Author/Authors :
Eischen، نويسنده , , Christine M. and Lozano، نويسنده , , Guillermina، نويسنده ,
Abstract :
Therapeutics that disrupt the p53-MDM2 interaction show promise for cancer treatment but surprisingly have different biological outcomes. A study by Enge et al. in this issue of Cancer Cell shows that the ability of MDM2 to target hnRNP K for degradation contributes to the decision to induce apoptosis rather than cell-cycle arrest.