MYC PROTEIN - PARTNERS AND ANTAGONISTS

One of the first oncogenes identified from human tumors was c-myc, whi ch is frequently activated in Burkitt's lymphomas due to chromosomal t ranslocations. Subsequently, members of the myc oncogene family were f ound to be amplified in neuroblastoma and small-cell lung cancer. In n ormal cells, Myc activity has been shown to be both necessary and suff icient for resting cells to enter the cell cycle. Interestingly, it ap pears that Myc not only drives the cell cycle, but also induces cell d eath by apoptosis in certain situations. Myc contains a transcriptiona l activation domain and a basic helix-loop-helix-leucine zipper DNA-bi nding and dimerization domain. As a heterodimer with a structurally re lated protein, Max, Myc can bind DNA in a sequence-specific manner. Th ese results suggest that the Myc/Max heterodimer functions as a transc riptional activator of genes that are critical for the regulation of c ell growth.