title: Nitric oxide evoked p53-accumulation and apoptosis.
abstract: The tumor suppressor p53 accumulates under conditions of cellular stress and affects cell cycle progression and/or apoptosis. This has been exemplified for endogenously produced or exogenously supplied nitric oxide (NO) and thus accounts at least in part for cell destructive signaling qualities of this bioactive molecule and/or derived reactive nitrogen species. However, detailed mechanisms of toxicity and pathways of cell demise remain to be elucidated. Establishing that NO-treatment left the ubiquitination and the p53-Mdm2 interaction intact may point to an impaired nuclear-cytoplasmic shuttling to account for p53 stabilization. This was verified by heterokaryon analysis. We conclude that attenuated nuclear export contributes to stabilization and activation of p53 under the influence of NO.
authors.affiliation: Department of Cell Biology, Faculty of Biology, University of Kaiserslautern, Erwin Schroedinger-Strasse 13/4, 67663 Kaiserslautern, Germany. bruene@rhrk.uni-kl.de
authors.forename: Bernhard
authors.initials: B
authors.lastname: Brüne
authors.forename: Nicole
authors.initials: N
authors.lastname: Schneiderhan
mesh_terms: D016475:3T3 Cells; D000818:Animals; D017209:Apoptosis; D051379:Mice; D009569:Nitric Oxide / Q000378:metabolism*; D014407:Tumor Cells, Cultured; D016159:Tumor Suppressor Protein p53 / Q000378:metabolism*
chemical_list: D016159:Tumor Suppressor Protein p53; D009569:Nitric Oxide