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
Oncogenejournal_title
Oncogeneauthors
Cowling VH,Cole MDdoi
10.1038/sj.onc.1210734subject
Has Abstractpub_date
2008-02-21 00:00:00pages
1327-32issue
9eissn
0950-9232issn
1476-5594pii
1210734journal_volume
27pub_type
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