Goswami S K, Zhao Y Y, Siddiqui M A, Kumar A
Department of Cell Biology and Anatomy, SUNY Health Science Center, Brooklyn 11203.
Cell Mol Biol Res. 1993;39(2):125-30.
MyoD is one of the regulatory genes that causes activation of the expression of muscle specific genes in fibroblasts through interaction with a cis-acting DNA element CANNTG (E-box). We show here that forced expression of MyoD in mouse fibroblast C3H10T1/2 cells induces the expression of the liver specific rat angiotensinogen gene promoter. In the absence of MyoD, the angiotensinogen promoter is not expressed in C3H10T1/2 fibroblasts. Cotransfection of MyoD has no significant effect on the angiotensinogen promoter activity in the liver-derived HepG2 cells, suggesting that the regulatory programs of HepG2 and C3H10T1/2 cells are different, at least in terms of the requirement for MyoD-mediated transactivation of the target angiotensinogen promoter.
肌分化抗原(MyoD)是一种调控基因,它通过与顺式作用DNA元件CANNTG(E盒)相互作用,导致成纤维细胞中肌肉特异性基因的表达激活。我们在此表明,在小鼠成纤维细胞C3H10T1/2细胞中强制表达MyoD可诱导肝脏特异性大鼠血管紧张素原基因启动子的表达。在没有MyoD的情况下,血管紧张素原启动子在C3H10T1/2成纤维细胞中不表达。MyoD的共转染对肝脏来源的HepG2细胞中血管紧张素原启动子活性没有显著影响,这表明HepG2和C3H10T1/2细胞的调控程序不同,至少在对MyoD介导的靶血管紧张素原启动子反式激活的需求方面是不同的。