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2002-07-26

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Si us plau utilitzeu sempre aquest identificador per citar o enllaçar aquest document: https://hdl.handle.net/2445/176737

NCS-1 Inhibits insulin stimulated GLUT4 translocation in 3T3L1 adipocytes through a phosphatidylinositol 4-kinase dependent pathway

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https://doi.org/10.1074/jbc.M203669200

Resum

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.

Matèries

Fosforilació, Teixit adipós, Receptors d'insulina

Matèries (anglès)

Phosphorylation, Adipose tissues, Insulin receptors

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Articles publicats en revistes (Bioquímica i Biomedicina Molecular)

Citació

MORA FAYOS, Sílvia, DURHAM, Paul l., SMITH, Jeffery r., RUSSO, Andrew f., JEROMIN, Andrea, PESSIN, Jeffrey e.. NCS-1 Inhibits insulin stimulated GLUT4 translocation in 3T3L1 adipocytes through a phosphatidylinositol 4-kinase dependent pathway. _Journal of Biological Chemistry_. 2002. Vol. 277, núm. 27494-27500. [consulta: 31 de gener de 2026]. ISSN: 0021-9258. [Disponible a: https://hdl.handle.net/2445/176737]

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