Abstract
Although there is general agreement that insulin receptor tyrosine kinase activity mediates many of the actions of insulin, two types of studies suggest that non-tyrosine kinase dependent pathways may also exist. First, both monoclonal and polyclonal antibodies to the receptor have been shown to mediate many of insulin's actions with little or no stimulation of receptor kinase. Second, insulin receptor mutants, with reduced or no tyrosine kinase activity, have been shown to mediate several actions of insulin. Non-tyrosine kinase pathways that could signal insulin effects through the insulin receptor include non-covalent activation of G proteins, phospholipase Cs, or docking proteins such as IRS-1. Further studies on the chemical structures of phospholipids and their hydrolysis products involved in insulin action will be required to sort out the underlying mechanisms of insulin action via non-tyrosine kinase dependent pathways.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.