Targeted deletion of p97 (VCP/CDC48) in mouse results in early embryonic lethality

被引：106

作者：

Mueller, J. M. M.

Deinhardt, K.

Rosewell, I.

Warren, G.

Shima, D. T.

机构：

[1] Canc Res UK, Endothelial Cell Biol Lab, London WC2A 3PX, England

[2] Canc Res UK, Transgen Serv, London WC2A 3PX, England

[3] Yale Univ, Sch Med, Dept Cell Biol, New Haven, CT 06520 USA

来源：

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 2007年 / 354卷 / 02期

关键词：

p97; CDC48; VCP; AAA ATPase; mouse; knock-out; early embryonic lethality; cell cycle; embryogenesis; ubiquitin; folding;

D O I：

10.1016/j.bbrc.2006.12.206

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

The highly conserved AAA ATPase p97 (VCP/CDC48) has well-established roles in cell cycle progression, proteasome degradation and membrane dynamics. Gene disruption in Saccromyces cerevisiae, Drosophila melanogaster and Trypanosoma brucei demonstrated that p97 is essential in unicellular and multicellular organisms. To explore the requirement for p97 in mammalian cell function and embryogenesis, we disrupted the p97 locus by gene targeting. Heterozygous p97(+/-) mice were indistinguishable from their wild-type littermates, whereas homozygous mutants did not survive to birth and died at a peri-implantation stage. These results show that p97 is an essential gene for early mouse development. (c) 2007 Elsevier Inc. All rights reserved.

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页码：459 / 465

页数：7

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