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The p19 ARF  tumor suppressor antagonizes Mdm2 to induce p53-dependent cell cycle arrest. Individual TKO (triple knock out) mice nullizygous for  ARF, p53 , and  Mdm2  develop multiple tumors at a frequency greater than those observed in animals lacking both  p53 and  Mdm2  or  p53  alone, demonstrating that p19 ARF  can act independently of the Mdm2-p53 axis in tumor surveillance. Reintroduction of  ARF  into TKO mouse embryo fibroblasts (MEFs), but not into those lacking both  p53  and ARF , arrested the cell division cycle in the G1 phase. Inhibition of the retinoblastoma protein had no effect on the ability of ARF to arrest TKO MEFs. Thus, in the absence of Mdm2, p19 ARF  interacts with other targets to inhibit cell proliferation.

p53-independent functions of the p19ARF tumor suppressor

p53-independent functions of the p19^ARF tumor suppressor