Regulation of circadian clock by DNA damage stress
| Project/Area Number |
23681009
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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 |
Risk sciences of radiation/Chemicals
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| Research Institution | Tokyo Medical and Dental University |
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Principal Investigator |
HIRAYAMA Jun 東京医科歯科大学, 難治疾患研究所, 准教授 (90510363)
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| Project Period (FY) |
2011-04-01 – 2014-03-31
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥27,430,000 (Direct Cost: ¥21,100,000、Indirect Cost: ¥6,330,000)
Fiscal Year 2013: ¥8,840,000 (Direct Cost: ¥6,800,000、Indirect Cost: ¥2,040,000)
Fiscal Year 2012: ¥8,840,000 (Direct Cost: ¥6,800,000、Indirect Cost: ¥2,040,000)
Fiscal Year 2011: ¥9,750,000 (Direct Cost: ¥7,500,000、Indirect Cost: ¥2,250,000)
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| Keywords | 概日リズム / DNA損傷応答 / 放射線 / 時計蛋白質 / MKK7 / JNK / 活性酸素種 / ストレス応答性リン酸化酵素 / MKK-JNKシグナル / JNKシグナル経路 / リン酸化修飾 |
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| Research Abstract |
Circadian clocks are intrinsic, time-tracking systems that endow organisms with a survival advantage. Studies of animal models and human tumor samples have revealed that the disruption of circadian rhythms is an important endogenous factor that can contribute to mammalian cancer development. The core of the circadian clock mechanism is molecular clock, a cell-autonomous and self-sustained oscillator system. This study tried to identify a molecular link between the molecular clock and DNA damage responses and have found that the stress kinase mitogen-activated protein kinase kinase 7 is a regulator of the molecular clock in mammalian cells.
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Report
(4 results)
Research Products
(27 results)
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[Journal Article] Linking oxygen to time: The bidirectional interaction between the hypoxic signaling pathway and the circadian clock2013
Author(s)
Egg M, Köblitz L, Hirayama J, Schwerte T, Folterbauer C, Kurz A, Fiechtner B, Möst M, Salvenmoser W, Sassone-Corsi P, and Pelster B
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Journal Title
Chronobiol. Int.
Volume: 30
Pages: 510-529
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