RESEARCH Amplification of Mdmx an M

Full list of author information is available at the end of the articleagainst cancer. The tumor protein 53 (TP53) becomes sta-bilized and regulates numerous downstream targets to in-duce cell cycle arrest, senescence, apoptosis, and DNA repair in response to diverse stresses. Mutation and LOH at the p53 locus occur as tumors progress under conditions of increasing genomic instability [1-3]. p53 is mutated in about 15 % to 50 % of the cases carry a mutant p53 gene and/or loss of heterozygosity (LOH) at chromosome loca-tion 17p13, where the p53 gene is located [5-7]. TP53 is negatively regulated by numerous factors. The murine double minute 2 (Mdm2) and Mdmx represent two important cellular regulators of p53. The Mdm2 gene was identified as one of three unknown genes (Mdm1-3) coamplified in the spontaneously transformed 3T3-DM mouse cell line [8]. Acting as an ubiquitin (Ub) protein ligase (E3), MDM2 (also called HDM2) can bind and ubi-* Correspondence