Intermolecular Phosphorylation between Insulin Holoreceptors Does Not Stimulate Substrate Kinase Activity
Author:
Publisher
Elsevier BV
Subject
Cell Biology,Molecular Biology,Biochemistry
Reference37 articles.
1. A mutation in the insulin receptor gene that impairs transport of the receptor to the plasma membrane and causes insulin-resistant diabetes.
2. A mutation in the extracellular domain of the insulin receptor impairs the ability of insulin to stimulate receptor autophosphorylation.
3. Intermolecular transphosphorylation between insulin receptors and EGF-insulin receptor chimerae.
4. Insulin binding to its receptor induces a conformational change in the receptor C-terminus
5. The insulin receptor activation process involves localized conformational changes
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1. Dimerization-Induced Activation of Soluble Insulin/IGF-1 Receptor Kinases: An Alternative Mechanism of Activation;Biochemistry;2001-11-01
2. Substitution of the insulin receptor transmembrane domain with that of glycophorin A inhibits insulin action;The FASEB Journal;1999-08
3. Journey beyond immunology. Regulation of receptor internalization by major histocompatibility complex class I (MHC-I) and effect of peptides derived from MHC-I;APMIS;1998-11
4. Multiple endosomal recycling pathways in rat adipose cells;Biochemical Journal;1998-05-01
5. Cellular effects of phosphotyrosine-binding domain inhibitors on insulin receptor signaling and trafficking;Molecular and Cellular Biology;1997-03
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