Fig. 15
From: Convergence and Divergence of the Signaling Pathways for Insulin and Phosphoinositolglycans
Hypothetical model for signal transduction from GPI lipids and GPI-anchored proteins across the plasma membrane of insulin-sensitive cells.
This signal transduction takes place through the trypsin/salt-and NEM sensitive component, bridge protein and dual acylated tyrosine kinase of the Src-class to tyrosine phosphorylation of signaling proteins, such as IRS-1, caveolin, cytoplasmic (acylated) protein kinases and G proteins. Soluble PIG molecules generated from endogenous GPI structures through cleavage by intrinsic or exog-enously added phospholipases or PIG molecules added exogenously cause displacement of endoge-neous GPI lipids or GPI membrane protein anchors from their binding site at the trypsin/salt-and NEM-sensitive component located in caveolae. For further details, see Discussion.