| Project/Area Number |
15H06410
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| Research Category |
Grant-in-Aid for Research Activity Start-up
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| Allocation Type | Single-year Grants |
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| Research Field |
Cell biology
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| Research Institution | Iwate University (2016)
Nara Institute of Science and Technology (2015) |
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Principal Investigator |
Shiba Yoko 岩手大学, 理工学部, 准教授 (50755866)
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| Project Period (FY) |
2015-08-28 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
Fiscal Year 2016: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2015: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Keywords | インスリン / IRE1alpha / 小胞体ストレス / 分泌 / IRE1a / 小胞体ストレスセンサー / 阻害剤 |
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| Outline of Final Research Achievements |
IRE1a is activated by the accumulation of unfolded proteins in the endoplasmic reticulum to induce gene transcription of chaperones. 4μ8C, a well-known inhibitor of IRE1a RNase activity, is commonly used to analyze IRE1a function during ER stress in cultured mammalian cells. However, the off-target effects of 4μ8C remain elusive. Pancreatic β-cells synthesize a large amount of insulin in response to high glucose stimulation, and IRE1a plays an important role in insulin secretion from pancreatic beta-cells. To analyze the role of IRE1a in pancreatic beta-cells, we examined insulin secretion after 4μ8C treatment. Unexpectedly, we found 4μ8C blocked the late stage of the insulin secretory process, independent of the IRE1a-XBP1 pathway. Our results indicate that 4μ8C has an off-target effect on insulin secretion in pancreatic β-cells. These finding inform the researchers in the field that the use of 4μ8C requires the special consideration for the future studies.
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