Regulatory mechanism of NLRP3 inflammasome in chronic inflammation
Project/Area Number |
16H06270
|
Research Category |
Grant-in-Aid for Young Scientists (A)
|
Allocation Type | Single-year Grants |
Research Field |
Functional basic dentistry
|
Research Institution | Osaka University |
Principal Investigator |
|
Project Period (FY) |
2016-04-01 – 2019-03-31
|
Project Status |
Completed (Fiscal Year 2018)
|
Budget Amount *help |
¥24,050,000 (Direct Cost: ¥18,500,000、Indirect Cost: ¥5,550,000)
Fiscal Year 2018: ¥7,800,000 (Direct Cost: ¥6,000,000、Indirect Cost: ¥1,800,000)
Fiscal Year 2017: ¥7,800,000 (Direct Cost: ¥6,000,000、Indirect Cost: ¥1,800,000)
Fiscal Year 2016: ¥8,450,000 (Direct Cost: ¥6,500,000、Indirect Cost: ¥1,950,000)
|
Keywords | 炎症 / インフラマソーム / NLRP3 / GNB1 |
Outline of Final Research Achievements |
The NLRP3 inflammasome has been reported to be important for the development of chronic inflammation. However the regulatory mechanism of the NLRP3 inflammasome is not completely understood. In this study, we searched for new proteins that bind to NLRP3 by mass spectrometry and found G protein subunit beta 1 (GNB1). Functional analysis of GNB1 in NLRP3 inflammasome revealed that GNB1 negatively regulates NLRP3 inflammasome by suppressing the binding of NLRP3 to ASC.
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Academic Significance and Societal Importance of the Research Achievements |
本研究では、NLRP3インフラマソームを負に制御する新規因子であるGNB1を見出した。Gタンパク質とNLRP3インフラマソームの関連を示したことは新規性が高く、学術的にも重要である。さらにNLRP3インフラマソームが慢性炎症の発症に重要であることが判明していることから、GNB1によるNLRP3インフラマソームの抑制効果を利用することで、慢性炎症性疾患に対する新規治療法あるいは新規予防法のに応用できる可能性が考えられる。
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Report
(4 results)
Research Products
(10 results)