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爱泼斯坦 - 巴尔病毒超感染的拉吉TK阴性细胞中胸苷激酶(TK)的合成

Synthesis of thymidine kinase (TK) in Epstein-Barr virus-superinfected Raji TK-negative cells.

作者信息

Roubal J, Klein G

出版信息

Intervirology. 1981;15(1):43-8. doi: 10.1159/000149213.

Abstract

Epstein-Barr virus (EBV) from P3HR-1 cells, but not from B95-8 cells, can induce the synthesis of thymidine kinase (TK) in TK-negative Raji cells. The synthesis of TK was slightly reduced, but not inhibited, when cells were cultivated in the presence of cytosine arabinoside (ara-C). On the other hand, the synthesis of TK in ordinary Raji cells was enhanced in the presence of the drug. Thymidine-beta-D-arabinofuranoside (ara-T) was capable of reducing the conversion rate of thymidine to TdR nucleotides by extracts prepared from superinfected Raji TK-cells, but had no influence on TK activity in cell extracts from ordinary Raji cells and EBV-negative Ramos cells. This suggested a broader substrate specificity of the virally induced enzyme.

摘要

来自P3HR - 1细胞而非B95 - 8细胞的爱泼斯坦 - 巴尔病毒(EBV)可诱导TK阴性的拉吉细胞合成胸苷激酶(TK)。当细胞在阿糖胞苷(ara - C)存在的情况下培养时,TK的合成略有减少,但未被抑制。另一方面,在该药物存在的情况下,普通拉吉细胞中TK的合成增强。胸苷 - β - D - 阿拉伯呋喃糖苷(ara - T)能够降低由超感染的拉吉TK细胞制备的提取物将胸苷转化为TdR核苷酸的转化率,但对普通拉吉细胞和EBV阴性的 Ramos细胞的细胞提取物中的TK活性没有影响。这表明病毒诱导酶具有更广泛的底物特异性。

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