MDM2 controls gene expression independently of p53 in both normal and cancer cells

被引：21

作者：

Arena, Giuseppe ^{[1
]}

Riscal, Romain ^{[2
,3
]}

Linares, Laetitia K. ^{[4
,5
]}

Le Cam, Laurent ^{[4
,5
]}

机构：

[1] INSERM, U1030, Lab Mol Radiotherapy, Gustave Roussy Canc Campus, Villejuif, France

[2] Univ Penn, Perelman Sch Med, Abramson Family Canc Res Inst, Philadelphia, PA 19104 USA

[3] Univ Penn, Perelman Sch Med, Dept Canc Biol, Philadelphia, PA 19104 USA

[4] Univ Montpellier, Inst Rech Cancerol Montpellier, Inst Reg Canc Montpellier, IRCM,INSERM,U1194, F-34298 Montpellier, France

[5] Equipe Labelisee Ligue Canc, Paris, France

来源：

CELL DEATH AND DIFFERENTIATION | 2018年 / 25卷 / 09期

关键词：

EMBRYONIC LETHALITY; MDM2-DEFICIENT MICE; MITOCHONDRIAL; ABSENCE; DISEASE; RESCUE;

D O I：

10.1038/s41418-018-0156-x

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

070307 [化学生物学]; 071010 [生物化学与分子生物学];

摘要：

The mouse double minute 2 (MDM2) protein is an E3-ubiquitin ligase recognized for its role as a negative regulator of the tumor suppressor protein p53 [1]. Genetic studies showing that embryonic lethality of mice lacking MDM2 could only be rescued by the concomitant deletion of Tp53 suggested that the main physiological role of MDM2 is to inhibit p53. Furthermore, MDM2/p53 double knock-out (KO) mice displayed a cancer incidence similar to that observed in Tp53 KO animals, supporting the notion that the major role of MDM2 is to interfere with p53 activities [2, 3]. However, several reports have challenged this notion and convincingly showed that MDM2 functions extend beyond p53 regulation both in normal and cancer cells.

引用

页码：1533 / 1535

页数：3

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