Potential role of 3-phosphoinositide-dependent protein kinase 1 (PDK1) in insulin-stimulated glucose transporter 4 translocation in adipocytes

被引：12
作者：
Grillo, S [1 ]
Grémeaux, T [1 ]
Le Marchand-Brustel, Y [1 ]
Tanti, JF [1 ]
机构：
[1] Fac Med, INSERM, U145, F-06107 Nice 02, France
来源：
FEBS LETTERS | 1999年 / 461卷 / 03期
关键词：
insulin effect; okadaic acid; glut; 4; translocation; adipocyte; 3-phosphoinositide-dependent protein kinase 1;
D O I：
10.1016/S0014-5793(99)01472-6
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：
Insulin stimulation of Glut 4 translocation requires the activation of phosphatidylinositol 3-kinase (PI 3-kinase) but the downstream pathway remains ill-defined. We demonstrated that the overexpression of PDK1 (3-phosphoinositide-dependent protein kinase 1), a downstream effector of PI 3-kinase, stimulated Glut 4 translocation in adipocytes. This effect does not require the PH domain of PDK1, but expression of the pleckstrin homology domain-deleted PDK1 inhibits the effect of insulin, but not okadaic acid, on Glut 4 translocation, These results support a role of the PDK1 pathway in the transmission of insulin signal to Glut translocation. (C) 1999 Federation of European Biochemical Societies.
引用
收藏
页码：277 / 279
页数：3
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