Functional analyses of the bHLH transcription factor DEC2 in cardiac and neural differentiations.

我们研究了Dec2调控基因表达的分子机制。凝胶滞留和荧光素酶分析表明，Dec2以同源二聚体的形式优先与B类E盒元件(CACGTG)结合，并以组蛋白脱乙酰酶(HDAC)依赖的方式抑制靶基因的转录。相反，Dec2通过A类E-box以不依赖于HDAC1的方式抑制MyoD激活的肌肉肌酸激酶基因启动子活性。这些发现表明，Dec2使用多种机制-包括DNA结合和蛋白质-蛋白质相互作用-来实现E-box依赖的转录表达。

We studied about the molecular mechanisms by which Dec2 regulates gene expression. Gel retardation and luciferase assays showed that Dec2 preferentially binds to class B E-box elements (CACGTG) as a homodimer and represses the transcription of target genes in a histone deacetylase (HDAC)-dependent manner. In contrast, Dec2 repressed a MyoD-activated promoter activity of muscle creatine kinase gene through class A E-box in an HDAC1-independent manner. These findings indicate that Dec2 employs multiple mechanisms -including DNA-binding and protein-protein interactions-to achieve E-box-dependent transcriptional repressions.