2014 Fiscal Year Final Research Report
Regulation of MAPK pathways by protein sumoylation and O-GlcNAcylation and its dysregulation in human diseases
| Project Area | Regulation of signal transduction by post-translational modifications and its pathogenic dysregulation |
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| Project/Area Number |
22117003
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| Research Category |
Grant-in-Aid for Scientific Research on Innovative Areas (Research in a proposed research area)
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| Allocation Type | Single-year Grants |
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| Review Section |
Biological Sciences
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| Research Institution | The University of Tokyo (2012-2014)
Nagoya University (2010-2011) |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
TOMIDA Taichiro 東京大学, 医科学研究所, 助教 (70396886)
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| Project Period (FY) |
2010-04-01 – 2015-03-31
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| Keywords | シグナル伝達 / 翻訳後修飾 / MAPキナーゼ / SUMO / 上皮間葉転換 / 癌 / ストレス応答 |
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| Outline of Final Research Achievements |
In human cells, a wide array of extracellular stimuli generates intracellular signals that converge on a limited number of protein kinase cascades, commonly referred to as mitogen-activated protein kinase (MAPK) pathways. MAPK cascades, which consist of a three-tiered core of protein kinases, are the major signaling systems that dictate cell fate decisions such as survival, proliferation, and apoptosis. There are at least three subfamilies of MAPKs, named p38, JNK, and ERK. Perturbation of these cellular signaling systems is involved in a variety of life-threatening diseases. Therefore, these signaling systems are of clinical importance. In this study, we identified: 1) The ERK pathway is regulated at least in part by protein sumoylation and O-GlcNAcylation ; 2) MCRIP1, a novel ERK substrate, regulates epithelial-mesenchymal transition; 3) Oscillation of the p38/JNK activities in cells is critical for the regulation of the immune response.
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| Free Research Field |
分子細胞生物学
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