Cdc25 cell-cycle phosphatase as a target of c-myc

The product of the proto-oncogene c-myc, in partnership with Max, forms a transcription factor that can promote either oncogenic transformation or apoptosis. The Myc/Max heterodimer binds to elements in the cdc25A gene and activates transcription. Like myc, cdc25A, itself a proto-oncogene, can induce apoptosis in cells depleted of growth factor, and Myc-induced apoptosis also requires cdc25A. These findings indicate that cdc25A is a physiologically relevant transcriptional target of c-myc

The Myc/Max/Mad network and the transcriptional control of cell behavior.

The Myc/Max/Mad network comprises a group of transcription factors whose distinct interactions result in gene-specific transcriptional activation or repression. A great deal of research indicates that the functions of the network play roles in cell proliferation, differentiation, and death. In this review we focus on the Myc and Mad protein families and attempt to relate their biological functions to their transcriptional activities and gene targets. Both Myc and Mad, as well as the more recently described Mnt and Mga proteins, form heterodimers with Max, permitting binding to specific DNA sequences. These DNA-bound heterodimers recruit coactivator or corepressor complexes that generate alterations in chromatin structure, which in turn modulate transcription. Initial identification of target genes suggests that the network regulates genes involved in the cell cycle, growth, life span, and morphology. Because Myc and Mad proteins are expressed in response to diverse signaling pathways, the network can be viewed as a functional module which acts to convert environmental signals into specific gene-regulatory programs