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脑心肌炎病毒感染艾氏腹水瘤细胞导致组蛋白合成停止。

Shutoff of histone synthesis by Mengovirus infection of Ehrlich ascites tumor cells.

作者信息

Egberts E, Hackett P B, Traub P

出版信息

Hoppe Seylers Z Physiol Chem. 1977 Apr;358(4):463-74. doi: 10.1515/bchm2.1977.358.1.463.

Abstract

The histone synthesizing capacity of mengovirus-infected Ehrlich ascites tumor cells and of their corresponding postnuclear supernatants was investigated as a funcion of time post-infection. In addition, histone synthesis was compared with the synthesis of other basic host proteins under identical conditions. In the scope of mengovirus infection of Ehrlich ascites tumor cells the less complex fraction comprising basic protein, separated from the acidic proteins by carboxymethyl cellulose chromatography, can be regarded as a representative of total host protein. Histones and the remaining basic host proteins therefore are well suited as easily identifiable indicators of the host protein synthesizing potential of mengovirus-infected Ehrlich ascites tumor cells. The cessation of histone synthesis proceeds faster than the arrest of the synthesis of other basic host protein.

摘要

研究了感染脑心肌炎病毒的艾氏腹水瘤细胞及其相应的核后上清液中组蛋白合成能力随感染后时间的变化。此外,在相同条件下,将组蛋白合成与其他碱性宿主蛋白的合成进行了比较。在脑心肌炎病毒感染艾氏腹水瘤细胞的范围内,通过羧甲基纤维素色谱法从酸性蛋白中分离出的包含碱性蛋白的较简单部分,可被视为总宿主蛋白的代表。因此,组蛋白和其余碱性宿主蛋白非常适合作为感染脑心肌炎病毒的艾氏腹水瘤细胞宿主蛋白合成潜力的易于识别的指标。组蛋白合成的停止比其他碱性宿主蛋白合成的停止进行得更快。

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