title: Germ-line-derived hinge domain p53 mutants have lost apoptotic but not cell cycle arrest functions.
abstract: The protein p53 is a critical tumor suppressor, as demonstrated by its frequent mutation in human cancers. Overexpression of the wild-type form of the p53 tumor suppressor gene in human cancer cell lines has been shown to lead to either cell cycle arrest or apoptosis. A study of two Li-Fraumeni syndrome-derived p53 hinge domain mutants shows that both mutants retain the ability to arrest cell growth but are significantly impaired for the induction of apoptosis in human p53-null cell lines. This indicates that the hinge domain may be important in the regulation of p53-dependent apoptosis.
authors.affiliation: Department of Microbiology and Molecular Genetics, University of California-Irvine, 92697-4025, USA.
authors.forename: O N
authors.initials: ON
authors.lastname: Aurelio
authors.forename: J F
authors.initials: JF
authors.lastname: Cajot
authors.forename: M L
authors.initials: ML
authors.lastname: Hua
authors.forename: Z
authors.initials: Z
authors.lastname: Khwaja
authors.forename: E J
authors.initials: EJ
authors.lastname: Stanbridge
mesh_terms: D000293:Adolescent; D000328:Adult; D017209:Apoptosis / Q000235:genetics*; D002453:Cell Cycle / Q000235:genetics*; D018095:Germ-Line Mutation; D006801:Humans; D009363:Neoplasm Proteins / Q000235:genetics*; D011487:Protein Conformation; D014407:Tumor Cells, Cultured; D014410:Tumor Stem Cell Assay; D016159:Tumor Suppressor Protein p53 / Q000235:genetics* / Q000502:physiology
chemical_list: D009363:Neoplasm Proteins; D016159:Tumor Suppressor Protein p53