| Project/Area Number |
24790840
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Kidney internal medicine
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| Research Institution | University of Miyazaki (2013)
University of Yamanashi (2012) |
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Principal Investigator |
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| Project Period (FY) |
2012-04-01 – 2014-03-31
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2013: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2012: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | 小胞体ストレス / タンパク質恒常性 / 腎臓病学 / タンパク質分解 / 腎障害 |
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| Research Abstract |
The unfolded protein response (UPR) and autophagy (Atg) serves protein homeostasis and implicates in renal diseases. Previous our studies demonstrated that the IRE1 signaling, which is known as UPR-mediated protein degradation pathway, related to renal tubular injury. Here, we investigated the role of Atg-related component in the IRE1 signaling. Our results demonstrated that; (1) Atg-related component could be interacted with cytosolic C-terminal region of IRE1; 2) level of this interaction changed during ER stress condition; 3) similar results were also observed in renal culture cells; 4) binding of Atg-related component activated the IRE1 signaling. Taken together, our results suggest a possibility that the Atg-related component regulated the renal function through modulation of UPR.
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