhibited several proteins which were completely resistant to interferon. We conclude that interferon primarily inhibits protein synthesis originating from a subset of newly transcribed messenger RNAs. The mechanism(s) for inhibition of protein synthesis and the possible relationship to the antiproliferative and antiviral effects of interferon are discussed.
在血清刺激的瑞士3T3小鼠成纤维细胞中，分析了干扰素抗增殖作用中蛋白质合成抑制的假定作用。我们观察到G1期蛋白质合成抑制与进入S期延迟之间存在明显的关联。为了揭示蛋白质合成抑制的任何特异性，我们通过使用同位素双标记和二维凝胶电泳测量了56种主要单个蛋白质的合成量。干扰素优先抑制血清刺激后增加的蛋白质的合成，而血清刺激后合成量恒定或减少的蛋白质则明显更具抗性。还将干扰素的作用与转录抑制剂5,6-二氯-1-β-呋喃核糖基苯并咪唑（DRB）的作用进行了比较。所有研究的对干扰素敏感的蛋白质都被DRB处理所抑制，但此外DRB还抑制了几种对干扰素完全抗性的蛋白质。我们得出结论，干扰素主要抑制源自新转录的信使RNA子集的蛋白质合成。讨论了蛋白质合成抑制的机制以及与干扰素抗增殖和抗病毒作用的可能关系。
