ARF-BP1/Mule is a critical mediator of the ARF tumor suppressor.

By Delin Chen, N. Kon, Muyang Li, Wenzhu Zhang, J. Qin, W. Gu. Cell, 2005

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Acetylation is indispensable for p53 activation. (2008, background): “To extend these findings, we identified Pirh2 as another p53 target (Leng et al., 2003), whose induction by p53 is independent of the acetylation status (Figure S10).”
Glycogen synthase kinase-3 regulates mitochondrial outer membrane permeabilization and apoptosis by destabilization of MCL-1. (2006, background): “Since the biological consequence of Mule activity, degrading MCL-1 and p53 (Chen et al., 2005), can be divergent, it is conceivable that substrate-specific levels of regulation exist.”
p53 ubiquitination: Mdm2 and beyond. (2006, background): “ARF suppresses aberrant cell growth in response to oncogene activation, at least in part, by inducing the p53 pathway (Sharpless and DePinho, 2004; Sherr, 2001). p53 induction by ARF is mediated through inhibiting the activities of either Mdm2 (Kamijo et al., 1998; Pomerantz et al., 1998; Zhang et a”