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DNA Damage Checkpoints: P53 Regulation of the Cell Cycle

Arnold Levine

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Department of Molecular Biology, Lewis Thomas Laboratory, Princeton University, Princeton, NJ 08540

The P53 tumor suppresser gene product responds to DNA damage or cellular stress by being activated for transcription of several down stream genes. This results in either a G1 or G2 arrest of the cell cycle, to permit repair of the DNA, or programmed cell death. The p53 mediated response to cellular DNA damage is regulated by the genetic background of an organism, the sex of the organism and possibly by the age of the organism. Individuals who do not have a wild type p53 gene or are heterozygous for the p53 gene develop cancer at a young age (Levine, A.J., 1997, P53, the cellular gatekeeper for growth and division, Cell 88: 323-331.)

Dr. Levine has just been named President of Rockefeller University. He comes to Rockefeller from Princeton University where he was the Harry C. Weiss Professor in the Life Sciences in the Department of Molecular Biology. Dr. Levine received his B.A. from Harpur College, SUNY, and his Ph.D. from the University of Pennsylvania, School of Medicine. He was a postdoctoral fellow with Dr. Robert L. Sinsheimer at California Institute of Technology. He is a member of the National Academy of Sciences and has received numerous awards and honors throughout his career, including the G.H.A. Clowes Award from the American Association for Cancer Research (1998), The Bertner Award from the MD Anderson Cancer Center (1998), and The Paul Ehrlich and Ludwig Darmstaeder Prize from the Paul Ehrlich Foundation (1998). He is a member of the Society of Sigma Xi, the American Society for Microbiology, the American Association for Cancer Research, the American Association of Virology, and the AAAS. In 1996 he led a review of the National Institute of HealthÕs AIDS program.