Regulation of the ERK-MAPK cascade and cell-transformation by MEKsumoylation
Project/Area Number |
23890077
|
Research Category |
Grant-in-Aid for Research Activity Start-up
|
Allocation Type | Single-year Grants |
Research Field |
Pathological medical chemistry
|
Research Institution | The University of Tokyo (2012) Nagoya University (2011) |
Principal Investigator |
KUBOTA Yuji 東京大学, 医科学研究所, 助教 (70614973)
|
Project Period (FY) |
2011 – 2012
|
Project Status |
Completed (Fiscal Year 2012)
|
Budget Amount *help |
¥3,250,000 (Direct Cost: ¥2,500,000、Indirect Cost: ¥750,000)
Fiscal Year 2012: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2011: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
|
Keywords | 癌 / ERK / SUMO / MAPK / Ras-MAPK症候群 / MEK |
Research Abstract |
We found MEK sumoylation strongly attenuated its kinase activity and inhibited the ERK pathway by disrupting the specific docking interaction between MEK and ERK. Interestingly, the Ras oncogene inhibited MEK sumoylation, and forced enhancement of MEK sumoylation suppressed Ras-induced cell transformation. These data indicates that the ablation of MEKsumoylation by the specific oncogene contributes to carcinogenesis.
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Report
(3 results)
Research Products
(15 results)