College of Life Sciences and Biotechnology, Korea University, Seoul 136-701, Republic of Korea.
Biochem Biophys Res Commun. 2010 May 28;396(2):238-45. doi: 10.1016/j.bbrc.2010.04.072. Epub 2010 Apr 23.
TRIM72 is known to be involved in the negative feedback regulation of myogenesis by targeting insulin receptor substrate-1. Here, we found that TRIM72 was more highly expressed in oxidative muscle with the higher activity of MEF2, compared to glycolytic muscle. Indeed, TRIM72 promoter contained an evolutionarily conserved MEF2 site juxtaposed to E-box. TRIM72 promoter activity was decreased by the site-directed mutagenesis of either E-boxes or a MEF2 site and synergistically enhanced by MyoD (or myogenin) and MEF2, which were associated with proximal E-box, and MEF2 site of the TRIM72 promoter, respectively. Taken together all these data, we concluded that the synergism of MyoD (or myogenin) and MEF2 is necessary for TRIM72 expression during C2C12 differentiation.
TRIM72 已知通过靶向胰岛素受体底物-1 参与肌生成的负反馈调节。在这里,我们发现与糖酵解肌肉相比,TRIM72 在具有更高 MEF2 活性的氧化肌肉中表达更高。事实上,TRIM72 启动子包含一个进化上保守的 MEF2 位点,与 E 盒并列。TRIM72 启动子活性通过 E 盒或 MEF2 位点的定点诱变降低,并通过与近端 E 盒结合的 MyoD(或 myogenin)和 MEF2 协同增强,以及 TRIM72 启动子的 MEF2 位点。综上所述,我们得出结论,MyoD(或 myogenin)和 MEF2 的协同作用对于 C2C12 分化过程中 TRIM72 的表达是必要的。