发明名称 |
Non-human transgenic animal whose germ cells and somatic cells contain a knockout mutation in DNA encoding 4E-BP1 |
摘要 |
The eukaryotic mRNA 5' cap structure is recognized by eIF4E, which plays an essential role in translational control and cell growth. Members of a family of proteins called eIF4E-binding proteins (4E-BPs) inhibit the activity of eIF4E and consequently repress translation. Following exposure of cells to hormones, cytokines and growth factors, 4E-BPs become hyperphosphorylated and dissociate from eIF4E, to relieve translation inhibition. The phosphorylation events leading to 4E-BP1 dissociation from eIF4E are mediated by the P13-kinase/FRAP/mTOR signaling pathway. The present study addresses the biological importance of 4E-BP1 in vivo by disrupting its gene in the mouse. Homozygous 4E-BP1 deficient mice are healthy and develop normally. However, they show an important decrease in white adipose tissue and blood glucose level, and the males show a decrease in total body weight and an increase in resting metabolic rate. Primary mouse embryo fibroblasts show accelerated cell growth and enhanced cap-dependent translation, coincident with an increase in eIF4E phosphorylation.
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申请公布号 |
US2003041341(A1) |
申请公布日期 |
2003.02.27 |
申请号 |
US20010973473 |
申请日期 |
2001.10.09 |
申请人 |
SONENBERG NAHUM;TREMBLAY MICHEL;TSUKIAYAMA-KOHARA KYOKO |
发明人 |
SONENBERG NAHUM;TREMBLAY MICHEL;TSUKIAYAMA-KOHARA KYOKO |
分类号 |
A01K67/027;A61K31/7088;A61K38/00;A61K45/00;A61K48/00;A61P3/00;A61P3/04;A61P3/08;A61P3/10;A61P43/00;C07K14/47;C12N5/10;C12N15/09;C12N15/85;G01N33/15;G01N33/50;(IPC1-7):A01K67/027;C12N5/06 |
主分类号 |
A01K67/027 |
代理机构 |
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