Kalinina N O, Skarlat I V
Biokhimiia. 1988 Jan;53(1):107-12.
As shown previously, the bulk of cellular mRNA in Krebs II ascite carcinoma cells infected with encephalomyocarditis virus during active virus-specific synthesis is bound to ribosomes within the 100S structure which is inactive in protein synthesis. In order to elucidate the reasons for the translation repression of cellular mRNA within the 100S structure, a fraction of loosely bound proteins which are liberated by treatment of the 100S structure with 0.5 M KCl an which contain sum translation factors, was obtained. This fraction was shown to contain an inhibitor which non-specifically represses the translation of endogenous viral and cellular mRNA within the composition of polyribosomes and of exogenous poly(A)-containing cellular mRNAs from ascite carcinoma cells.
如前所示,在活跃的病毒特异性合成过程中,感染脑心肌炎病毒的克雷布斯II腹水癌细胞中的大部分细胞mRNA与100S结构内的核糖体结合,该结构在蛋白质合成中无活性。为了阐明100S结构内细胞mRNA翻译抑制的原因,获得了一部分松散结合的蛋白质,这些蛋白质通过用0.5M KCl处理100S结构而释放出来,并且含有一些翻译因子。结果表明,该部分含有一种抑制剂,该抑制剂在多核糖体组成中可非特异性地抑制内源性病毒和细胞mRNA以及腹水癌细胞中外源含poly(A)细胞mRNA的翻译。