title: AKT down-regulates insulin-like growth factor-1 receptor as a negative feedback.
abstract: 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.
authors: Department of Biochemistry, Purdue University, West Lafayette, IN 47907, USA. lqin@purdue.edu
authors: Liang
authors: L
authors: Qin
authors: Yun
authors: Y
authors: Wang
authors: Lianyuan
authors: L
authors: Tao
authors: Zheng
authors: Z
authors: Wang