Figure 1 | Cell Death & Differentiation

Figure 1

From: In the race for protection, ARF comes second

Figure 1

Schematic representation of ARF regulation by differential oncogenic burden. Left: low oncogenic burden, as exemplified by Ras activation alone, activates ATM and the DDR. ATM promotes ULF-mediated ARF degradation, preventing ARF accumulation. Mild c-Myc activation induces ARF mRNA, but ARF protein is not accumulated. Thus, the ARF activation threshold is not reached. Right: high oncogenic burden, as achieved by a combination of two oncogenes (exemplified by Ras and Wnt pathway activation) will override the inhibitory effect of the DDR and enable ARF accumulation. Likewise, excessive c-Myc will inhibit ULF and enable effective ARF accumulation. Thus, the ARF activation threshold is reached, eliciting ARF-driven, p53-dependent and p53-independent antiproliferative effects

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