Cross-talk between viral. infection and bacterial infection in oral region
| Project/Area Number |
18591994
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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 |
Morphological basic dentistry
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| Research Institution | Hokkaido University |
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Principal Investigator |
YASUDA Motoaki Hokkaido University, Graduate school of Dental medicine, Associate professor (90239765)
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| Co-Investigator(Kenkyū-buntansha) |
SHIBATA Ken-ichiro Hokkaido University, Graduate school of Dental medicine, professor (50145265)
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| Project Period (FY) |
2006 – 2007
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| Project Status |
Completed (Fiscal Year 2007)
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| Budget Amount *help |
¥3,730,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥330,000)
Fiscal Year 2007: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2006: ¥2,300,000 (Direct Cost: ¥2,300,000)
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| Keywords | Adenovirus / Innate immune / Transcription factor / TLR |
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| Research Abstract |
In the present study, we demonstrated the involvement of toll-like receptor 2 (TLR2) in the recognition of human adenovirus type 5 (Ad5) and the repressive effect of adenovirus E1A to the NF-κB activation via TLR2 pathways. Mutational analysis revealed that adenovirus E1A inhibited the NF-κB activation utilizing two independent pathways involving transcriptional co-activator p300 and the transcription factor E2Fs. Molecular mechanism of the NF-κB repression was explained by the competition between E1A and NF-κB for the limited amount of nuclear p300/CBP coactivator or the complex formation between RelA/ p65 and E2Fs which are displaced from Rb family proteins by competitive E1A binding to Rb proteins. The complex formation between RelA/ p65 and E2Fs also abolished the E2F dependent transcriptional activation. It is revealed that human adenovirus possess the transcriptional interference strategy involving NF-κB /Rel family and E2F family proteins and that human adenovirus utilize the strategy for the activation of host cell cycle and the repression of host innate immunological response.
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Report
(3 results)
Research Products
(2 results)
