title: The ARF-B23 connection: implications for growth control and cancer treatment.
abstract: The tumor suppressor ARF induces a p53-dependent and -independent cell cycle arrest. Unlike nucleoplasmic localized MDM2 and p53, ARF localizes in the nucleolus. The role of ARF in the nucleolus and the molecular target and mechanism of ARF's p53-independent function remain both controversial and a fertile field of research. Recent study has identified the nucleolar protein B23 as a target of ARF for implementing its growth inhibitory function. The ability of ARF to block cell cycle progression through the MDM2-p53 pathway and to suppress ribosomal biogenesis through B23 suggest a role for ARF in coordinating inhibitions of growth and proliferation.
authors.affiliation: Department of Molecular and Cellular Oncology, University of Texas, MD Anderson Cancer Center, Houston, Texas 77030-4009, USA. ypzhang@mdanderson.org
authors.forename: Yanping
authors.initials: Y
authors.lastname: Zhang
mesh_terms: D000818:Animals; D002466:Cell Nucleolus / Q000378:metabolism; D049109:Cell Proliferation; D006801:Humans; D009369:Neoplasms / Q000378:metabolism / Q000473:pathology* / Q000628:therapy*; D009687:Nuclear Proteins / Q000378:metabolism*; D000090243:Nucleophosmin; D025803:Tumor Suppressor Protein p14ARF / Q000378:metabolism*
chemical_list: D009687:Nuclear Proteins; D025803:Tumor Suppressor Protein p14ARF; D000090243:Nucleophosmin