Cross-talk between viral. infection and bacterial infection in oral region

病毒之间的串扰。

• 批准号: 18591994
• 负责人: YASUDA Motoaki
• 金额: $ 2.39万
• 依托单位: Hokkaido University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (C)
• 财政年份: 2006
• 资助国家: 日本
• 起止时间: 2006 至 2007
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-18591994/
• 关键词: Adenovirus; Innate immune; Transcription factor; TLR

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.

在本研究中，我们证明了Toll样受体2（TLR 2）参与识别人5型腺病毒（Ad 5），以及腺病毒E1 A通过TLR 2途径对NF-κB激活的抑制作用。突变分析显示腺病毒E1 A通过转录辅激活因子p300和转录因子E2 Fs两条独立的途径抑制NF-κB的活化。NF-κB抑制的分子机制可能是E1 A和NF-κB竞争有限量的核内p300/CBP共激活因子，或E1 A与Rb蛋白竞争结合，导致Rb家族蛋白中的E2 Fs与RelA/ p65形成复合物。RelA/ p65与E2 Fs之间的复合物的形成也消除了E2 F依赖的转录激活。结果表明，人腺病毒具有NF-κB /Rel家族和E2 F家族蛋白的转录干扰策略，人腺病毒具有激活宿主细胞周期和抑制宿主天然免疫应答的策略。

项目成果

DNAがんウイルスは自然免疫応答を抑制する

DNA癌症病毒抑制先天免疫反应

• 发表时间: 2007
• 作者: Atsushi;Tabata;et. al.;安田元昭
• 通讯作者: 安田元昭