Abstract
The members of the MYC family of oncogenes, in particular c-Myc, N-Myc, and L-Myc, are activated either directly or indirectly in many, if not most, human tumors. These structurally and functionally related nuclear phosphoproteins (Fig. (Fig.1A)1A) appear to promote cell growth and transformation by regulating the transcription of target genes required for proliferation (33, 44, 57). Myc's transcription functions require a C-terminal basic helix-loop-helix–leucine zipper (bHLHZip) DNA-protein interaction motif and conserved regulatory domains in the N terminus (Myc boxes, MB1 and MB2), which regulate Myc's transactivation and/or transrepression functions (Fig. (Fig.1A).1A). Normally, the expression of Myc family genes is cell context specific, mutually exclusive, and tightly dependent upon mitogens (8, 47, 71, 88). Furthermore, the life span of Myc proteins is brief, and they are rapidly degraded by the ubiquitin-linked proteasome machinery (45). However, these controls are lost in cancer cells, resulting in aberrantly high levels of Myc proteins (2, 57).
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