An N-Myc truncation analogous to c-Myc-S induces cell proliferation independently of transactivation but dependent on Myc homology box II

V. H. Cowling, M. D. Cole

    Research output: Contribution to journalArticle

    12 Citations (Scopus)

    Abstract

    Myc promotes both normal cell proliferation and oncogenic transformation through the activation and repression of target genes. The c-Myc-S protein is a truncated form of c-Myc that is produced in some cells from translation initiation at an internal AUG codon. We report that c-Myc-S and a similar truncated form of N-MycWT can fully rescue the proliferation defect in myc-null fibroblasts, but rescue is dependent on the highly conserved Myc homology box II (MBII). Global gene expression studies show that the N-Myc equivalent of c-Myc-S is defective for virtually all transcriptional activation of Myc target genes but remains active for the majority of transcriptional repression. Repression by Myc-S is dependent on MBII, but it does not bind to several known nuclear cofactors. These data suggest that repression by Myc involves recruitment of a novel MBII-dependent cofactor.
    Original languageEnglish
    Pages (from-to)1327-1332
    Number of pages6
    JournalOncogene
    Volume27
    Issue number9
    Early online date20 Aug 2007
    DOIs
    Publication statusPublished - 21 Feb 2008

    Keywords

    • c-Myc-S
    • Myc
    • Transcriptional repression
    • Transactivation
    • Cell proliferation

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