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Repression of the c‐ fms gene in fibroblast cells by c‐Myc‐MM‐1‐TIF1β complex
Author(s) -
Satou Akiko,
Hagio Yuko,
Taira Takahiro,
Iguchi-Ariga Sanae M.M,
Ariga Hiroyoshi
Publication year - 2004
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2004.07.034
Subject(s) - promoter , psychological repression , microbiology and biotechnology , transcription (linguistics) , gene , hdac1 , histone deacetylase , biology , histone , gene expression , transcription factor , cell culture , fibroblast , oncogene , chemistry , genetics , cell cycle , linguistics , philosophy
MM‐1 has been reported to repress the E‐box‐dependent transcription activity of c‐Myc by recruiting histone deacetylase 1 complex via TIF1β/KAP1. In this study, to identify target genes for c‐Myc‐MM‐1‐TIF1β, we established rat‐1 cells harboring the dominant‐negative form of TIF1β to abrogate the pathway from TIF1β 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.