Please use this identifier to cite or link to this item: https://doi.org/10.4161/cc.10.13.16249
Title: Kinetic profiling of the c-Myc transcriptome and bioinformatic analysis of repressed gene promoters
Authors: Yap, C.-S. 
Peterson, A.L.
Castellani, G.
Sedivy, J.M.
Neretti, N.
Keywords: c-Myc
Expression profiling
Gene regulation
Microarray
Promoter
Proto-oncogene
Transcriptome
Issue Date: 1-Jul-2011
Citation: Yap, C.-S., Peterson, A.L., Castellani, G., Sedivy, J.M., Neretti, N. (2011-07-01). Kinetic profiling of the c-Myc transcriptome and bioinformatic analysis of repressed gene promoters. Cell Cycle 10 (13) : 2184-2196. ScholarBank@NUS Repository. https://doi.org/10.4161/cc.10.13.16249
Abstract: Mammalian c-Myc is a member of a small family of three related proto-oncogenic transcription factors. c-Myc has an unusually broad array of regulatory functions, which include roles in cell cycle and apoptosis, a variety of metabolic functions, cell differentiation, senescence and stem cell maintenance. c-Myc modulates the expression of a very large number of genes, but the magnitude of the majority of the regulatory effects is only 2-fold or less. c-Myc can both activate and repress the promoters of its target genes. Identification of genes directly regulated by c-Myc has been an enduring question in the field. We report here microarray expression profiling of a high resolution time course of c-Myc induction, using fibroblast cells in which c-Myc activity can be modulated from null to physiological. The c-Myc transcriptome data set presented is the largest reported to date with 4,186 differentially regulated genes (1,826 upregulated, 2,360 downregulated, 1% FDR). The gene expression patterns fit well with the known biological functions of c-Myc. We describe several novel findings and present tools for further data mining. Although the mechanisms of transcriptional activation by c-Myc are well understood, how c-Myc represses an even greater number of genes remains incompletely described. One mechanism involves the binding of c-Myc to other, positively acting transcription factors and interfering with their activities. We identified rapid-response genes likely to be direct c-Myc targets and analyzed the promoters of the repressed genes to identify transcription factors that could be targets of c-Myc repression. © 2011 Landes Bioscience.
Source Title: Cell Cycle
URI: http://scholarbank.nus.edu.sg/handle/10635/124750
ISSN: 15384101
DOI: 10.4161/cc.10.13.16249
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