Growth retardation and increased apoptosis in mice with homozygous disruption of the akt1 gene

被引：775

作者：

Chen, WS ^{[1
]}

Xu, PZ

Gottlob, K

Chen, ML

Sokol, K

Shiyanova, T

Roninson, I

Weng, W

Suzuki, R

Tobe, K

Kadowaki, T

Hay, N

机构：

[1] Univ Illinois, Coll Med, Dept Mol Genet, Chicago, IL 60607 USA

[2] Univ Illinois, Res Resources Ctr, Chicago, IL 60612 USA

[3] Rockefeller Univ, New York, NY 10021 USA

[4] Ingenious Targeting Lab, Stony Brook, NY 11790 USA

[5] Univ Tokyo, Dept Metab Dis, Tokyo 1138655, Japan

来源：

GENES & DEVELOPMENT | 2001年 / 15卷 / 17期

关键词：

gamma irradiation; glucose tolerance; seminiferous tubular atrophy; thymocytes; mouse embryo fibroblasts;

D O I：

10.1101/gad.913901

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

The serine/threonine kinase Akt has been implicated in the control of cell survival and metabolism. Here we report the disruption of the most ubiquitously expressed member of the akt family of genes, akt1, in the mouse. Akt1(-/-) mice are viable but smaller when compared to wild-type littermates. In addition, the life span of Akt1(-/-) mice, upon exposure to genotoxic stress, is shorter. However, Akt1(-/-) mice do not display a diabetic phenotype. Increased spontaneous apoptosis in testes, and attenuation of spermatogenesis is observed in Akt1(-/-) male mice. Increased spontaneous apoptosis is also observed in the thymi of Akt1(-/-) mice, and Akt1(-/-)thymocytes are more sensitive to apoptosis induced by gamma -irradiation and dexamethasone. Finally, Akt1(-/-)mouse embryo fibroblasts (MEFs) are mote susceptible to apoptosis induced by TNF, anti-Fas, UV irradiation, and serum withdrawal.

引用

页码：2203 / 2208

页数：6

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