title: Micromanagement of the mitochondrial apoptotic pathway by p53.
abstract: It is now well established that p53 is the primary arbiter of stress-response and the principal barrier to neoplastic processes at the cellular level. Perhaps the most potent weapon in p53's tumor suppressive arsenal is apoptosis, enacted as a last resort when all other remedies are exhausted. Initially, the mechanism was thought to be simply activation or repression of Bcl-2 family members by p53. More recently, evidence of a more rapid pathway emerged whereby p53 physically interacts with Bcl-2 family members to tip the balance toward apoptosis. This review details the multiple levels of regulation of mitochondrially-directed apoptosis by p53, including recent findings of how p53 translocation is regulated.
authors.affiliation: Department of Pharmacology and Simmons Cancer Institute, Southern Illinois University School of Medicine, Springfield, Illinois 62794, USA.
authors.forename: Vijay
authors.initials: V
authors.lastname: Walia
authors.forename: Smita
authors.initials: S
authors.lastname: Kakar
authors.forename: Randolph
authors.initials: R
authors.lastname: Elble
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000235:genetics*; D018118:Chloride Channels / Q000378:metabolism; D016158:Genes, p53; D006801:Humans; D008928:Mitochondria / Q000187:drug effects / Q000502:physiology*; D033681:Mitochondrial Membrane Transport Proteins / Q000378:metabolism; D000083162:Mitochondrial Permeability Transition Pore; D021381:Protein Transport / Q000187:drug effects; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000378:metabolism*; D016159:Tumor Suppressor Protein p53 / Q000502:physiology*; D051028:bcl-2-Associated X Protein / Q000502:physiology
chemical_list: C464459:CLIC4 protein, human; D018118:Chloride Channels; D033681:Mitochondrial Membrane Transport Proteins; D000083162:Mitochondrial Permeability Transition Pore; D019253:Proto-Oncogene Proteins c-bcl-2; D016159:Tumor Suppressor Protein p53; D051028:bcl-2-Associated X Protein