Jang Moon Kyoo, Mochizuki Kazuki, Zhou Meisheng, Jeong Ho-Sang, Brady John N, Ozato Keiko
Laboratory of Molecular Growth Regulation, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland 20892, USA.
Mol Cell. 2005 Aug 19;19(4):523-34. doi: 10.1016/j.molcel.2005.06.027.
Brd4 is a mammalian bromodomain protein that binds to acetylated chromatin. Proteomic analysis revealed that Brd4 interacts with cyclinT1 and Cdk9 that constitutes core positive transcription elongation factor b (P-TEFb). Brd4 interacted with P-TEFb in the living nucleus through its bromodomain. About half of P-TEFb was bound to the inhibitory subunit and functionally inactive. Brd4 interacted with P-TEFb that was free of the inhibitory subunit. An increase in Brd4 expression led to increased P-TEFb-dependent phosphorylation of RNA polymerase II (RNAPII) CTD and stimulation of transcription from promoters in vivo. Conversely, a reduction in Brd4 expression by siRNA reduced CTD phosphorylation and transcription, revealing that Brd4 is a positive regulatory component of P-TEFb. In chromatin immunoprecipitation (ChIP) assays, the recruitment of P-TEFb to a promoter was dependent on Brd4 and was enhanced by an increase in chromatin acetylation. Together, P-TEFb alternately interacts with Brd4 and the inhibitory subunit to maintain functional equilibrium in the cell.
Brd4是一种与乙酰化染色质结合的哺乳动物溴结构域蛋白。蛋白质组学分析显示,Brd4与构成核心正转录延伸因子b(P-TEFb)的细胞周期蛋白T1和Cdk9相互作用。Brd4通过其溴结构域在活细胞核中与P-TEFb相互作用。约一半的P-TEFb与抑制性亚基结合且功能失活。Brd4与不含抑制性亚基的P-TEFb相互作用。Brd4表达的增加导致RNA聚合酶II(RNAPII)CTD的P-TEFb依赖性磷酸化增加,并在体内刺激启动子转录。相反,通过小干扰RNA(siRNA)降低Brd4表达会减少CTD磷酸化和转录,表明Brd4是P-TEFb的正调控成分。在染色质免疫沉淀(ChIP)试验中,P-TEFb募集到启动子上依赖于Brd4,并且染色质乙酰化增加会增强这种募集。总之,P-TEFb与Brd4和抑制性亚基交替相互作用,以维持细胞内的功能平衡。