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MdmX regulates transformation and chromosomal stability in p53-deficient cells

Zdenka Matijasevic, Anna Krzywicka-Racka, Greenfield Sluder and Stephen N. Jones

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The cellular homologues Mdm2 and MdmX play critical roles in regulating the activity of the p53 tumor suppressor in damaged and non-damaged cells and during development in mice. Recently, we have utilized genetically defined primary cells and mice to reveal that endogenous levels of MdmX can also suppress multipolar mitosis and transformation in hyperploid p53-deficient cells and tumorigenesis in p53-deficient mice. These MdmX functions are not shared by Mdm2, and are distinct from the well-established ability of MdmX to complex with and inhibit p53 activity. Here we discuss some of the ramifications of MdmX loss in p53-deficient cells and mice, and we explore further the fate of MdmX/p53-double null embryonic fibroblasts undergoing multi-polar cell division using time-lapse video microscopy. We also discuss the relationship between chromosomal loss, cell proliferation, and the tumorigenic potential of p53-deficient cells lacking MdmX.

Authors

Zdenka Matijasevic

University of Massachusetts Medical School; Worcester, MA

Anna Krzywicka-Racka

University of Massachusetts Medical School; Worcester, MA

Greenfield Sluder

University of Massachusetts Medical School; Worcester, MA

Stephen N. Jones

University of Massachusetts Medical School; Worcester, MA

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If the document does not open, please right-click on the link (control-click on a Macintosh) and select the option to save the file to disk.