Experimental Immunology, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA.
Proc Natl Acad Sci U S A. 2012 May 1;109(18):6927-32. doi: 10.1073/pnas.1120422109. Epub 2012 Apr 16.
The bromodomain protein, BRD4, has been identified recently as a therapeutic target in acute myeloid leukemia, multiple myeloma, Burkitt's lymphoma, NUT midline carcinoma, colon cancer, and inflammatory disease; its loss is a prognostic signature for metastatic breast cancer. BRD4 also contributes to regulation of both cell cycle and transcription of oncogenes, HIV, and human papilloma virus (HPV). Despite its role in a broad range of biological processes, the precise molecular mechanism of BRD4 function remains unknown. We report that BRD4 is an atypical kinase that binds to the carboxyl-terminal domain (CTD) of RNA polymerase II and directly phosphorylates its serine 2 (Ser2) sites both in vitro and in vivo under conditions where other CTD kinases are inactive. Phosphorylation of the CTD Ser2 is inhibited in vivo by a BRD4 inhibitor that blocks its binding to chromatin. Our finding that BRD4 is an RNA polymerase II CTD Ser2 kinase implicates it as a regulator of eukaryotic transcription.
溴结构域蛋白 BRD4 最近被确定为急性髓性白血病、多发性骨髓瘤、伯基特淋巴瘤、NUT 中线癌、结肠癌和炎症性疾病的治疗靶点;其缺失是转移性乳腺癌的预后标志。BRD4 还参与调节细胞周期和癌基因、HIV 和人乳头瘤病毒 (HPV) 的转录。尽管 BRD4 在广泛的生物学过程中发挥作用,但 BRD4 功能的确切分子机制尚不清楚。我们报告 BRD4 是一种非典型激酶,可与 RNA 聚合酶 II 的羧基末端结构域 (CTD) 结合,并在其他 CTD 激酶失活的条件下直接体外和体内磷酸化其丝氨酸 2 (Ser2) 位点。BRD4 抑制剂可阻止其与染色质结合,从而抑制体内 CTD Ser2 的磷酸化。我们发现 BRD4 是 RNA 聚合酶 II CTD Ser2 激酶,这表明它是真核转录的调节剂。