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    Cell. 2002 Aug 23;110(4):467-78.

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

    Tapon N, Harvey KF, Bell DW, Wahrer DC, Schiripo TA, Haber DA, Hariharan IK.

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    Massachusetts General Hospital Cancer Center, Building 149, 13th Street, Charlestown 02129, USA.

    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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    PMID:
    12202036
    [PubMed - indexed for MEDLINE]

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