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从感染脑心肌炎病毒的艾氏腹水瘤细胞中分离出的多聚腺苷酸加尾信使核糖核酸的编码能力。

Coding capacity of poly(A)+mRNA isolated from mengovirus-infected Ehrlich ascites tumor cells.

作者信息

Hackett P B, Egberts E, Buchwald I, Traub P

出版信息

Mol Biol Rep. 1977 Sep;3(5):387-95. doi: 10.1007/BF00420398.

Abstract

Total poly (A)+mRNA was isolated from mengovirus-infected Ehrlich ascites tumor cells at various times postinfection and quantitated in a cell-free system derived from uninfected ascites cells. Basic proteins were separated from acidic proteins by carboxymethyl cellulose chromatography. At the end of the infectious cycle, 8h postinfection, the cellular contents of most mRNAs coding for basic ribosomal proteins are still between 70 and 90 percent of those measured at the beginning of infection or in uninfected cells. On the basis of this result, the rapid shutoff of host protein synthesis after mengovirus infection of Ehrlich ascites tumor cells cannot be the consequence of the inactivation of host template RNA.

摘要

在感染后不同时间从感染脑心肌炎病毒的艾氏腹水瘤细胞中分离出总聚腺苷酸加尾信使核糖核酸(poly (A)+mRNA),并在源自未感染腹水细胞的无细胞系统中进行定量分析。通过羧甲基纤维素色谱法将碱性蛋白与酸性蛋白分离。在感染周期结束时,即感染后8小时,大多数编码碱性核糖体蛋白的信使核糖核酸的细胞含量仍为感染开始时或未感染细胞中所测含量的70%至90%。基于这一结果,脑心肌炎病毒感染艾氏腹水瘤细胞后宿主蛋白合成的快速关闭并非宿主模板核糖核酸失活的结果。

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