Originally discovered as one of three genes amplified on double minute chromosomes in a tumorigenic derivative of NIH 3T3 cells, MDM2 was later shown to possess oncogenic potential when overexpressed. High-level expression of MDM2 has also been shown to confer tumorigenic potential upon nontransformed rodent fibroblasts in athymic nude mice. MDM2 can immortalize rat embryo fibroblasts and can cooperate with activated RAS to transform these cells. Elevated levels of MDM2 protein have been found in a variety of human tumors, most notably in soft tissue sarcomas where up to 30% of primary tumors contain multiple copies of the MDM2 gene. One mechanism by which MDM2 overexpression promotes tumor development is through its ability to bind to the p53 tumor suppressor, thereby blocking the transactivation, cell cycle arrest, and apoptotic functions of p53. MDM2 can inhibit p53 activity in a number of ways including preventing p53 from recruiting TAFs, promoting nuclear export, inhibiting p53 acetylation, and perhaps most importantly by virtue of its function as an E3 ubiquitin ligase with specificity for, among others, p53. In addition to regulating p53 levels by targeting p53 for proteasomal degradation MDM2 also transfers ubiquitin to itself, MDMX, the ß2 adrenergic receptor, glucocorticoid receptor, TIP60, and PCAF.

Clear and colorless frozen liquid solution.
MDM2 is stored in 20mM Tris-Cl (pH 8.0), 20% Glycerol, 100mM KCl, 1mM DTT and 0.2mM EDTA buffer.

Use a manual defrost freezer and avoid repeated freeze-thaw cycles. While working, please keep sample on ice.