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Citation
Tapon, N., Harvey, K.F., Bell, D.W., Wahrer, D.C.R., Schiripo, T.A., Haber, D.A., Hariharan, I.K. (2002). Salvador promotes both cell cycle exit and apoptosis in Drosophila and is mutated in human cancer cell lines.  Cell 110(4): 467--478.
FlyBase ID
FBrf0151717
Publication Type
Research paper
Abstract

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.

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Related Publication(s)
Note

Competition and compensation: coupled to death in development and cancer.
Abrams, 2002, Cell 110(4): 403--406 [FBrf0151812]

Stop and die.
Wells, 2002, J. Cell Biol. 158(4): 607 [FBrf0188714]

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Secondary IDs
    Language of Publication
    English
    Additional Languages of Abstract
    Parent Publication
    Publication Type
    Journal
    Abbreviation
    Cell
    Title
    Cell
    Publication Year
    1974-
    ISBN/ISSN
    0092-8674
    Data From Reference
    Aberrations (2)
    Alleles (11)
    Genes (7)
    Human Disease Models (1)
    Physical Interactions (1)
    Experimental Tools (1)
    Transgenic Constructs (5)