Different Pathways of Postreceptor Desensitization following Chronic Insulin Treatment and in Cells Overexpressing Constitutively Active Insulin Receptors
Open Access
- 1 November 1996
- journal article
- Published by Elsevier in Journal of Biological Chemistry
- Vol. 271 (45) , 28206-28211
- https://doi.org/10.1074/jbc.271.45.28206
Abstract
No abstract availableKeywords
This publication has 35 references indexed in Scilit:
- Divergent Mechanisms for Homologous Desensitization of p21 by Insulin and Growth FactorsPublished by Elsevier ,1995
- Desensitization of Ras Activation by a Feedback Disassociation of the SOS-Grb2 ComplexJournal of Biological Chemistry, 1995
- Shc Isoform-specific Tyrosine Phosphorylation by the Insulin and Epidermal Growth Factor ReceptorsPublished by Elsevier ,1995
- Thiazolidine Derivatives Ameliorate High Glucose-induced Insulin Resistance via the Normalization of Protein-tyrosine Phosphatase ActivitiesJournal of Biological Chemistry, 1995
- Biochemical Analysis of MEK Activation in NIH3T3 FibroblastsPublished by Elsevier ,1995
- Insulin Stimulates the Tyrosine Dephosphorylation of pp125 Focal Adhesion KinaseJournal of Biological Chemistry, 1995
- PDGF- and insulin-dependent pp70S6k activation mediated by phosphatidylinositol-3-OH kinaseNature, 1994
- Regulation of phosphatidylinositol 3-kinase activity in liver and muscle of animal models of insulin-resistant and insulin-deficient diabetes mellitus.Journal of Clinical Investigation, 1993
- Phospholipase C-γ1 and phosphatidylinositol 3 kinase are the downstream mediators of the PDGF receptor's mitogenic signalCell, 1993
- Insulin receptor down-regulation is linked to an insulin-induced postreceptor defect in the glucose transport system in rat adipocytes.Journal of Clinical Investigation, 1985