2016 Fiscal Year Final Research Report
Elucidation of regulatory mechanisms of stress signaling whose dysregulation causes inflammation and autoimmune diseases
| Project/Area Number |
26293011
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Partial Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Biological pharmacy
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| Research Institution | Tohoku University |
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Principal Investigator |
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Keywords | ストレス / シグナル伝達 / 活性酸素 / 炎症 / 自己免疫疾患 |
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| Outline of Final Research Achievements |
ASK1 (Apoptosis signal-regulating kinase 1), a stress-responsive kinase, induces a variety of physiological functions including cell death and immune responses in response to various types of stress such as reactive oxygen species, and the dysregulation of ASK1 leads to various diseases including inflammation and autoimmune diseases. Therefore, the activation of ASK1 should be strictly regulated in response to stress. However, the regulatory mechanisms of ASK1 had not been completely understood. In this study, we revealed that the activation of ASK1 is fine-tuned by several ubiquitination-related molecules such as USP9X, Roquin-2, and TRIM48, which have been originally identified in our laboratory, and that the fine-tuning of ASK1 provides appropriate responses including cell death and immune responses in response to a type, intensity, and duration of stress.
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| Free Research Field |
分子生物学
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