Analyses of function of ASC and PYNOD in skin
| Project/Area Number |
21590329
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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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 | Kanazawa University |
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Principal Investigator |
IMAMURA Ryu 金沢大学, がん進展制御研究所, 助教 (10311680)
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| Project Period (FY) |
2009 – 2011
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| Project Status |
Completed (Fiscal Year 2011)
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| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2011: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2010: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2009: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 自然免疫 / NLRファミリー蛋白 / 皮膚 / PYNOD / ASC |
|---|
| Research Abstract |
PYNOD(Nlrp10) is one of the NLR family member we recently identified, however, the physiological function of PYNOD is still totally unclear. To investigate physiological/pathological function of PYNOD, we succeeded to establish PYNOD deficient mice. We found that keratinocytes from PYNOD deficient mice show lower potential to produce TNFαafter UVB treatment than that of wild-type mice. We further found TNFαproduction in skin after UVB treatment also decreased in PYNOD deficient mice. Moreover, we discovered IFNγproduction in serum after UVB treatment is higher in PYNOD deficient mice. These results suggest that PYNOD plays important roles to produce TNFαproduction after UVB treatment in skin and contributes local inflammatory responses.
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Report
(4 results)
Research Products
(33 results)
