Regulation of the cellular thymidine kinase gene promoter in simian virus 40-infected cells.
Regulation of the cellular thymidine kinase gene promoter in simian virus 40-infected cells.
复制标题
猿猴病毒 40 感染细胞中细胞胸苷激酶基因启动子的调节。
DOI：
10.1128/jvi.67.8.4964-4971.1993
复制
发表时间：
1993
影响因子：
5.4
通讯作者：
Conrad,SE
中科院分区：
文献类型：
--
作者：
Roehl,HH;Anderson,MM;Mehigh,CS;Conrad,SE
我们检查了猿猴病毒 40 (SV40) 感染的猿猴 CV1 细胞中细胞胸苷激酶 (TK) 基因启动子的调节。核连续转录测定表明，病毒感染后 14 至 16 小时内源基因的转录率增加了三至四倍。此外，SV40在稳定转染的细胞中诱导了含有与细菌新霉素抗性基因连接的人TK启动子的杂合基因，表明启动子序列足以赋予病毒调节作用。对人 TK 启动子缺失突变体的分析表明，相对于转录起始位点位于 -67 和 +30 bp 之间的序列足以对 SV40 感染的细胞进行调节。这些序列元件与血清诱导所需的序列元件不同，后者先前定位于-135和-67之间的区域。这些结果表明 SV40 激活新的细胞途径，而静息细胞的血清刺激不会激活这些途径。
We examined the regulation of the cellular thymidine kinase (TK) gene promoter in simian virus 40 (SV40)-infected simian CV1 cells. Nuclear run-on transcription assays demonstrated a three- to fourfold increase in the rate of transcription of the endogenous gene at 14 to 16 h following viral infection. In addition, hybrid genes containing the human TK promoter linked to the bacterial neomycin resistance gene were induced by SV40 in stably transfected cells, indicating that promoter sequences are sufficient to confer viral regulation. Analysis of human TK promoter deletion mutants indicated that sequences localized between -67 and +30 bp relative to the transcriptional initiation site are sufficient to confer regulation on SV40-infected cells. These sequence elements are distinct from those required for serum induction, which were previously localized to the region between -135 and -67. These results suggest that SV40 activates novel cellular pathways that are not activated by serum stimulation of quiescent cells.