Proteasome‐dependent decrease in Akt by growth factors in vascular smooth muscle cells

FEBS Letters

Adachi, Mayumi²  Aoki, Hiroki²  Kobayashi, Sei¹  Katsumura, Koichi Ricardo²  Fujii, Kozo²  Matsuzaki, Masunori² 

[1] Department of Molecular Physiology, Yamaguchi University School of Medicine, 1-1-1 Minami Kogushi, Ube, Yamaguchi 755-8505, Japan;Department of Molecular Cardiovascular Biology, Yamaguchi University School of Medicine, 1-1-1 Minami Kogushi, Ube, Yamaguchi 755-8505, Japan

关键词: Akt;    Vascular smooth muscle cell;    Proteasome;    Ubiquitin;    Platelet-derived growth factor;    Insulin-like growth factor-1;    Phosphatidylinositol 3-kinase;    GAPDH;    glyceraldehyde-3-phosphate dehydrogenase;    IGF-1;    insulin-like growth factor-1;    IRS;    insulin receptor substrate;    PDGF;    platelet-derived growth factor;    PI3-kinase;    phosphatidylinositol 3-kinase;    VSMC;    vascular smooth muscle cell;   

DOI  :  10.1016/S0014-5793(03)01109-8

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

Akt is activated by growth factors to regulate various aspects of vascular smooth muscle cell function. Platelet-derived growth factor (PDGF) and insulin-like growth factor-1 activated Akt in vascular smooth muscle cells with a rapid reduction of total Akt protein that lasted for several hours. The downregulation of Akt required phosphatidylinositol 3-kinase activity, but not intrinsic Akt activity. The downregulation of Akt was abrogated by MG-132, a proteasome inhibitor, but not by inhibitors of calpain or cathepsins. Akt was found in ubiquitin immune complex after PDGF treatment. Proteasome-dependent degradation of Akt may provide a counter-regulatory mechanism against overactivation of Akt.

【 授权许可】

Unknown