| Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2017: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2016: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2015: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Outline of Final Research Achievements |
ER-associated degradation (ERAD) contributes to the maintenance of cellular homeostasis by degrading and eliminating structurally abnormal proteins generated in the endoplasmic reticulum. In this study, we focused on Derlin-3 whose expression is induced by endoplasmic reticulum stress and analyzed the importance of its function. In the in vivo experiments using hypoxic conditions, we found that Derlin-3 deficient mice exhibited the survival vulnerability. Herp (a protein forming an ERAD complex with Derlin-3)-deficient mice also exhibited the vulnerability. We also found that these mice have functional abnormalities in their hearts. Our findings that Herp controls the level of IP3 receptor, an intracellular signal transduction protein in the heart, may partly explain the cardiac abnormalities of Derlin-3 and Herp deficient mice.
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