MdmX regulates transformation and chromosomal stability in p53-deficient cells

UMMS Affiliation

Department of Cell Biology

Publication Date


Document Type



Animals; Cell Division; *Cell Transformation, Neoplastic; Centrosome; Chromosomal Instability; Humans; Mice; Mitosis; Proto-Oncogene Proteins c-mdm2; Tumor Suppressor Protein p53


Cell Biology | Life Sciences | Medicine and Health Sciences


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.

DOI of Published Version



Cell Cycle. 2008 Oct;7(19):2967-73. Epub 2008 Oct 15. doi: 10.4161/cc.7.19.6797. Link to article on publisher's website

Journal/Book/Conference Title

Cell cycle (Georgetown, Tex.)

Related Resources

Link to Article in PubMed

PubMed ID