| Project/Area Number |
16K09764
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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 |
Metabolomics
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| Research Institution | Gunma University |
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Principal Investigator |
Fukunaka Ayako 群馬大学, 生体調節研究所, 助教 (60586402)
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| Research Collaborator |
Fujitani Yoshio
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| Project Period (FY) |
2016-04-01 – 2019-03-31
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| Project Status |
Completed (Fiscal Year 2018)
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| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2018: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2017: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2016: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
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| Keywords | 亜鉛シグナル / 脂肪細胞褐色化 / ベージュ脂肪細胞 / 亜鉛トランスポーター / ZIP13 / 亜鉛輸送 / エネルギー代謝 / 脂肪褐色化 / エネルギー消費 |
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| Outline of Final Research Achievements |
We have previously reported that zinc transporter ZIP13, a protein associated with the recessive human connective tissues disorders (Fukada T, et al.,PLoS One, 2008), negatively regulates the adipocyte browning pathway (Fukunaka A, et al.,PLoS Genet., 2017). However, underlined mechanism has been obscured.
We have noted that the unique amino acid sequence of ZIP13 facing the cytosol, named intracellular loop2 (Int-L2), which is distinct from the other ZIP family members, is involved in the inhibition of adipocyte browning. We identified binding molecules that associate with the Int-L2 of ZIP13. We are now clarifying the molecular mechanism as to how ZIP13 Int-L2 binding protein X regulate adipocyte browning via ZIP13.
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| Academic Significance and Societal Importance of the Research Achievements |
「亜鉛シグナル」が生命活動に深く関わるシグナル伝達システムの一端を担うことが明示され、亜鉛シグナルの健康と病気への関与に注目が集まっている。一方で、「亜鉛シグナルがどのように標的分子の発現・活性を制御するのか」という生命現象の重大な命題が解明できていない(Fukunaka A, Int J Mol Sci.2018)。我々は、自身が開発したベージュ脂肪細胞分化系を用いて、ZIP13の直接の標的分子Xを同定することができたが、ZIP13がどのように分子Xを制御し、脂肪細胞褐色化を抑制するかは今後の課題である。
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