A novel function of p53 in TR3-MDM2 cross-talk  

作　　者：Hang-Zi Chen Qiao wu 

机构地区：[1]Key Laboratory of the Ministry of Education for Cell Biology and Tumor Cell Engineering, School of Life Sciences, Xiamen University,Fujian 361005, China

出　　处：《Cell Research》2007年第4期293-294,共2页细胞研究（英文版）

摘　　要：TR3 (也作为 Nur77，或 NGFI-B 知道) 属于 steroid/thyroid/retinoidreceptor 总科，并且因为它的特定的 ligand 没被识别，作为孤儿受体被分类。原来， TR3 作为生长被识别因素可诱导的基因。TR3in apoptosis 的角色首先在 1994 被报导，在 TR3 表示被显示被 T-cellreceptor 发信号导致并且为 T 房间调停受体的 apoptosis 要求了的地方。TR3 的快速的正式就职被导致 apoptosis 代理人也在刺激以后在癌症房间的不同类型观察，显示 TR3 的那正式就职贡献 apoptotic 过程。TR3 （also known as Nur77, or NGFI-B） belongs to the steroid/thyroid/retinoid receptor superfamily, and is classified as an orphan receptor because its specific ligand has not been identified [1 ]. Originally, TR3 was identified as a growth factor-inducible gene [2]. The role of TR3 in apoptosis was first reported in 1994, where TR3 expression was shown to be induced by T-cell receptor signaling and required for T-cell receptor-mediated apoptosis [3,4]. Rapid induction of TR3 is also observed in different types of cancer cells after stimulation by apoptosis-inducing agents [5-7], indicating that induction of TR3 contributes to the apoptotic process.

关 键 词：孤儿受体超家族 TR3 生长因子诱导基因 MDM2 P53 相互作用 细胞凋亡 

分 类 号：Q26[生物学—细胞生物学] Q255