Transcriptional activation of cKi-ras proto-oncogene resulting from retroviral promoter insertion.
Transcriptional activation of cKi-ras proto-oncogene resulting from retroviral promoter insertion.
复制标题
逆转录病毒启动子插入导致 cKi-ras 原癌基因的转录激活。
DOI：
10.1093/nar/17.22.9259
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发表时间：
1989
影响因子：
14.9
通讯作者：
George,DL
中科院分区：
文献类型：
--
作者：
Trusko,SP;Hoffman,EK;George,DL
在骨髓来源的小鼠细胞系416 B中，Ki-ras原癌基因的增强表达已被证明与Friend病毒DNA整合到细胞基因中有关。在这里，我们报告的实验结果，旨在澄清的分子机制负责的Ki-ras过度表达。基于引物延伸分析和cKi-rascDNA克隆的DNA测序，我们获得了证据，416 B细胞含有病毒宿主嵌合转录本，其起始于整合的前病毒的3′长末端重复序列（LTR）内。来自重组的cKi-ras基因的转录物的加工包括与在前病毒和细胞DNA序列之间的连接处偶然产生隐蔽供体剪接位点相关的意外剪接事件。这些数据表明，cKi-ras在416 B细胞中的表达增强是由逆转录病毒启动子插入转录激活机制引起的。
Enhanced expression of thecKi-rasproto-oncogene in a bone marrow-derived mouse cell line, 416B, has been shown to be associated with the integration of Friend viral DNA into the cellular gene. Here we report the results of experiments designed to clarify the molecular mechanism responsible for thecKi-rasoverexpression. Based on primer extension analyses and DNA sequencing ofcKi-rascDNA clones, we have obtained evidence that the 416B cells contain viral-host chimaeric transcripts that initiate within the 3′ long terminal repeat (LTR) of the integrated provirus. Processing of the transcripts from the rearrangedcKi-rasgene includes an unexpected splicing event associated with the fortuitous creation of a cryptic donor splice site at the junction between the proviral and cellular DNA sequences. These data demonstrate that enhancedcKi-rasexpression in the 416B cells results from a retroviral promoter insertion mechanism of transcriptional activation.