c-Myc-MM-1-TIF1β复合物对成纤维细胞中c-fms基因的抑制作用。
Repression of the c-fms gene in fibroblast cells by c-Myc-MM-1-TIF1beta complex.
作者信息
Satou Akiko, Hagio Yuko, Taira Takahiro, Iguchi-Ariga Sanae M M, Ariga Hiroyoshi
机构信息
Graduate School of Pharmaceutical Sciences, Hokkaido University, Kita-ku, Sapporo 060-0812, Japan.
出版信息
FEBS Lett. 2004 Aug 13;572(1-3):211-5. doi: 10.1016/j.febslet.2004.07.034.
MM-1 has been reported to repress the E-box-dependent transcription activity of c-Myc by recruiting histone deacetylase 1 complex via TIF1beta/KAP1. In this study, to identify target genes for c-Myc-MM-1-TIF1beta, we established rat-1 cells harboring the dominant-negative form of TIF1beta to abrogate the pathway from TIF1beta to MM-1-c-Myc. This cell line, in which transcription activity of c-Myc was activated, was found to be tumorigenic. By DNA-microarray analysis of this cell line, expression and promoter activity of the c-fms oncogene were found to be upregulated. Of the two promoters, pE1 and pE2, in the c-fms gene, pE1 promoter activity was found to be activated in an E-box-dependent manner.
据报道，MM-1通过TIF1β/KAP1募集组蛋白去乙酰化酶1复合物来抑制c-Myc的E盒依赖性转录活性。在本研究中，为了鉴定c-Myc-MM-1-TIF1β的靶基因，我们建立了携带TIF1β显性负性形式的大鼠-1细胞，以消除从TIF1β到MM-1-c-Myc的信号通路。发现这种c-Myc转录活性被激活的细胞系具有致瘤性。通过对该细胞系进行DNA微阵列分析，发现c-fms癌基因的表达和启动子活性上调。在c-fms基因的两个启动子pE1和pE2中，发现pE1启动子活性以E盒依赖性方式被激活。
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