| Budget Amount *help |
¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2015: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2014: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2013: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Outline of Final Research Achievements |
G protein-coupled receptors (GPCRs) are heptahelical membrane proteins that comprise one of the largest families of cell surface signaling receptors in the human genome. GPCRs are the targets of ~30% of the drugs currently used for the treatment of a wide range of human diseases. Thus, elucidating the mechanism of regulation of GPCR signaling is essential for the development of more effective and safer therapeutic agents. Endocytic internalization of G protein-coupled receptors (GPCRs) plays a critical role in down-regulation of GPCR signaling. In this study, we screened for yeast single-gene deletion mutants exhibiting defects in GPCR endocytosis. By using fluorescent endocytic cargo, we identified 195 mutants that exhibited delay in endocytic transport of GPCR. Among these genes, we focused on yeast Rab5, Vps21p. We found that yeast Rab5 mutant shows significant delay of GPCR transport to the vacuole. We also found a novel endocytic pathway mediated by the AP-3 complex.
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