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Experimental & Molecular Medicine ; : 180-189, 2006.
Artículo en Inglés | WPRIM | ID: wpr-15693

RESUMEN

In adipocytes, insulin stimulates glucose transport primarily by promoting the translocation of GLUT4 to the plasma membrane. Requirements for Ca2+/ calmodulin during insulin-stimulated GLUT4 translocation have been demonstrated; however, the mechanism of action of Ca2+ in this process is unknown. Recently, myosin II, whose function in non-muscle cells is primarily regulated by phosphorylation of its regulatory light chain by the Ca2+/calmodulin-dependent myosin light chain kinase (MLCK), was implicated in insulin-stimulated GLUT4 translocation. The present studies in 3T3- F442A adipocytes demonstrate the novel finding that insulin significantly increases phosphorylation of the myosin II RLC in a Ca2+-dependent manner. In addition, ML-7, a selective inhibitor of MLCK, as well as inhibitors of myosin II, such as blebbistatin and 2,3-butanedione monoxime, block insulin- stimulated GLUT4 translocation and subsequent glucose transport. Our studies suggest that MLCK may be a regulatory target of Ca2+/calmodulin and may play an important role in insulin-stimulated glucose transport in adipocytes.


Asunto(s)
Ratones , Animales , Transporte de Proteínas/efectos de los fármacos , Fosforilación , Naftalenos/farmacología , Quinasa de Cadena Ligera de Miosina/antagonistas & inhibidores , Miosina Tipo II/metabolismo , Insulina/farmacología , Transportador de Glucosa de Tipo 4/metabolismo , Inhibidores Enzimáticos/farmacología , Relación Dosis-Respuesta a Droga , Calmodulina/antagonistas & inhibidores , Azepinas/farmacología , Adipocitos/citología , Células 3T3
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