Exit from Arsenite-Induced Mitotic Arrest Is p53 Dependent

Background: Arsenic is both a human carcinogen and a chemotherapeutic agent, but the mechanism of neither arsenic-induced carcinogenesis nor tumor selective cytotoxicity is clear. Using a model cell line in which p53 expression is regulated exogenously in a tetracycline-off system (TR9-7 cells), our...

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Veröffentlicht in:	Environmental health perspectives 2006-09, Vol.114 (9), p.1401-1406
Hauptverfasser:	McNeely, Samuel C., Xu, Xiaogiang, Taylor, B. Frazier, Zacharias, Wolfgang, McCabe, Michael J., States, J. Christopher
Format:	Artikel
Sprache:	eng
Schlagworte:	Apoptosis Apoptosis - drug effects Apoptosis - physiology Arsenic Arsenites Arsenites - toxicity Benzimidazoles - pharmacology Cell cycle Cell Cycle - drug effects Cell Cycle - physiology Cell lines Cells, Cultured DNA Dose-Response Relationship, Drug Fibroblasts G2 Phase - drug effects G2 Phase - physiology Gene therapy Genes, p53 - drug effects Genes, p53 - physiology Humans Inhibitor of Differentiation Protein 1 - metabolism Interphase KB cells Kinetics Microarray Analysis Mitosis Mitosis - drug effects Mitosis - physiology RNA, Messenger - metabolism Sodium Compounds - toxicity Time Factors
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