A functional proteomics approarch to mechanism of radiation sensitivity.
| Project/Area Number |
26461880
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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 |
Radiation science
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| Research Institution | The University of Tokyo |
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Principal Investigator |
Enomoto Atsushi 東京大学, 大学院医学系研究科(医学部), 講師 (20323602)
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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 |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2016: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2015: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2014: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | Proteomics / STK38 / Radiation sensitivity / DNA damage responses / DNA損傷応答 / プロテオーム / リン酸化 / DNA損傷シグナル / DNA二重鎖切断 / 放射線感受性 / 放射線応答 |
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| Outline of Final Research Achievements |
STK38 (serine/threonine kinase 38), also known as NDR1 (nuclear Dbf2-related 1, is a serine/threonine protein kinase belonging to a subclass of the protein kinase A (PKA)/PKG/PKC-like (AGC) family, which includes cAMP-dependent kinase, protein kinase B, and protein kinase C. Knockdown of STK38 enhacnes cellular radio-sensitivity. However, its substrates and downstream signaling pathways remain to be determined. The fuction proteomics approarch revealved that STK38 endogenouly interact with CDC25A and that STK38 directly regulates CDC25A’s stability by phosphorylating Ser-76.Moreover, the STK38/CDC25A signaling module is demonstrated to be required to regulate the DNA-damage-induced G2/M checkpoint. Together, the results suggest thatthe STK38 knockdown-mediated radiosensitization may be due, at least in part, to impaired DNA damage-induced G2 arrest resulting from defective CDC25A degradation.
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Report
(4 results)
Research Products
(13 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] PI-3K/mTOR pathway inhibition overcomes radioresistance via suppression of the HIF1-alpha/VEGF pathway in endometrial cancer2015
Author(s)
A. Miyasaka, K. Oda, Y. Ikeda, K. Sone, T. Fukuda, K. Inaba, C. Makii, A. Enomoto, N. Hosoya, M. Tanikawa, Y. Uehara, T. Arimoto, H. Kuramoto, O. Wada-Hiraike, K. Miyagawa, T. Yano, K. Kawana, Y. Osuga, T. Fujii
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Journal Title
Gynecologic Oncology
Volume: 印刷中
Related Report
Peer Reviewed
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