Figure 2.

Myc regulation of gene transcription in healthy and cancer cells. Schematic representation of abundancy-dependent Myc binding at target promoters. (a) In healthy cells, Myc/Max and coregulators preferentially bind to high-affinity E-boxes (h-a-E-box). By inducing both the opening of chromatin through histone acetylation and RNAPII pause and release via PTEFb-dependent phosphorylation of Ser2 on RNAPII, Myc/Max heterodimers tune the transcription, splicing, and RNA capping of genes pivotal to cellular homeostasis. (b) In overexpressing Myc cancer cells, Myc/Max heterodimers also invade low-affinity binding sites (l-a-E-box) and push transcription, leading to the execution of aberrant gene expression programs.