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salvador Promotes both cell cycle exit and apoptosis in Drosophila and is mutated in human cancer cell lines.

The number of cells in an organism is determined by regulating both cell proliferation and cell death. Relatively few mechanisms have been identified that can modulate both of these processes. In a screen for Drosophila mutations that result in tissue overgrowth, we identified salvador (sav), a gene that promotes both cell cycle exit and cell death. Elevated Cyclin E and DIAP1 levels are found in mutant cells, resulting in delayed cell cycle exit and impaired apoptosis. Salvador contains two WW domains and binds to the Warts (or LATS) protein kinase. The human ortholog of salvador (hWW45) is mutated in three cancer cell lines. Thus, salvador restricts cell numbers in vivo by functioning as a dual regulator of cell proliferation and apoptosis.

Pubmed ID: 12202036

Authors

  • Tapon N
  • Harvey KF
  • Bell DW
  • Wahrer DC
  • Schiripo TA
  • Haber D
  • Hariharan IK

Journal

Cell

Publication Data

August 23, 2002

Associated Grants

  • Agency: NCI NIH HHS, Id: CA87691
  • Agency: NEI NIH HHS, Id: EY11632
  • Agency: NIGMS NIH HHS, Id: GM61672

Mesh Terms

  • Amino Acid Sequence
  • Animals
  • Apoptosis
  • Base Sequence
  • Cell Cycle Proteins
  • Cell Division
  • Cell Transformation, Neoplastic
  • Drosophila Proteins
  • Eukaryotic Cells
  • Eye
  • Eye Abnormalities
  • Female
  • Gene Expression Regulation, Developmental
  • Gene Expression Regulation, Neoplastic
  • Genes, cdc
  • Genetic Testing
  • Humans
  • Male
  • Molecular Sequence Data
  • Mutation
  • Neoplasms
  • Phenotype
  • Photoreceptor Cells, Invertebrate
  • Protein Kinases
  • Protein Structure, Tertiary
  • Protein-Serine-Threonine Kinases
  • Proteins
  • Tumor Cells, Cultured