Mice thrive without Cdk4 and Cdk2

被引：92

作者：

Barriere, Cedric ^{[1
,2
]}

Santamaria, David ^{[1
]}

Cerqueira, Antonio ^{[1
]}

Galan, Javier ^{[1
]}

Martin, Alberto ^{[1
]}

Ortega, Sagrario ^{[1
]}

Malumbres, Marcos ^{[1
]}

Dubus, Pierre ^{[2
]}

Barbacid, Mariano ^{[1
]}

机构：

[1] CNIO, Biotechnol Program, E-28029 Madrid, Spain

[2] Univ Bordeaux 2, EA2406, F-33076 Bordeaux, France

来源：

MOLECULAR ONCOLOGY | 2007年 / 1卷 / 01期

关键词：

Cyclin-dependent kinases; Mouse development; Cell proliferation; Conditional knock outs; Liver regeneration;

D O I：

10.1016/j.molonc.2007.03.001

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

Mammalian cell division is thought to be driven by sequential activation of several Cyclin-dependent kinases (Cdk), mainly Cdk4, Cdk6, Cdk2 and Cdk1. Since mice lacking Cdk4, Cdk6 or Cdk2 are viable, it has been proposed that they play compensatory roles. We report here that mice lacking Cdk4 and Cdk2 complete embryonic development to die shortly thereafter presumably due to heart failure. However, conditional ablation of Cdk2 in adult mice lacking Cdk4 does not result in obvious abnormalities. Moreover, these double mutant mice recover normally after partial hepatectomy. In culture, Cdk4(-/-); Cdk2(-/-) embryonic fibroblasts become immortal, display robust pRb phosphorylation. and have normal S phase kinetics. These observations indicate that Cdk4 and Cdk2 are dispensable for the mammalian cell cycle and for adult homeostasis. (C) 2007 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.

引用

页码：72 / 83

页数：12

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