ras oncogene activation of a VL30 transcriptional element is linked to transformation.
ras oncogene activation of a VL30 transcriptional element is linked to transformation.
复制标题
ras 癌基因激活 VL30 转录元件与转化有关。
DOI：
10.1128/mcb.10.1.1-9.1990
复制
发表时间：
1990
影响因子：
5.3
通讯作者：
Ostrowski,MC
中科院分区：
文献类型：
--
作者：
Owen,RD;Bortner,DM;Ostrowski,MC
The activity of a murine VL30 transcriptional element was increased 20-fold in transient assays by coexpression of mutantrasgenes. Theciselement did not respond torasin a revertant cell line that was transformation defective. Therefore,ras-dependent alterations in transcription andrastransformation are linked. Deletion analysis of the VL30 long-terminal-repeat U3 region showed that a minimal 53-base-pair segment is required incisfor oncogene activation of transcription. Gel retention assays using a probe that contained the minimalciselement revealed that a unique complex was formed with nuclear proteins prepared from transformed cells. Exonuclease III footprinting and gel retention experiments that used oligonucleotide probes and competitors indicated that two distinct nuclear factors interact with the minimal cw-responsive element. Site-directed deletion of the 5'-proximal binding site (TGACTCT) resulted in a complete loss ofrasresponsiveness. However, deletion of this site did not affect stimulation by the phorbol ester 12-0-tetradecanoylphorbol-13-acetate (TPA). These data are consistent with the hypothesis thatrasand TPA signal transduction mechanisms for transcriptional activation are distinct.
