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. 2014 Nov 3;6(12):1509–1511. doi: 10.15252/emmm.201404735

Figure 1. MIZ1–MYC equilibrium controls cell fate.

Figure 1

In normal cells, HUWE1-directed ubiquitylation of MIZ1 controls its levels to balance the control of MYC transcription targets. In cancer, MYC oncoproteins are overexpressed, which tips the balance to activating MYC:MAX complexes that activate direct targets, which in turn lead to a hyperproliferative state that includes an amplification of transcription (Lin et al, 2012; Nie et al, 2012; Sabo et al, 2014; Walz et al, 2014). Inhibition or silencing of HUWE1 in cancer cells re-establishes a proper equilibrium, by provoking increases in the levels of MIZ1 that forms repressive MIZ1:MYC:MAX ternary complexes on growth-associated target genes that are activated by MYC.