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Oncogene. 2008 Feb 21;27(9):1327-32. Epub 2007 Aug 20.

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

Author information

1
Department of Pharmacology and Toxicology, Dartmouth Medical School, Norris Cotton Cancer Center, Lebanon, NH 03756, USA.

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.

PMID:
17704800
DOI:
10.1038/sj.onc.1210734
[Indexed for MEDLINE]

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