| Project/Area Number |
26440060
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Functional biochemistry
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| Research Institution | Prefectural University of Hiroshima |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
内匠 透 国立研究開発法人理化学研究所, 脳科学総合研究センター, チームリーダー (00222092)
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| Co-Investigator(Renkei-kenkyūsha) |
TAKUMI Toru 国立研究開発法人理化学研究所, 脳科学総合研究センター, シニアチームリーダー (00222092)
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2016: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2015: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2014: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | 細胞情報伝達 / ノックアウトマウス / アダプタータンパク質 / 細胞増殖因子 |
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| Outline of Final Research Achievements |
GAREM1 (Grb2-associated regulator of Erk/MAPK1) is an adaptor protein that is involved in the EGF pathway. The nuclear localization of GAREM1 depends on the nuclear localization sequence (NLS), which is located at the N-terminal CABIT (cysteine-containing, all in Themis) domain. Here, we identified 14-3-3ε as a GAREM-binding protein, and its binding site is closely located to the NLS. Moreover, the binding of 14-3-3 had an effect on the nuclear localization of GAREM1. We suggest that the interplay between 14-3-3, the C-terminal SAM (sterile alpha motif) domain and CABIT domain might be responsible for the distribution of GAREM1 in mammalian cells.
In contrast to GAREM1 that is expressed ubiquitously in human organs and cultured cells, GAREM2 is specifically expressed in the mouse, rat, and human brain. Moreover, GAREM2 does not possess the NLS sequence. To analyze the physiological functions of each GAREM subtype, we established and characterized a GAREM knockout (KO) mouse.
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