SIMIAN VIRUS-40 REPLICATION IN ADENOVIRUS-TRANSFORMED HUMAN-CELLS ANTAGONIZES GENE-EXPRESSION
SIMIAN VIRUS-40 REPLICATION IN ADENOVIRUS-TRANSFORMED HUMAN-CELLS ANTAGONIZES GENE-EXPRESSION
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DOI：
10.1038/317169a0
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发表时间：
1985-01-01
期刊：
影响因子：
64.8
通讯作者：
CALOS, MP
中科院分区：
文献类型：
--
作者：
LEBKOWSKI, JS;CLANCY, S;CALOS, MP
猴病毒40（SV40）在猴肾细胞中有效复制。然而，我们现在已经发现，基于SV40的载体转染到大多数人类细胞中，复制效果很差，如果有的话。相反，在用腺病毒早期区域转化的人胚肾（HEK）细胞中观察到强SV40复制，但在未转化的HEK细胞中未观察到。腺病毒转化细胞中的载体复制依赖于SV40复制起点和大T抗原的存在。然而，在免疫荧光检测不到的大T抗原水平下发生剧烈复制。这些数据表明，腺病毒癌基因创造了一个复制许可的环境，SV40复制子响应。此外，在我们的载体上，复制和基因表达似乎是拮抗的。只有当载体复制被大T抗原基因或复制起点突变阻断，或被阿非迪霉素直接抑制DNA聚合酶阻断时，才能观察到高水平的大T抗原。
Simian virus 40 (SV40) replicates efficiently in monkey kidney cells. However, we have now found that SV40-based vectors transfected into most human cells replicate poorly, if at all. In contrast, strong SV40 replication is observed in human embryonic kidney (HEK) cells transformed with the adenovirus early region, but not in untransformed HEK cells. Vector replication in adenovirus-transformed cells is dependent on the presence of the SV40 origin of replication and large-T antigen. However, vigorous replication occurs at levels of large-T antigen that are undetectable by immunofluorescence. These data suggest that the adenovirus oncogenes create a replication-permissive environment to which the SV40 replicon responds. Furthermore, replication and gene expression seem to be antagonistic on our vectors. High levels of large-T antigen are observed only when vector replication is blocked by mutations in the gene for large-T antigen or the origin of replication, or by direct inhibition of DNA polymerase with aphidicolin.