The members of the Myc/Max/Mad network function as transcriptional regulato
rs. Substantial evidence has been accumulated over the last years that supp
ort the model that Myc/Max/Mad proteins affect different aspects of cell be
havior, including proliferation, differentiation, and apoptosis, by modulat
ing distinct target genes. The unbalanced expression of these genes, e.g. i
n response to deregulated Myc expression, is most likely an important aspec
t of Myc's ability to stimulate tumor formation. Myc and Mad proteins affec
t target gene expression by recruiting chromatin remodeling activities. In
particular Myc interacts with a SWI/SNF-like complex that may contain ATPas
e activity. In addition Myc binds to TRRAP complexes that possess histone a
cetyl transferase activity. Mad proteins, that antagonize Myc function, rec
ruit an mSin3 repressor complex with histone deacetylase activity. Thus the
antagonism of Myc and Mad proteins is explained at the molecular level by
the recruitment of opposing chromatin remodeling activities. (C) 2001 Publi
shed by Elsevier Science B.V.