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Role of Glycosyl-Phosphatidylinositols in Insulin Signalling

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Activation and Desensitization of Transducing Pathways

Abstract

Insulin is one of the best studied hormones. The main actions of insulin are to stimulate the synthesis of glycogen, lipids and proteins, through the modulation of the metabolic pathways implicated in these processes, and the stimulation of cell growth. The physiological effects of insulin include the stimulation of the uptake of glucose, amino acids and ions; the regulation of the state of serine-and threonine-phosphorylation of a variety of proteins and rate-limiting enzymes like glycogen phosphorylase, hormone-sensitive lipase and ATP citrate lyase; and the regulation of the expression of the genes for several regulatory enzymes (review by Denton, 1986). All these effects, whose chronology vary from seconds to hours, are initiated by the interaction of the hormone with the insulin receptor, an integral membrane glycoprotein composed of two α (Mr about 130 kDa) and two ß (95 kDa) subunits. The α subunits bind insulin and are linked by disulphide bonds to each other and to the ß-subunits. Following insulin binding, the ß-subunits are rapidly autophosphorylated predominantly at tyrosine residues. Direct evidence, indicating that insulin action depends on the protein tyrosine kinase activity of the insulin receptor, has been obtained by site-directed mutagenesis of the insulin receptor cDNA as well as with monoclonal antibodies to the insulin receptor kinase domain (review by Rosen, 1987).

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© 1990 Springer-Verlag Berlin Heidelberg

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Varela, I. et al. (1990). Role of Glycosyl-Phosphatidylinositols in Insulin Signalling. In: Konijn, T.M., Houslay, M.D., Van Haastert, P.J.M. (eds) Activation and Desensitization of Transducing Pathways. NATO ASI Series, vol 44. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-83618-3_10

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  • DOI: https://doi.org/10.1007/978-3-642-83618-3_10

  • Publisher Name: Springer, Berlin, Heidelberg

  • Print ISBN: 978-3-642-83620-6

  • Online ISBN: 978-3-642-83618-3

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