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首页> 外文期刊>Journal of Cellular Physiology >Inhibition of NF-κB activity by HIV-1 Vpr is dependent on Vpr binding protein
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Inhibition of NF-κB activity by HIV-1 Vpr is dependent on Vpr binding protein

机译：抑制hiv - 1 NF -κB活性的冲程体积依赖冲程体积结合蛋白

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Numerous studies have reported that Vpr alters NF-κB signaling in various cell types, however, the findings have been largely conflicting with reports of both stimulatory and inhibitory effects of Vpr. Our aim was to investigate the role of Vpr signaling in myeloid cells using an adenovirus based expression and indicator system. Our results show that Vpr is inhibitory to NF-κB, however, this effect is dependent on the particular manner of NF-κB stimulation. Consistent with this notion, we report that Vpr has inhibitory effects that are specific to the TNF-α pathway, but not affecting the LPS pathway, suggesting that differential targets of Vpr may exist for NF-κB regulation. Further, we identify VprBP as one possible cellular component of Vpr's regulation of IκBα in response to TNF-α stimulation. We did not identify such a role for HSP27, which instead seems to inhibit Vpr functions. Chronically HIV-1 infected U1 cells with knockdown constructs for Vpr were unexpectedly less responsive to TNF-α mediated viral replication, perhaps suggesting that other HIV-1 components may antagonize these anti-NF-κB effects in infected cells. We hypothesize that Vpr may serve an important role in the context of viral infection and immune function in vivo, through its selective inhibition of NF-κB pathways.
机译：大量研究报道,冲程体积改变NF -κB信号在不同的细胞类型,然而,研究结果很大程度上是相互矛盾的刺激和抑制的报告冲程体积的影响。使用一个冲程体积信号在骨髓细胞中的作用腺病毒表达和指标体系。我们的结果表明,冲程体积是抑制NF -κB,然而,这种效果依赖于NF -κB刺激的特定方式。符合这个概念,我们报告,冲程体积抑制作用是具体的肿瘤坏死因子-α通路,但不影响有限合伙人的通路,这表明微分冲程体积可能的目标NF -κB监管存在。VprBP冲程体积的作为一个可能的细胞组件调节我在应对TNF -ακBα刺激。HSP27,相反似乎抑制冲程体积功能。冲程体积是可拆卸的结构肿瘤坏死因子-α介导出人意料地减少响应病毒复制,也许暗示hiv - 1组件可能对抗这些anti-NF -κB在感染细胞的影响。冲程体积可能服务上下文中的一个重要的角色病毒感染和体内免疫功能,通过选择性抑制NF -κB通路。

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