title: Too much of a good thing: the Prl-3 in p53's oyster.
abstract: In this issue of Molecular Cell, Basak et al. (2008) identify Prl-3 as a p53-inducible gene acting in DNA damage-induced cell-cycle arrest. Both deletion and overexpression of Prl-3 can be cytostatic, adding to a growing list of genes whose expression must be carefully titrated for proper cell proliferation.
authors.affiliation: Molecular Oncology Research Institute, Tufts Medical Center, 800 Washington Street #5609, Boston, MA 02111, USA. phinds@tuftsmedicalcenter.org
authors.forename: Philip W
authors.initials: PW
authors.lastname: Hinds
mesh_terms: D002453:Cell Cycle / Q000502:physiology; D049109:Cell Proliferation; D004249:DNA Damage; D005786:Gene Expression Regulation; D006801:Humans; D009363:Neoplasm Proteins / Q000235:genetics / Q000378:metabolism*; D017027:Protein Tyrosine Phosphatases / Q000235:genetics / Q000378:metabolism*; D016159:Tumor Suppressor Protein p53 / Q000235:genetics / Q000378:metabolism*
chemical_list: D009363:Neoplasm Proteins; C495901:TP53 protein, human; D016159:Tumor Suppressor Protein p53; C484730:PTP4A3 protein, human; D017027:Protein Tyrosine Phosphatases