Synthesis of thymidine kinase (TK) in Epstein-Barr virus-superinfected Raji TK-negative cells.
Synthesis of thymidine kinase (TK) in Epstein-Barr virus-superinfected Raji TK-negative cells.
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Epstein-Barr 病毒重复感染的 Raji TK 阴性细胞中胸苷激酶 (TK) 的合成。
DOI：
10.1159/000149213
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发表时间：
1981
期刊：
影响因子：
4.6
通讯作者：
G. Klein
中科院分区：
文献类型：
--
作者：
J. Roubal;G. Klein
来自P3 HR-1细胞的EB病毒（EBV）可诱导胸苷激酶（TK）阴性Raji细胞合成TK，而来自B 95 -8细胞的EBV不能诱导TK阴性Raji细胞合成TK。当细胞在阿糖胞苷（ara-C）存在下培养时，TK的合成略有减少，但不受抑制。另一方面，在药物存在下，普通Raji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Raji TK-细胞制备的提取物的胸苷向TdR核苷酸的转化率，但对普通Raji细胞和EBV阴性拉莫斯细胞提取物的TK活性没有影响。这表明病毒诱导的酶具有更广泛的底物特异性。
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.