Repression of the c-fms gene in fibroblast cells by c-Myc-MM-1-TIF1β complex
Repression of the c-fms gene in fibroblast cells by c-Myc-MM-1-TIF1β complex
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DOI：
10.1016/j.febslet.2004.07.034
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发表时间：
2004-08-13
期刊：
影响因子：
3.5
通讯作者：
Ariga, H
中科院分区：
文献类型：
--
作者：
Satou, A;Hagio, Y;Ariga, H
据报道，MM-1通过TIF 1 β/KAP 1募集组蛋白脱乙酰酶1复合物，抑制c-Myc的E-box依赖性转录活性。在这项研究中，为了鉴定c-Myc-MM-1-TIF 1 β的靶基因，我们建立了携带TIF 1 β显性阴性形式的大鼠-1细胞，以消除从TIF 1 β到MM-1-c-Myc的通路。该细胞系中c-Myc的转录活性被激活，被发现是致瘤性的。通过对该细胞系的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pE 1和pE 2中，发现pE 1启动子活性以E-box依赖性方式被激活。(C)2004年由Elsevier B. V.代表欧洲生物化学学会联合会出版。
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. (C) 2004 Published by Elsevier B.V. on behalf of the Federation of European Biochemical Societies.