Key Laboratory of the Ministry of Education for Cell Biology and Tumor Cell Engineering, School of Life Sciences, Xiamen University, Xiamen 361005, Fujian, China.
Methods. 2011 Jan;53(1):85-90. doi: 10.1016/j.ymeth.2010.04.005. Epub 2010 Apr 10.
Originally identified as a factor crucial for RNA polymerase (Pol) II transcriptional elongation of cellular genes, the P-TEFb kinase was subsequently shown to also serve as a specific host co-factor required for HIV-1 transcription. Recruited by either the bromodomain protein Brd4 to cellular promoters for general transcription or the HIV-1 Tat protein to the viral LTR for activated HIV-1 transcription, P-TEFb stimulates the processivity of Pol II through phosphorylating the C-terminal domain of Pol II and a pair of negative elongation factors, leading to the synthesis of full-length transcripts. However, abundant evidence indicates that P-TEFb does not act alone in the cell and that all of its known biological functions are likely mediated through the interactions with various regulators. Although a number of P-TEFb-associated factors have already been identified, there are likely more yet to be discovered. Given that P-TEFb plays an essential role in HIV-1 transcription, a major challenge facing the field is to identify all the P-TEFb-associated factors and determine how they may modulate Tat-transactivation and HIV-1 replication. Described here is a set of experimental procedures that have not only enabled us to isolate and identify several P-TEFb-associated factors, but also provided the means to characterize their biochemical functions in HIV-1 transcriptional control. In light of the recent demonstrations that transcriptional elongation plays a much more important role in controlling metazoan gene expression than previously thought, the techniques presented here will also be useful for analyzing Pol II elongation of cellular genes.
最初被鉴定为 RNA 聚合酶(Pol)II 转录细胞基因所必需的因子,P-TEFb 激酶随后被证明也是 HIV-1 转录所需的特定宿主共因子。P-TEFb 通过磷酸化 Pol II 的 C 末端结构域和一对负延伸因子来刺激 Pol II 的连续性,从而招募溴结构域蛋白 Brd4 到细胞启动子进行一般转录,或 HIV-1 Tat 蛋白到病毒 LTR 以激活 HIV-1 转录,导致全长转录本的合成。然而,大量证据表明,P-TEFb 在细胞中并非单独发挥作用,其所有已知的生物学功能可能都是通过与各种调节剂的相互作用介导的。尽管已经鉴定出许多与 P-TEFb 相关的因子,但可能还有更多尚未被发现。鉴于 P-TEFb 在 HIV-1 转录中起着至关重要的作用,该领域面临的主要挑战是确定所有与 P-TEFb 相关的因子,并确定它们如何调节 Tat 转录激活和 HIV-1 复制。本文描述了一组实验程序,这些程序不仅使我们能够分离和鉴定几种与 P-TEFb 相关的因子,而且还提供了用于表征它们在 HIV-1 转录控制中生化功能的手段。鉴于最近的研究表明,转录延伸在控制后生动物基因表达方面的作用比以前认为的要重要得多,因此这里介绍的技术也将有助于分析细胞基因的 Pol II 延伸。