| Project/Area Number |
15K19019
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Pathological medical chemistry
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| Research Institution | The University of Tokyo |
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Principal Investigator |
Kubota Yuji 東京大学, 医科学研究所, 助教 (70614973)
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| Research Collaborator |
Takagi Yusuke 東京大学, 医科学研究所, 大学院生
Kawabe Yosuke 東京大学, 医科学研究所, 大学院生
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| Project Period (FY) |
2015-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2016: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2015: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | MAPK経路 / 癌 / 先天性疾患 / 遺伝子変異 / シグナル伝達 |
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| Outline of Final Research Achievements |
The ERK pathway is a signaling pathway responsible for various cellular functions such as cell proliferation and differentiation. Recently, genetic mutations of MEK1 which is MAPKK of the ERK pathway were identified by genetic analysis of sporadic cancers and congenital Ras/MAPK syndromes. I found that the abnormal ERK activity caused by these MEK mutations leads to the expression of novel genes; a function-unknown protein (about 10 kDa) and long non-coding RNA (lncRNA). I confirmed that these molecules were expressed in various cancer cell lines with high ERK activity, and their strong expression was observed in several clinical cancer samples. In addition, cellular and molecular experiments showed that these gene expressions were important for cell functions such as cell proliferation and motility.
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