Clarification of molecular basis of transporter diseases by the comprehensive detection of protein-rotein interactions.

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Transporter diseases are caused by disorders of various membrane transporter and channel proteins. We analyzed the comprehensive protein-protein interactions that alter intracellular traffic of transporters by utilizing the hereditary defects of glutamate transporter GLAST in Japanese dog red cells as a model of the transporter disease. The PDZ domain proteins NHERF1 and NHERF2 interacted with the GLAST proteins in the endoplasmic reticulum and the post-Golgi compartments during the traffic to the plasma membrane, respectively. Since coexpression of these proteins altered the cell surface expression level of GLAST, it is suggested that the interaction of PDZ domain proteins with GLAST is associated with the disorder of intracellular trafficking of GLAST.