共 25 条
Proteasome-dependent decrease in Akt by growth factors in vascular smooth muscle cells
被引:37
作者:

Adachi, M
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机构: Yamaguchi Univ, Sch Med, Dept Mol Cardiovasc Biol, Ube, Yamaguchi 7558505, Japan

Katsumura, KR
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机构: Yamaguchi Univ, Sch Med, Dept Mol Cardiovasc Biol, Ube, Yamaguchi 7558505, Japan

Fujii, K
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机构: Yamaguchi Univ, Sch Med, Dept Mol Cardiovasc Biol, Ube, Yamaguchi 7558505, Japan

Kobayashi, S
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机构: Yamaguchi Univ, Sch Med, Dept Mol Cardiovasc Biol, Ube, Yamaguchi 7558505, Japan

Aoki, H
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机构: Yamaguchi Univ, Sch Med, Dept Mol Cardiovasc Biol, Ube, Yamaguchi 7558505, Japan

Matsuzaki, M
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机构: Yamaguchi Univ, Sch Med, Dept Mol Cardiovasc Biol, Ube, Yamaguchi 7558505, Japan
机构:
[1] Yamaguchi Univ, Sch Med, Dept Mol Cardiovasc Biol, Ube, Yamaguchi 7558505, Japan
[2] Yamaguchi Univ, Sch Med, Dept Mol Physiol, Ube, Yamaguchi 7558505, Japan
关键词:
Akt;
vascular smooth muscle cell;
proteasome;
ubiquitin;
platelet-derived growth factor;
insulin-like growth factor-1;
phosphatidylinositol;
3-kinase;
D O I:
10.1016/S0014-5793(03)01109-8
中图分类号:
Q5 [生物化学];
Q7 [分子生物学];
学科分类号:
071010 ;
081704 ;
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. (C) 2003 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.
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页码:77 / 80
页数:4
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