Simmons Comprehensive Cancer Center, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.
Mol Cell. 2013 Mar 7;49(5):843-57. doi: 10.1016/j.molcel.2012.12.006. Epub 2013 Jan 11.
Bromodomain-containing protein 4 (Brd4) is an epigenetic reader and transcriptional regulator recently identified as a cancer therapeutic target for acute myeloid leukemia, multiple myeloma, and Burkitt's lymphoma. Although chromatin targeting is a crucial function of Brd4, there is little understanding of how bromodomains that bind acetylated histones are regulated, nor how the gene-specific activity of Brd4 is determined. Via interaction screen and domain mapping, we identified p53 as a functional partner of Brd4. Interestingly, Brd4 association with p53 is modulated by casein kinase II (CK2)-mediated phosphorylation of a conserved acidic region in Brd4 that selectively contacts either a juxtaposed bromodomain or an adjacent basic region to dictate the ability of Brd4 binding to chromatin and also the recruitment of p53 to regulated promoters. The unmasking of bromodomains and activator recruitment, concurrently triggered by the CK2 phospho switch, provide an intriguing mechanism for gene-specific targeting by a universal epigenetic reader.
溴结构域蛋白 4(Brd4)是一种表观遗传阅读器和转录调节剂,最近被确定为急性髓性白血病、多发性骨髓瘤和伯基特淋巴瘤的癌症治疗靶点。尽管染色质靶向是 Brd4 的一个关键功能,但对于结合乙酰化组蛋白的溴结构域如何被调节,以及 Brd4 的基因特异性活性如何确定,人们知之甚少。通过相互作用筛选和结构域映射,我们确定了 p53 是 Brd4 的功能伙伴。有趣的是,Brd4 与 p53 的结合受 CK2 介导的 Brd4 中保守酸性区域磷酸化的调节,该磷酸化选择性地接触毗邻的溴结构域或相邻的碱性区域,从而决定 Brd4 结合染色质的能力,以及 p53 募集到受调控的启动子的能力。由 CK2 磷酸开关同时触发的溴结构域的暴露和激活剂募集,为通用表观遗传阅读器的基因特异性靶向提供了一个有趣的机制。