Description
Book SynopsisWith contributions from the leading researchers in the field, this volume brings together the latest studies on insulin action and signal transduction to provide a state-of-the-art reference for graduate researchers and students in diabetes and endocrinology. Insulin Signaling is a comprehensive study of the regulation of molecular events by insulin at a cellular level, utilizing experimental techniques ranging from molecular systems through phenotypic expression in transgenic and knockout models.
Table of ContentsStructural Aspects of the Insulin Receptor and its Downstream Effectors. Mutations in the Insulin Receptor Gene. Insulin Receptor Folding. IRS Protein Structure. Insulin Signaling Cascades. The Molecular Basis of Insulin Action. Grb-10 in Peptide Hormone Action. Regulation of Protein Kinase B: Implications for Insulin Signaling. Insulin-Mediated S6 Kinase Activation: Role in Translation Cell Growth and Insulin Production. Role of Serine/Threonine Protein Kinase Raf-1, in Insulin-Mediated Metabolic Signaling. PKC as Downstream Effector of P13 Kinase in Rat Adipocytes. Molecular Aspects of Insulin Action 10. PIKfyve and the Acute Insulin Actions. Insulin Action in Vascular Endothelium. GLUT4 Traffic Report: Molecular Mechanisms of Insulin-Stimulated GLUT4 Trafficking in Adipocytes. Insulin Receptor Trafficking. Ser/Thr Phosphorylation of Insulin Receptor Signaling Molecules and Insulin Resistance. Tyrosine Kinase Inhibitors. Abnormal p85/p110 Type PI-Kinase Activation in Zucker Fatty Rats and High-Fat Fed Rats. The Role of PKC for Insulin Receptor Signaling. Pharmacological Approaches to Insulin Resistance in the Zucker Diabetic Fatty Rat. Transgenics and Gene Knockout Models of Insulin Action. Lessons from Targeted Gene Knockouts of the Insulin receptor. Animal Models of IRS-1/IRS-2 Knockouts. Metabolic Perturbations in Mice Engineered to have Altered GLUT4 Content. Glucose Transporters and Cardiac Function: Insights from Heart Selective GLUT4 Knockout Mice. Insights from Mouse Models Deficient in Protein-Tyrosine Phosphatases that Regulate the Insulin Action Pathway.
