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Potential role of 3‐phosphoinositide‐dependent protein kinase 1 (PDK1) in insulin‐stimulated glucose transporter 4 translocation in adipocytes
Author(s) -
Grillo Sophie,
Grémeaux Thierry,
Le Marchand-Brustel Yannick,
Tanti Jean-François
Publication year - 1999
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(99)01472-6
Subject(s) - pleckstrin homology domain , glut4 , chromosomal translocation , microbiology and biotechnology , glucose transporter , map kinase kinase kinase , chemistry , insulin receptor , protein kinase b , phosphatidylinositol , ask1 , phosphoinositide 3 kinase , cyclin dependent kinase 9 , mitogen activated protein kinase kinase , signal transduction , kinase , insulin , biology , protein kinase a , endocrinology , biochemistry , insulin resistance , gene
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.