2011 Fiscal Year Final Research Report
Regulation of cell death and proliferation by the MTK1 SAPKKK and its failure in cancer
| Project/Area Number |
21390090
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Pathological medical chemistry
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| Research Institution | Nagoya University |
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Principal Investigator |
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| Project Period (FY) |
2009 – 2011
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| Keywords | 分子病態学 / 分子腫瘍学 / シグナル伝達 / MAPキナーゼ |
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| Research Abstract |
Stress-responsive MAPK pathways are activated by a wide array of stress stimuli such as DNA-damage, and play pivotal roles in the regulation of cellular stress responses, ranging from survival to apoptotic cell death. Perturbation of these critical signaling systems is involved in a variety of life-threatening disorders including cancer. In this study, we investigated physiological functions of a stress-responsive MAPKKK, MTK1. We found that, under stress conditions, MTK1 participated in down-regulation of cyclin expression. Furthermore, we screened for molecules that interact with MTK1, and identified a protein kinase(termed Mip1) as a novel substrate of MTK1. In response to stress, Mip1 was phosphorylated and activated by MTK1, thereby inhibiting stress-induced apoptosis. Interestingly, we confirmed that Mip1 expression was aberrantly regulated in human cancer.
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