The novel mechanism of stress recognition through the interaction of SOD1 with Derlin-1
Project/Area Number |
22770187
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Research Category |
Grant-in-Aid for Young Scientists (B)
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Allocation Type | Single-year Grants |
Research Field |
Cell biology
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Research Institution | The University of Tokyo |
Principal Investigator |
KADOWAKI Hisae 東京大学, 大学院・薬学系研究科, 特任研究員 (40568200)
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Project Period (FY) |
2010 – 2011
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Project Status |
Completed (Fiscal Year 2011)
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Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2011: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2010: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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Keywords | タンパク質 / 小胞体ストレス / Derlin-1 / SOD1 |
Research Abstract |
The structure of wild type SOD1 is thought to be changed by some cellular stress, and induces the endoplasmic reticulum stress through the interaction with Derlin-1, which is the important component of endoplasmic reticulum quality control system. Then, we tried to identify the factor which induces the interaction between wild type SOD1 and Derlin-1. Then, we identified the serum starvation induces the interaction and triggers endoplasmic reticulum stress.
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Report
(3 results)
Research Products
(9 results)
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[Journal Article] A novel monoclonal antibody reveals a conformational alteration shared by amyotrophic lateral sclerosis-linked SOD1 mutants
Author(s)
Fujisawa T, Homma K, Yamaguchi N, Kadowaki H, Tsuburaya N, Naguro I, Matsuzawa A, Takeda K, Takahashi Y, Goto J, Tsuji S, Nishitoh, Ichijo H
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Journal Title
Ann. Neurol
Volume: (印刷中)
Related Report
Peer Reviewed
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