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Proteasome‐dependent decrease in Akt by growth factors in vascular smooth muscle cells
Author(s) -
Adachi Mayumi,
Katsumura Koichi Ricardo,
Fujii Kozo,
Kobayashi Sei,
Aoki Hiroki,
Matsuzaki Masunori
Publication year - 2003
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(03)01109-8
Subject(s) - protein kinase b , downregulation and upregulation , microbiology and biotechnology , proteasome , pi3k/akt/mtor pathway , growth factor , vascular smooth muscle , platelet derived growth factor receptor , chemistry , biology , phosphorylation , endocrinology , signal transduction , biochemistry , receptor , smooth muscle , gene
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.