| Budget Amount *help |
¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2016: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2015: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2014: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Outline of Final Research Achievements |
The endoplasmic reticulum (ER) is an organelle where newly synthesized secretory and membrane proteins are folded and assembled. Various stresses cause the accumulation of unfolded proteins in the ER, resulting in dysfunction of the ER. This condition is called ER stress. ER stress sensors are activated in pancreatic β cells, and loss of these sensors causes diabetes. Although the function of each sensor has been well studied, their precise roles in animal tissues are largely unknown.
To examine this physiological role of the IRE1α (one of the ER stress sensors) in pancreatic β cells, we generated pancreatic-β-cell-specific IRE1α conditional KO (CKO) mice and IRE1α-CKO insulinoma cell lines. IRE1α CKO mice developed insulin-dependent diabetes. We found that expression of some genes encoding folding enzymes was decreased in the insulinoma cells. From these observations, we concluded that IRE1α was found to be necessary for the folding process of insulin.
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