Proteasome-dependent decrease in Akt by growth factors in vascular smooth muscle cells
Proteasome-dependent decrease in Akt by growth factors in vascular smooth muscle cells
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DOI：
10.1016/s0014-5793(03)01109-8
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发表时间：
2003-11-06
期刊：
影响因子：
3.5
通讯作者：
Matsuzaki, M
中科院分区：
文献类型：
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作者：
Adachi, M;Katsumura, KR;Matsuzaki, M
Akt被生长因子激活以调节血管平滑肌细胞功能的各个方面。血小板源性生长因子（PDGF）和胰岛素样生长因子-1激活血管平滑肌细胞中的Akt，总Akt蛋白迅速减少，持续数小时。Akt的下调需要磷脂酰肌醇3-激酶活性，但不需要固有的Akt活性。Akt的下调被MG-132（一种蛋白酶体抑制剂）废除，但不被钙蛋白酶或组织蛋白酶抑制剂所废除。PDGF处理后，Akt表达于泛素免疫复合物中。Akt的蛋白酶体依赖性降解可能提供了一种对抗Akt过度激活的反调节机制。(C)2003年欧洲生物化学学会联合会。Elsevier B. V.出版，保留所有权利。
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. (C) 2003 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.