Analysis and establishment of crinophagy research
| Project/Area Number |
16H06167
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| Research Category |
Grant-in-Aid for Young Scientists (A)
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| Allocation Type | Single-year Grants |
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| Research Field |
Cell biology
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| Research Institution | Chiba University |
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Principal Investigator |
Itakura Eisuke 千葉大学, 大学院理学研究院, 助教 (90754218)
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| Project Period (FY) |
2016-04-01 – 2020-03-31
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| Project Status |
Completed (Fiscal Year 2019)
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| Budget Amount *help |
¥23,660,000 (Direct Cost: ¥18,200,000、Indirect Cost: ¥5,460,000)
Fiscal Year 2019: ¥3,250,000 (Direct Cost: ¥2,500,000、Indirect Cost: ¥750,000)
Fiscal Year 2018: ¥3,250,000 (Direct Cost: ¥2,500,000、Indirect Cost: ¥750,000)
Fiscal Year 2017: ¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2016: ¥11,960,000 (Direct Cost: ¥9,200,000、Indirect Cost: ¥2,760,000)
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| Keywords | タンパク質分解 / タンパク質品質管理 / 細胞外タンパク質 / crinopahgy / crinophagy / オートファジー / クリノファジー |
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| Outline of Final Research Achievements |
There are abundant proteins in extracellular spaces including blood and body fluid in mammals. On the other hand, the stress induce protein denature. It is well known that intracellular protein degradation systems degrade aberrant intracellular proteins to maintain proteostasis. However, degradation system for aberrant extracellular proteins remained unclear. We identified Chaperone and Receptor mediated Extracellular protein degradation (CRED) pathway which leads to selective degradation of aberrant extracellular protein via an extracellular chaperone. These data indicate that the extracellular protein degradation pathway has important role for extracellular proteostasis.
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| Academic Significance and Societal Importance of the Research Achievements |
細胞外へのタンパク質沈着は神経変性疾患などの疾患の要因となることが知られている。しかし細胞外タンパク質を除去するシステムはよくわかっていない。本研究成果は、細胞外変性タンパク質を選択的にリソソーム分解するシステムを世界で初めて明らかにした。このことはタンパク質分解関連学術分野に新しい知見を導入し、当該分野が新しい方向性へも発展することが期待される。今後このシステムを応用することで、疾患の原因となる異常タンパク質を選択的に取り除く新規疾患治療方法の開発へと発展し、いまだ治療法の開発に至っていない難治性の神経疾患への応用も期待される。
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Report
(5 results)
Research Products
(32 results)
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[Journal Article] Receptor-Interacting Protein Kinase 3 (RIPK3) inhibits autophagic flux during necroptosis in intestinal epithelial cells.2020
Author(s)
Otsubo K, Maeyashiki C, Nibe Y, Tamura A, Aonuma E, Matsuda H, Kobayashi M, Onizawa M, Nemoto Y, Nagaishi T, Okamoto R, Tsuchiya K, Nakamura T, Torii S, Itakura E, Watanabe M, Oshima S.
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Journal Title
FEBS letters
Volume: 594
Issue: 10
Pages: 1586-1595
DOI
Related Report
Peer Reviewed / Open Access
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[Journal Article] Systemic Analysis of Atg5-Null Mice Rescued from Neonatal Lethality by Transgenic ATG5 Expression in Neurons.2016
Author(s)
Yoshii SR, Kuma A, Akashi T, Hara T, Yamamoto A, Kurikawa Y, Itakura E, Tsukamoto S, Shitara H, Eishi Y, Mizushima N.
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Journal Title
Developmental cell
Volume: 39
Issue: 1
Pages: 116-130
DOI
Related Report
Peer Reviewed
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