期刊
FASEB JOURNAL
卷 15, 期 2, 页码 501-514出版社
FEDERATION AMER SOC EXP BIOL
DOI: 10.1096/fj.00-0222com
关键词
IRF-3; transcription; defense; gene expression
资金
- NCI NIH HHS [P01CA28146, R01CA50773] Funding Source: Medline
An apoptotic cellular defense mechanism is triggered in response to viral dsRNA generated during the course of infection by many DNA and RNA viruses. We demonstrate that apoptosis induced by dsRNA or a paramyxovirus is independent of the action of interferon as it can proceed in a variety of cell lines and primary cells deficient in an interferon response. Initiation of apoptosis appears to be triggered by activation of a cellular transcription factor, the dsRNA-activated factor (DRAF1), DRAF1 is composed of interferon regulatory factor 3 (IRF-3) and the transcriptional coactivators CREB binding protein (CBP) or p300. We find that activation of IRF-3 in the absence of viral infection stimulates apoptosis, In addition, a negative interfering mutant blocks both target gene induction and apoptosis, demonstrating a requirement for gene expression by IRF-3/DRAF1 to promote apoptosis. IRF-3/DRAF1 target gene expression is also induced in response to a distinct apoptotic stimulus, the DNA damaging agent: etoposide, The activity of the p53 tumor suppressor does not appear to be required for IRF-3/DRAF1-mediated apoptosis.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据