The essential cofactor TRRAP recruits the histone acetyltransferase hGCN5 to c-Myc

The c-Myc protein functions as a transcription factor to facilitate oncogen ic transformation; however, the biochemical and genetic pathways leading to transformation remain undefined. We demonstrate here that the recently des cribed c-Myc cofactor TRRAP recruits histone acetylase activity, which is c atalyzed by the human GCN5 protein. Since c-Myc function is inhibited by re cruitment of histone deacetylase activity through Mad family proteins, thes e opposing biochemical activities are likely to be responsible for the anta gonistic biological effects of c-Myc and Mad on target genes and ultimately on cellular transformation.