Department of Microbiology, Brain Korea 21 Project for Biological Science, Chungnam National University, Daejeon, 305-764, Republic of Korea.
Mol Biol Rep. 2010 Oct;37(7):3593-600. doi: 10.1007/s11033-010-0008-3. Epub 2010 Feb 24.
Cancer-upregulated gene 2 (CUG2), which was named since it was originally identified as a putative oncogene up-regulated in various human cancers, was recently renamed CENP-W based on the new findings that it is a component of the centromeric complex playing a crucial role in the assembly of functional kinetochore complex during mitosis. To understand the transcriptional regulation of CENP-W, we analyzed its TATA-less promoter and identified a GC-rich putative Sp1 binding site located at -46 to -36 that was critical in CENP-W expression. Competitive electrophoretic gel mobility shift assay using mutated oligos and supershift assays with Sp1 and Sp3 antibodies demonstrated that both proteins specifically bound to this promoter region. Moreover, we found that CENP-W was highly induced by serum stimulation followed by serum deprivation, with Sp1 and Sp3 transcription factors involved in this transactivation. Taken together, our results suggest that Sp1 together with Sp3 may function as the main regulator of the basal and serum-induced transcription of CENP-W.
癌基因上调基因 2（CUG2）最初被鉴定为在各种人类癌症中上调的假定癌基因，因此得名，最近根据新的发现将其重新命名为 CENP-W，因为它是着丝粒复合物的组成部分，在有丝分裂过程中组装功能性动粒复合物中起着至关重要的作用。为了了解 CENP-W 的转录调控，我们分析了其无 TATA 的启动子，并鉴定出位于-46 到-36 的富含 GC 的假定 Sp1 结合位点，该位点对于 CENP-W 的表达至关重要。使用突变寡核苷酸的竞争电泳凝胶迁移率变动分析和 Sp1 和 Sp3 抗体的超迁移分析表明，这两种蛋白都特异性地结合到该启动子区域。此外，我们发现 CENP-W 可被血清刺激诱导，然后血清剥夺，涉及 Sp1 和 Sp3 转录因子参与这种反式激活。总之，我们的结果表明 Sp1 与 Sp3 可能共同作为 CENP-W 的基础和血清诱导转录的主要调节剂。
