Yamaguchi Y, Wada T, Handa H
Department of Biomolecular Engineering, Faculty of Bioscience and Biotechnology, Tokyo Institute of Technology, Yokohama, Japan.
Genes Cells. 1998 Jan;3(1):9-15. doi: 10.1046/j.1365-2443.1998.00162.x.
DRB is a classic inhibitor of transcription by RNA polymerase II (pol II). Although it has been demonstrated that DRB inhibits the elongation step of transcription, its mode of action has been elusive. DRB also markedly inhibits human immunodeficiency virus (HIV) transcription, by targeting the elongation which is enhanced by the HIV-encoded transactivator Tat. Two factors essential for DRB action have recently been identified. These factors, positive transcription elongation factor b (P-TEFb) and DRB sensitivity-inducing factor (DSIF), positively and negatively regulate pol II elongation, and are likely to be relevant to the function of Tat. In this review, we summarize the recent findings on these factors, and discuss a possible model for the molecular mechanism of DRB action.
5,6-二氯-1-β-D-呋喃核糖基苯并咪唑(DRB)是RNA聚合酶II(pol II)转录的经典抑制剂。尽管已经证明DRB抑制转录的延伸步骤,但其作用方式一直难以捉摸。DRB还通过靶向由人类免疫缺陷病毒(HIV)编码的反式激活因子Tat增强的延伸来显著抑制HIV转录。最近已经鉴定出DRB作用所必需的两个因子。这些因子,即正转录延伸因子b(P-TEFb)和DRB敏感性诱导因子(DSIF),分别对pol II延伸起正向和负向调节作用,并且可能与Tat的功能相关。在这篇综述中,我们总结了关于这些因子的最新发现,并讨论了DRB作用分子机制的可能模型。