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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Repression of the c-fms gene in fibroblast cells by c-Myc-MM-1-TIF1beta complex.

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.[1]


  1. Repression of the c-fms gene in fibroblast cells by c-Myc-MM-1-TIF1beta complex. Satou, A., Hagio, Y., Taira, T., Iguchi-Ariga, S.M., Ariga, H. FEBS Lett. (2004) [Pubmed]
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