The ARF tumor suppressor connects pathways regulated by the retinoblastoma protein and p53. ARF inactivation reduces p53-dependent apoptosis induced by oncogenic signals. Nucleolar relocalization of Mdm2 by ARF connotes a novel mechanism for preventing p53 turnover and provides a framework for understanding how stress signals cooperate to regulate p53 function.
Department of Tumor Cell Biology, Howard Hughes Medical Institute, St Jude Children's Research Hospital, Memphis, Tennessee 38105, USA. sherr@stjude.org.
