American Association for Cancer Research
Browse
00085472can076552-sup-stable_2.pdf (225.5 kB)

Supplementary Table 2 from Myc-Mediated Transcriptional Repression by Recruitment of Histone Deacetylase

Download (225.5 kB)
journal contribution
posted on 2023-03-30, 17:45 authored by John F. Kurland, William P. Tansey
Supplementary Table 2 from Myc-Mediated Transcriptional Repression by Recruitment of Histone Deacetylase

History

ARTICLE ABSTRACT

Myc is a transcription factor that features prominently in cancer. The oncogenicity of Myc stems from its ability to regulate expression of genes required for cell growth and proliferation. Although the mechanisms through which Myc activates transcription have been extensively studied, less is known about how Myc represses transcription. Recently, we reported that a conserved element within Myc–MbIII– is important for transcriptional repression. Here, we investigate the mechanism through which MbIII contributes to repression. We show that Myc represses transcription of target genes Id2 and Gadd153 by a process that involves histone deacetylation. We show that MbIII is important for repression of these genes and present evidence that this element contributes to repression by recruiting the histone deacetylase HDAC3 to the Id2 and Gadd153 promoters. These results describe a mechanistic role for MbIII in transcription, and reveal that recruitment of HDAC3 is a process by which Myc represses gene activity. [Cancer Res 2008;68(10):3624–9]

Usage metrics

    Cancer Research

    Categories

    Keywords

    Licence

    Exports

    RefWorks
    BibTeX
    Ref. manager
    Endnote
    DataCite
    NLM
    DC