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由脑心肌炎病毒RNA编程的小鼠腹水无细胞系统中多肽提前终止的机制。

Mechanism of premature polypetide termination in a mouse ascites cell-free system programmed by encephalomyocarditis viral RNA.

作者信息

Hunt L A

出版信息

J Virol. 1976 May;18(2):788-92. doi: 10.1128/JVI.18.2.788-792.1976.

Abstract

The premature termination and release of encephalomyocarditis viral RNA-programmed polypeptides were analyzed in a cell-free system from mouse ascites tumor cells. The KCL concentration affects the size distribution of products but not the extent of polypeptide release. The same major products (60,000 to 140,000 molecular weight) are found in both the soluble and particulate fractions. The majority of released polypeptides are free protein, whereas the ribosome-bound product is mostly in the form of peptidyl-tRNA.

摘要

在来自小鼠腹水肿瘤细胞的无细胞系统中,对脑心肌炎病毒RNA编程多肽的提前终止和释放进行了分析。氯化钾浓度影响产物的大小分布,但不影响多肽释放的程度。在可溶性和颗粒部分均发现了相同的主要产物(分子量为60,000至140,000)。大多数释放的多肽是游离蛋白,而核糖体结合产物大多是肽基-tRNA的形式。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/db16/515609/1467467f71a0/jvirol00221-0431-a.jpg

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