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

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.

journal_name

Oncogene

journal_title

Oncogene

authors

Cowling VH,Cole MD

doi

10.1038/sj.onc.1210734

subject

Has Abstract

pub_date

2008-02-21 00:00:00

pages

1327-32

issue

9

eissn

0950-9232

issn

1476-5594

pii

1210734

journal_volume

27

pub_type

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