作者: Sara Piccinin , Elena Tonin , Sara Sessa , Silvia Demontis , Sabrina Rossi
DOI: 10.1016/J.CCR.2012.08.003
关键词:
摘要: Twist proteins have been shown to contribute cancer development and progression by impinging on different regulatory pathways, but their mechanism of action is poorly defined. By investigating the role in sarcomas, we found that Twist1 acts as a alternative TP53 mutation MDM2 overexpression inactivate p53 mesenchymal tumors. We provide evidence binds C terminus through box. This interaction hinders key posttranslational modifications facilitates its MDM2-mediated degradation. Our study suggests existence box code inactivation provides proof principle targeting box:p53 might offer additional avenues for treatment.