摘要: Type I interferon (IFN-I) is critical for a host against viral and bacterial infections via induction of hundreds of interferon-stimulated genes (ISGs), but the mechanism underlying the regulation of IFN-I remains largely unknown. In this study, we first demonstrate that ISG expression is required for optimal IFN-beta levels, an effect that is further enhanced by endoplasmic reticulum (ER) stress. Furthermore, we identify mitochondrial calcium uniporter protein (MCU) as a mitochondrial antiviral signaling protein (MAVS)-interacting protein that is important for ER stress induction and amplified MAVS signaling activation. In addition, by performing an ectopic expression assay to screen a library of 117 human ISGs for effects on IFN-beta levels, we found that tumor necrosis factor receptor 1 (TNFR1) significantly increases IFN-beta levels independent of ER stress. Altogether, our findings suggest that MCU and TNFR1 are involved in the regulation of RIG-I-like receptors (RLR) signaling.
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期刊:
SCIENTIFIC REPORTS
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分类:
生物学
>>
生物物理学
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引用:
ChinaXiv:201605.00768
(或此版本
ChinaXiv:201605.00768V1)
doi:10.12074/201605.00768
CSTR:32003.36.ChinaXiv.201605.00768.V1
- 推荐引用方式:
Cheng, Jinbo,Liao, Yajin,Zhou, Lujun,Peng, Shengyi,Chen, Hong,Yuan, Zengqiang,Liao, Yajin,Zhou, Lujun,.(2016).Amplified RLR signaling activation through an interferon-stimulated gene-endoplasmic reticulum stress-mitochondrial calcium uniporter protein loop.SCIENTIFIC REPORTS.[ChinaXiv:201605.00768]
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