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Title: NCS-1 Inhibits insulin stimulated GLUT4 translocation in 3T3L1 adipocytes through a phosphatidylinositol 4-kinase dependent pathway
Author: Mora Fayos, Sílvia
Durham, Paul L.
Smith, Jeffery R.
Russo, Andrew F.
Jeromin, Andrea
Pessin, Jeffrey E.
Keywords: Fosforilació
Teixit adipós
Receptors d'insulina
Adipose tissues
Insulin receptors
Issue Date: 26-Jul-2002
Publisher: American Society for Biochemistry and Molecular Biology
Abstract: Expression of NCS-1 (neuronal calcium sensor-1, also termed frequenin) in 3T3L1 adipocytes strongly inhibited insulin-stimulated translocation of GLUT4 and insulin-responsive aminopeptidase. The effect of NCS-1 was specific for GLUT4 and the insulin-responsive aminopeptidase translocation as there was no effect on the trafficking of the cation-independent mannose 6-phosphate receptor or the GLUT1 glucose transporter isoform. Moreover, NCS-1 showed partial colocalization with GLUT4-EGFP in the perinuclear region. The inhibitory action of NCS-1 was independent of calcium sequestration since neither treatment with ionomycin nor endothelin-1, both of which elevated the intracellular calcium concentration, restored insulin-stimulated GLUT4 translocation. Furthermore, NCS-1 did not alter the insulin-stimulated protein kinase B (PKB/Akt) phosphorylation or the recruitment of Cbl to the plasma membrane. In contrast, expression of the NCS-1 effector phosphatidylinositol 4-kinase (PI 4-kinase) inhibited insulin-stimulated GLUT4 translocation, whereas co-transfection with an inactive PI 4-kinase mutant prevented the NCS-1-induced inhibition. These data demonstrate that PI 4-kinase functions to negatively regulate GLUT4 translocation through its interaction with NCS-1.
Note: Reproducció del document publicat a:
It is part of: Journal of Biological Chemistry, 2002, vol. 277, p. 27494-27500
Related resource:
ISSN: 0021-9258
Appears in Collections:Articles publicats en revistes (Bioquímica i Biomedicina Molecular)

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