| Budget Amount *help |
¥218,010,000 (Direct Cost: ¥167,700,000、Indirect Cost: ¥50,310,000)
Fiscal Year 2016: ¥43,290,000 (Direct Cost: ¥33,300,000、Indirect Cost: ¥9,990,000)
Fiscal Year 2015: ¥43,680,000 (Direct Cost: ¥33,600,000、Indirect Cost: ¥10,080,000)
Fiscal Year 2014: ¥46,930,000 (Direct Cost: ¥36,100,000、Indirect Cost: ¥10,830,000)
Fiscal Year 2013: ¥43,680,000 (Direct Cost: ¥33,600,000、Indirect Cost: ¥10,080,000)
Fiscal Year 2012: ¥40,430,000 (Direct Cost: ¥31,100,000、Indirect Cost: ¥9,330,000)
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| Outline of Final Research Achievements |
Three major homeostasis in the ER, protein, calcium ion and redox, are closely regulating each other through a crosstalk. We found a novel ER-resident reductase ERdj5 and revealed that ERdj5 plays a pivotal role in facilitating the ER-associated degradation (ERAD) of misfolded proteins. We found that ERdj5 is also involved in the regulation of calcium ion pump SERCA2b though its reducing activity. ERdj5 reduces the disulfide bond in the ER lumen of SERCA2b and activates its ATPase activity. When Ca2+ concentration in the ER lumen is low, ERdj5 reduces and activates the SERCA2b, but when Ca2+ is high enough, ERdj5 makes a oligomer, which is no more active in activating the SERCA2b. Thus, ERdj5 regulates the SERCA2b activity by sensing the Ca2+ concentration in the ER lumen. We also revealed that the redox homeostasis in the ER is interfered by the protein homeostasis in the cytosol, which suggests the crosstalk between cytosolic protein homeostasis and ER redox homeostasis.
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