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首页> 外文期刊>Journal of Virology >Inhibition of Protein Synthesis in Cell-Free Systems from Interferon-Treated, Infected Cells: Further Characterization and Effect of Formylmethionyl-tRNAF
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Inhibition of Protein Synthesis in Cell-Free Systems from Interferon-Treated, Infected Cells: Further Characterization and Effect of Formylmethionyl-tRNAF

机译：抑制来自干扰素处理的感染细胞的无细胞系统中的蛋白质合成：进一步表征和甲酰基甲基乙烯 - TRNAF的作用

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The translation of encephalomyocarditis virus (EMC) RNA is markedly inhibited in cell-free systems from interferon-treated, vaccinia virus-infected L-cells (10, 11). The polypeptide products synthesized in response to EMC RNA in cell-free systems from these and untreated infected cells have been analyzed by electrophoresis on polyacrylamide gels. Qualitatively, the same EMC-specific polypeptides were synthesized throughout. In experiments using preincubated microsomes from normal Krebs cells to assay cell sap from L-cells which had been exposed to interferon prior to infection, only the amount of the EMC-specific polypeptide products was reduced. This result suggests that there is an inhibition very early in translation in interferon-treated, infected cells. Initiation seems a priori the more attractive site for this inhibition, but an effect shortly after initiation cannot be excluded. With unfractionated cell-free systems from interferon-treated infected L-cells, however, there appeared to be an additional minor inhibitory effect on polypeptide chain elongation, in that the EMC-specific polypeptides synthesized showed not only a reduction in amount but also a bias towards lower molecular weight. The formylated methionyl initiator tRNA (Fmet-tRNAF) was used as a further probe into the apparent effect on intiation. With this reagent we have confirmed that there is one major initiation site for the translation of EMC RNA in these cell-free systems. In addition, the results have shown that EMC-specific polypeptide chains initiated with Fmet escape the major interferon-mediated inhibition at or shortly after initiation.
机译：脑膜炎炎病毒（EMC）RNA的翻译显着抑制来自干扰素处理的无细胞系统，疫苗病毒感染的L细胞（10,11）。通过电泳在聚丙烯酰胺凝胶上的电泳分析了响应于来自这些和未处理的感染细胞的无细胞系统中的EMC RNA的多肽产物。定性地，在整个中合成相同的EMC特异性多肽。在使用从正常克雷斯细胞的预孵育微粒体的实验中，在感染之前从L细胞进行测定细胞SAP，只有在感染之前暴露于干扰素的细胞，仅降低了EMC特异性多肽产物的量。该结果表明，在干扰素治疗的感染细胞中存在抑制在翻译中。启动似乎是这种抑制的最有吸引力的部位，但在发起后不久的效果就不能排除在外。然而，通过来自干扰素处理的感染的L-细胞的未分配细胞系统，似乎是对多肽链伸长的额外较小的抑制作用，因为合成的EMC特异性多肽不仅表现出量的还原而且还为偏差而显示朝较低的分子量。甲型内甲硫醇引发剂TRNA（FEMET-TRNA F ）用作进一步的探针进入对抗动性的表观效果。用这种试剂，我们已经证实有一个主要的起始位点用于在这些无细胞系统中翻译EMC RNA。此外，结果表明，在发起后，用Fimmet引发的EMC特异性多肽链逸出或短暂的主要干扰素介导的抑制。

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