Groner B, Hynes N E, Rahmsdorf U, Ponta H
Nucleic Acids Res. 1983 Jul 25;11(14):4713-25. doi: 10.1093/nar/11.14.4713.
A chimeric gene, recombined in vitro, containing a long terminal repeat (LTR) sequence from the proviral DNA of mouse mammary tumor virus and the thymidine kinase (tk) gene of Herpes Simplex Virus was introduced into L tk- cells. No transcription of LTR RNA was observed in transfected cells when glucocorticoid hormones were absent from the growth medium. Accumulation of LTR initiated RNA was measured upon hormone addition by the single strand specific nuclease RNA mapping procedure. The accumulation was rapid (detectable after 7.5 minutes), independent of simultaneous protein synthesis and mediated by a functional glucocorticoid receptor complex. Glucocorticoid hormones affect LTR transcription at the level of initiation. The rate of initiation (1.8 X 10(-2) molecules/cell/sec) and a half life of about 30 minutes could be calculated for LTR RNA. The half life of LTR RNA is independent of the presence of hormone.
一种体外重组的嵌合基因被导入L tk-细胞,该基因含有来自小鼠乳腺肿瘤病毒前病毒DNA的长末端重复序列(LTR)和单纯疱疹病毒的胸苷激酶(tk)基因。当生长培养基中不存在糖皮质激素时,在转染细胞中未观察到LTR RNA的转录。通过单链特异性核酸酶RNA图谱分析方法,在添加激素后测量LTR起始RNA的积累。这种积累迅速(7.5分钟后可检测到),与同时进行的蛋白质合成无关,并由功能性糖皮质激素受体复合物介导。糖皮质激素在起始水平上影响LTR转录。可以计算出LTR RNA的起始速率(1.8×10(-2)分子/细胞/秒)和约30分钟的半衰期。LTR RNA的半衰期与激素的存在无关。