Analysis of ubiquitin network regulation by TRIM family proteins
Project/Area Number |
18H02607
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Research Category |
Grant-in-Aid for Scientific Research (B)
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Allocation Type | Single-year Grants |
Section | 一般 |
Review Section |
Basic Section 48040:Medical biochemistry-related
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Research Institution | Hokkaido University |
Principal Investigator |
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Project Period (FY) |
2018-04-01 – 2021-03-31
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Project Status |
Completed (Fiscal Year 2020)
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Budget Amount *help |
¥17,290,000 (Direct Cost: ¥13,300,000、Indirect Cost: ¥3,990,000)
Fiscal Year 2020: ¥5,850,000 (Direct Cost: ¥4,500,000、Indirect Cost: ¥1,350,000)
Fiscal Year 2019: ¥5,850,000 (Direct Cost: ¥4,500,000、Indirect Cost: ¥1,350,000)
Fiscal Year 2018: ¥5,590,000 (Direct Cost: ¥4,300,000、Indirect Cost: ¥1,290,000)
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Keywords | ユビキチン / TRIMタンパク質 / 細胞内シグナル / 質量分析 / 細胞周期 / タンパク質分解 / 細胞内情報伝達 |
Outline of Final Research Achievements |
It has been reported that TRIM family ubiquitin ligases are involved in the regulation of signal transduction and autophagy that control immune response, oncogenesis and cell differentiation, and has recently attracted attention in many fields of intracellular signal transduction system. In this application, we comprehensively analyzed the intracellular network system based on TRIM family ubiquitin ligase by comprehensive knockdown screening and proteomics method specialized in ubiquitination. Furthermore, by elucidating the functions of TRIM family in oncogenesis and the immune system, we proceeded to obtain findings that contribute to the diagnosis and treatment of autoimmune diseases, allergic diseases and cancers.
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Academic Significance and Societal Importance of the Research Achievements |
これまでは各TRIMタンパク質の機能が個別に報告されてきたが、本申請研究では網羅的にTRIMタンパク質が関するさまざまな細胞内シグナルを解析し、新たな基質タンパク質の同定に結び付いた。本研究成果により、TRIMファミリーによる翻訳後修飾(特にユビキチン化)の生理機能および疾患との関連の解明が進み、最終的にはがん化、細胞分化・個体発生・神経変性疾患・自己免疫疾患などの多様な方面おける総合的理解にも貢献する可能性が高い。
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Report
(4 results)
Research Products
(12 results)
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[Journal Article] The role of Mediator and Little Elongation Complex in transcription termination2020
Author(s)
Takahashi H, Ranjan A, Chen S, Suzuki H, Shibata M, Hirose T, Hirose H, Sasaki K, Abe R, Chen K, He Y, Zhang Y, Takigawa I, Tsukiyama T, Watanabe M, Fujii S, Iida M, Yamamoto J, Yamaguchi Y, Suzuki Y, Matsumoto M, Nakayama KI, Washburn P, Saraf A, Florens L, Sato S, Tomomori-Sato C, Conaway RC, Conaway JW, Hatakeyama S
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Journal Title
Nature Communications
Volume: 11
Issue: 1
Pages: 1-20
DOI
Related Report
Peer Reviewed / Open Access / Int'l Joint Research
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[Journal Article] Loss of TRIM29 Alters Keratin Distribution to Promote Cell Invasion in Squamous Cell Carcinoma.2018
Author(s)
Yanagi T, Watanabe M, Hata H, Kitamura S, Imafuku K, Yanagi H, Homma A, Wang L, Takahashi H, Shimizu H, Hatakeyama S.
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Journal Title
Cancer Res
Volume: 78
Issue: 24
Pages: 6795-6806
DOI
Related Report
Peer Reviewed
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[Journal Article] Anti-Sez6l2 antibody, detected in a patient with immune-mediated cerebellar ataxia, inhibits complex formation of GluR1 and Sez6l22018
Author(s)
Yaguchi, H., Yabe, I., Takahashi, H., Watanabe, M., Nomura, T., Kano, T., Watanabe, M. and Hatakeyama, S.
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Journal Title
J. Neurol.
Volume: 265
Issue: 4
Pages: 962-965
DOI
Related Report
Peer Reviewed
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[Journal Article] TRIM59 promotes gliomagenesis by inhibiting TC45 dephosphorylation of STAT32018
Author(s)
Sang, Y., Li, Y., Song, L., Alvarez, A.A., Zhang, W., Lv, D., Tang, J., Liu, F., Chang, Z., Hatakeyama, S., Hu, B., Cheng, S. and Feng, H.
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Journal Title
Cancer Res.
Volume: 78
Issue: 7
Pages: 1792-1804
DOI
Related Report
Peer Reviewed / Int'l Joint Research
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