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Germ-Line-derived Hinge Domain p53 Mutants Have Lost Apoptotic but not Cell Cycle Arrest Functions¹

Department of Microbiology and Molecular Genetics, University of California-Irvine, Irvine, California 92697-4025

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.

¹ Supported by National Cancer Institute Grants CA19401 and CA68230. O. N. A. is supported in part by National Cancer Institute/National Institute of General Medical Sciences Fellowship 1F31CA7718-01.

² O. N. A. and J-F. C. contributed equally to this study.

³ Present address: Department of Experimental Pathology, Swiss Institute of Experimental Cancer Research (ISREC) 1066 Epalinges, Switzerland.

⁴ To whom requests for reprints should be addressed, at Dept. of Microbiology and Genetics, University of California-Irvine, Irvine, CA 92697-4025.

Received 10/29/97. Accepted 3/19/98.

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