Role of mCG8863 for the activation of NF-kB
| Project/Area Number |
25860038
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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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) |
2013-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2014: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2013: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | NF-κB |
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| Outline of Final Research Achievements |
The NF-κB pathway is a phylogenetically conserved signaling pathway that has a central role for inflammatory and immune responses. Ｗe demonstrated that a co-chaperone protein CG8863 is involved in the activation of the canonical NF-κB signaling in flies and in human cultured cells. Overexpression of CG8863 induced an antimicrobial pepide expression in Drosophila. Conversely, knockdown of CG8863 resulted in the reduced expression of antimicrobial peptides and higher susceptibility to Gram-negative bacterial infection in flies. Similarly, Toll-like receptor-stimulated IκB phosphorylation and NF-κB activation was supressed by the knockdown of human CG8863 in HEK293 cells. IKK-overexpession induced NF-κB phosphorylation was also compromised in the CG8863-knockdown cells. Our study reveals a novel conserved regulator of the NF-κB pathway acting at the level of IκB phosphorylation.
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Report
(3 results)
Research Products
(16 results)
