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RNA interference directed against viral and cellular targets inhibits human immunodeficiency Virus Type 1 replication.针对病毒和细胞靶点的RNA干扰可抑制1型人类免疫缺陷病毒的复制。
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The IkappaB-NF-kappaB signaling module: temporal control and selective gene activation.IκB-NF-κB信号转导模块:时间控制与选择性基因激活
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Human T-lymphotropic virus type I tax activates I-kappa B kinase by inhibiting I-kappa B kinase-associated serine/threonine protein phosphatase 2A.人类I型嗜T淋巴细胞病毒的Tax蛋白通过抑制IκB激酶相关的丝氨酸/苏氨酸蛋白磷酸酶2A来激活IκB激酶。
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NF-kappaB regulation in the immune system.免疫系统中的核因子-κB调控
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核因子-κB与病毒感染:谁控制谁

NF-kappaB and virus infection: who controls whom.

作者信息

Santoro M Gabriella, Rossi Antonio, Amici Carla

机构信息

Department of Biology, University of Rome Tor Vergata, Via della Ricerca Scientifica and INeMM, CNR, 00133 Rome, Italy.

出版信息

EMBO J. 2003 Jun 2;22(11):2552-60. doi: 10.1093/emboj/cdg267.

DOI:10.1093/emboj/cdg267
PMID:12773372
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC156764/
Abstract

Among the different definitions of viruses, 'pirates of the cell' is one of the most picturesque, but also one of the most appropriate. Viruses have been known for a long time to utilize a variety of strategies to penetrate cells and, once inside, to take over the host nucleic acid and protein synthesis machinery to build up their own components and produce large amounts of viral progeny. As their genomes carry a minimal amount of information, encoding only a few structural and regulatory proteins, viruses are largely dependent on their hosts for survival; however, despite their apparent simplicity, viruses have evolved different replicative strategies that are regulated in a sophisticated manner. During the last years, the study of the elaborate relationship between viruses and their hosts has led to the understanding of how viral pathogens not only are able to alter the host metabolism via their signaling proteins, but are also able to hijack cellular signaling pathways and transcription factors, and control them to their own advantage. In particular, the nuclear factor-kappaB (NF-kappaB) pathway appears to be an attractive target for common human viral pathogens. This review summarizes what is known about the control of NF-kappaB by viruses, and discusses the possible outcome of NF-kappaB activation during viral infection, which may benefit either the host or the pathogen.

摘要

在对病毒的不同定义中,“细胞海盗”是最生动形象的定义之一,也是最恰当的定义之一。长期以来,人们都知道病毒会利用多种策略侵入细胞,一旦进入细胞,就会接管宿主的核酸和蛋白质合成机制,以构建自身成分并产生大量病毒后代。由于病毒基因组携带的信息极少,仅编码少数结构蛋白和调节蛋白,因此病毒在很大程度上依赖宿主生存;然而,尽管病毒看似简单,却已进化出以复杂方式调控的不同复制策略。在过去几年中,对病毒与其宿主之间复杂关系的研究,使人们了解到病毒病原体不仅能够通过其信号蛋白改变宿主代谢,还能够劫持细胞信号通路和转录因子,并将其控制为自身所用。特别是,核因子-κB(NF-κB)通路似乎是常见人类病毒病原体的一个有吸引力的靶点。本综述总结了关于病毒对NF-κB的调控的已知信息,并讨论了病毒感染期间NF-κB激活可能产生的结果,这可能对宿主或病原体有益。