Quantitative phosphoproteomic analysis of mTOR signaling perturbation in glioblastoma stem cells
| Project/Area Number |
26505001
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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 |
オミクス計測科学
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| Research Institution | The University of Tokyo |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
尾山 大明 東京大学, 医科学研究所, 准教授 (30422398)
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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 |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2016: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000)
Fiscal Year 2015: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2014: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | プロテオミクス / 膠芽腫幹細胞 / mTORシグナル / リン酸化 / SILAC / mTOR シグナル |
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| Outline of Final Research Achievements |
Glioblastoma is the most malignant brain tumor with poor prognosis and shows high resistance to the conventional treatment such as chemotherapy or radiation. In this study, we performed global quantitative proteome and phosphoproteome analyses of EGF-dependent mTOR signaling in patient-derived gliblastoma stem cells through perturbation by mTOR specific inhibitor, Torin1.
As a result of integrated statistical and mathematical analyses of these large-scale data, it was strongly suggested that DNA damage checkpoint might be involved in the maintenance of stemness properties in the glioblastoma stem cells.
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Report
(4 results)
Research Products
(36 results)
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[Journal Article] Extremotolerant tardigrade genome and improved radiotolerance of human cultured cells by tardigrade-unique protein.2016
Author(s)
Hashimoto T, Horikawa DD, Saito Y, Kuwahara H, Kozuka-Hata H, Shin-I T, Minakuchi Y, Ohishi K, Motoyama A, Aizu T, Enomoto A, Kondo K, Tanaka S, Hara Y, Koshikawa S, Sagara H, Miura T, Yokobori S, Miyagawa K, Suzuki Y, Kubo T, Oyama M, Kohara Y, Fujiyama A, Arakawa K, Katayama T, Toyoda A and Kunieda T
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Journal Title
Nature Communications
Volume: 7
Issue: 1
Pages: 12808-12808
DOI
NAID
Related Report
Peer Reviewed / Open Access
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[Journal Article] Long noncoding RNA UPAT promotes colon tumorigenesis by inhibiting degradation of UHRF1.2016
Author(s)
Taniue K, Kurimoto A, Sugimasa H, Nasu E, Takeda Y, Iwasaki K, Nagashima T, Okada-Hatakeyama M, Oyama M, Kozuka-Hata H, Hiyoshi M, Kitayama J, Negishi L, Kawasaki Y, Akiyama T.
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Journal Title
Proceedings of the National Academy of Sciences U S A.
Volume: 113
Issue: 5
Pages: 1273-8
DOI
Related Report
Peer Reviewed / Acknowledgement Compliant
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[Journal Article] Scaffold Protein Ahk1, Which Associates with Hkr1, Sho1, Ste11, and Pbs2, Inhibits Cross Talk Signaling from the Hkr1 Osmosensor to the Kss1 Mitogen-Activated Protein Kinase.2016
Author(s)
Nishimura A, Yamamoto K, Oyama M, Kozuka-Hata H, Saito H, Tatebayashi K.
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Journal Title
Mol Cell Biol
Volume: 36
Issue: 7
Pages: 1109-1123
DOI
Related Report
Peer Reviewed
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[Journal Article] 5-Hydroxymethylcytosine plays a critical role in glioblastomagenesis by recruiting the CHTOP-methylosome complex.2014
Author(s)
Takai H, Masuda K, Sato T, Sakaguchi Y, Suzuki T, Suzuki T, Koyama-Nasu R, Nasu-Nishimura Y, Katou Y, Ogawa H, Morishita Y, Kozuka-Hata H, Oyama M, Todo T, Ino Y, Mukasa A, Saito N, Toyoshima C, Shirahige K, Akiyama T.
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Journal Title
Cell Rep.
Volume: 9
Pages: 48-60
Related Report
Peer Reviewed
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[Journal Article] Influenza virus-host interactome screen as a platform for antiviral drug development.2014
Author(s)
Watanabe T, Kawakami E, Shoemaker JE, Lopes TJ, Matsuoka Y, Tomita Y, Kozuka-Hata H, Gorai T, Kuwahara T, Takeda E, Nagata A, Takano R, Kiso M, Yamashita M, Sakai-Tagawa Y, Katsura H, Nonaka N, Fujii H, Fujii K, Sugita Y, Noda T, Goto H, Fukuyama S, Watanabe S, Neumann G, Oyama M, Kitano H, Kawaoka Y.
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Journal Title
Cell Host Microbe
Volume: 16
Pages: 795-805
Related Report
Peer Reviewed
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