Affiliation:
1. Department of Molecular Biology, Princeton University, Princeton, New Jersey 08544-1014
Abstract
ABSTRACT
The c-Myc protein functions as a transcription factor to facilitate oncogenic transformation; however, the biochemical and genetic pathways leading to transformation remain undefined. We demonstrate here that the recently described c-Myc cofactor TRRAP recruits histone acetylase activity, which is catalyzed by the human GCN5 protein. Since c-Myc function is inhibited by recruitment of histone deacetylase activity through Mad family proteins, these opposing biochemical activities are likely to be responsible for the antagonistic biological effects of c-Myc and Mad on target genes and ultimately on cellular transformation.
Publisher
American Society for Microbiology
Subject
Cell Biology,Molecular Biology
Cited by
392 articles.
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