Journal
MOLECULAR AND CELLULAR BIOLOGY
Volume 20, Issue 2, Pages 556-562Publisher
AMER SOC MICROBIOLOGY
DOI: 10.1128/MCB.20.2.556-562.2000
Keywords
-
Categories
Ask authors/readers for more resources
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.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available