Functions of the p53 Protein in Growth Regulation and Tumor Suppression

  1. J. Lin,
  2. X. Wu,
  3. J. Chen,
  4. A. Chang, and
  5. A.J. Levine
  1. Department of Molecular Biology, Princeton University, Princeton, New Jersey 08544-1014

This extract was created in the absence of an abstract.

Excerpt

The wild-type p53 protein is the product of a tumor suppressor gene that has been shown to block oncogenic transformation (Eliyahu et al. 1989; Finlay et al. 1989), negatively regulate progress through the cell cycle (Baker et al. 1990; Martinez et al. 1991), and induce apoptosis in some cell types (Yonish-Rouach et al. 1991; Shaw et al. 1992). The wild-type p53 protein is a transcription factor (Fields and Jang 1990; Raycroft et al. 1990), and that property may mediate its tumor suppressor phenotype, because mutant p53 proteins from human cancers have lost both their transcriptional trans-activation activity (Raycroft et al. 1990) and their tumor suppressor activity (Hinds et al. 1990). The transcriptional activation domain of p53 has been mapped to amino acid residues 1–42 (Raycroft et al. 1990), and the sequence-specific DNA-binding domain of the p53 protein has been shown to reside within residues 120–290 (Pavletich et al. 1994).

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