期刊
JOURNAL OF BIOCHEMISTRY
卷 150, 期 2, 页码 151-156出版社
OXFORD UNIV PRESS
DOI: 10.1093/jb/mvr066
关键词
AKT; IGF1; IGF1R; IRS1; mTOR
资金
- municipal key discipline of Beijing, China [HK100230446]
As a member of receptor tyrosine kinase (RTK) family, insulin-like growth factor-1 (IGF1) receptor (IGF1R) activates several downstream pathways to transmit proliferative signals from extracellular stimulation. AKT as a major effector plays a pivotal role in integrating various survival signalling cascades. Our data here show that hyperactive AKT leads to the decrease of IGF1R at the transcriptional level, which could be partly restored by phosphatidylinositol-3 kinase (PI3K) inhibitors including wortmannin and LY294002. Moreover, the decrease of IGF1R impairs the sensitivity of IRS1 to the stimulation by IGF1. mTOR as a main downstream target of AKT is not involved in the AKT-mediated down-regulation of IGF1R.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据