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Open Access research that shapes economic thinking...

Strathprints makes available scholarly Open Access content by the Fraser of Allander Institute (FAI), a leading independent economic research unit focused on the Scottish economy and based within the Department of Economics. The FAI focuses on research exploring economics and its role within sustainable growth policy, fiscal analysis, energy and climate change, labour market trends, inclusive growth and wellbeing.

The open content by FAI made available by Strathprints also includes an archive of over 40 years of papers and commentaries published in the Fraser of Allander Economic Commentary, formerly known as the Quarterly Economic Commentary. Founded in 1975, "the Commentary" is the leading publication on the Scottish economy and offers authoritative and independent analysis of the key issues of the day.

Explore Open Access research by FAI or the Department of Economics - or read papers from the Commentary archive [1975-2006] and [2007-2018]. Or explore all of Strathclyde's Open Access research...

Glucagon activates two distinct signal transduction systems in hepatocytes, which leads to the desensitization of G-protein-regulated adenylate cyclase, the phosphorylation and inactivation of Gi-2 and the phosphorylation and stimulation of a specific cyclic AMP phosphodiesterase

Houslay, M.D. and Bushfield, M and Kilgour, E and Lavan, B E and Griffiths, S and Pyne, Nigel and Tang, I and Murphy, G (1990) Glucagon activates two distinct signal transduction systems in hepatocytes, which leads to the desensitization of G-protein-regulated adenylate cyclase, the phosphorylation and inactivation of Gi-2 and the phosphorylation and stimulation of a specific cyclic AMP phosphodiesterase. In: Activation and Desensitisation of Transducing Pathways. NATO ASI series, 44 . Springer-Verlag, pp. 63-83. ISBN 9783642836183

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Abstract

Book chapter explains how glucagon activates two distinct signal transduction systems in hepatocytes, which leads to the desensitization of G-protein-regulated adenylate cyclase, the phosphorylation and inactivation of Gi-2 and the phosphorylation and stimulation of a specific cyclic AMP phosphodiesterase.