Ko Soo-Il, Lee In-Seon, Kim Ji-Young, Kim Sung-Mi, Kim Dong-Wook, Lee Kyu-Sun, Woo Kyung-Mi, Baek Jeong-Hwa, Choo Jong-Kil, Seo Sang-Beom
Department of Life Science, College of Natural Sciences, Chung-Ang University, Seoul 156-756, Republic of Korea.
FEBS Lett. 2006 May 29;580(13):3217-22. doi: 10.1016/j.febslet.2006.04.081. Epub 2006 May 4.
The proto-oncogene protein DEK has been implicated in the t(6;9) chromosomal translocation associated with a subtype of acute myelogenous leukemia (AML), which results in the formation of a DEK-CAN fusion protein. Histone acetylation is an important post-translational modification which is involved in transcriptional regulation. In this study, we report that the acidic domain containing protein DEK interacts with histones and exerts a potent inhibitory effect on both p300 and PCAF-mediated histone acetyltransferase activity and transcription. Using chromatin immunoprecipitation assays, we have demonstrated that the recruitment of DEK to the appropriate promoter induces the histone H3 and H4 hypoacetylation of chromatin. Collectively, our data illustrate the important regulatory role played by protein DEK in transcriptional regulation, and suggest that transcription-regulating acidic domain regions may play a role in leukemogenesis.
原癌基因蛋白DEK与一种与急性髓性白血病（AML）亚型相关的t(6;9)染色体易位有关，该易位导致形成DEK-CAN融合蛋白。组蛋白乙酰化是一种重要的翻译后修饰，参与转录调控。在本研究中，我们报告含酸性结构域的蛋白DEK与组蛋白相互作用，并对p300和PCAF介导的组蛋白乙酰转移酶活性及转录发挥强大的抑制作用。通过染色质免疫沉淀试验，我们证明将DEK募集至适当的启动子可诱导染色质的组蛋白H3和H4低乙酰化。总体而言，我们的数据阐明了蛋白DEK在转录调控中发挥的重要调节作用，并表明转录调节酸性结构域区域可能在白血病发生中起作用。
