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本文引用的文献

1
Leader protein of encephalomyocarditis virus binds zinc, is phosphorylated during viral infection, and affects the efficiency of genome translation.脑心肌炎病毒的前导蛋白结合锌，在病毒感染期间被磷酸化，并影响基因组翻译效率。
Virology. 2001 Nov 25;290(2):261-71. doi: 10.1006/viro.2001.1193.
2
The leader protein of Theiler's virus inhibits immediate-early alpha/beta interferon production.泰勒病毒的前导蛋白可抑制即刻早期α/β干扰素的产生。
J Virol. 2001 Sep;75(17):7811-7. doi: 10.1128/jvi.75.17.7811-7817.2001.
3
Chemistry and biology of eukaryotic iron metabolism.真核生物铁代谢的化学与生物学
Int J Biochem Cell Biol. 2001 Oct;33(10):940-59. doi: 10.1016/s1357-2725(01)00063-2.
4
Ferritin and the response to oxidative stress.铁蛋白与对氧化应激的反应。
Biochem J. 2001 Jul 1;357(Pt 1):241-7. doi: 10.1042/0264-6021:3570241.
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Immunosuppressive effects of melanoma-derived heavy-chain ferritin are dependent on stimulation of IL-10 production.
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Biphasic regulation of NF-kappa B activity underlies the pro- and anti-inflammatory actions of nitric oxide.核因子κB活性的双相调节是一氧化氮促炎和抗炎作用的基础。
J Immunol. 2001 Mar 15;166(6):3873-81. doi: 10.4049/jimmunol.166.6.3873.
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Reactive oxygen species in cell signaling.细胞信号传导中的活性氧物质。
Am J Physiol Lung Cell Mol Physiol. 2000 Dec;279(6):L1005-28. doi: 10.1152/ajplung.2000.279.6.L1005.
8
Interleukin-1beta increases binding of the iron regulatory protein and the synthesis of ferritin by increasing the labile iron pool.白细胞介素-1β通过增加不稳定铁池来增加铁调节蛋白的结合和铁蛋白的合成。
Biochim Biophys Acta. 2000 Sep 20;1497(3):279-88. doi: 10.1016/s0167-4889(00)00066-5.
9
Ability of foot-and-mouth disease virus to form plaques in cell culture is associated with suppression of alpha/beta interferon.口蹄疫病毒在细胞培养中形成蚀斑的能力与α/β干扰素的抑制作用相关。
J Virol. 1999 Dec;73(12):9891-8. doi: 10.1128/JVI.73.12.9891-9898.1999.
10
Nuclear factor-kappaB-dependent induction of interleukin-8 gene expression by tumor necrosis factor alpha: evidence for an antioxidant sensitive activating pathway distinct from nuclear translocation.肿瘤坏死因子α通过核因子-κB依赖性诱导白细胞介素-8基因表达：存在一条不同于核转位的抗氧化剂敏感激活途径的证据。
Blood. 1999 Sep 15;94(6):1878-89.

脑心肌炎病毒前导蛋白通过抑制铁/铁蛋白介导的核因子κB激活来抑制α/β干扰素的产生。

The mengovirus leader protein suppresses alpha/beta interferon production by inhibition of the iron/ferritin-mediated activation of NF-kappa B.

作者信息

Zoll Jan, Melchers Willem J G, Galama Jochem M D, van Kuppeveld Frank J M

机构信息

Department of Medical Microbiology, Nijmegen Center for Molecular Life Sciences, University Medical Center Nijmegen, 6500 HB Nijmegen, The Netherlands.

出版信息

J Virol. 2002 Oct;76(19):9664-72. doi: 10.1128/jvi.76.19.9664-9672.2002.

DOI:10.1128/jvi.76.19.9664-9672.2002
PMID:12208945
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC136484/
Abstract

In our studies on the biological function of the mengovirus leader protein, we identified a casein kinase II (CK-2) phosphorylation site in the protein. Here we report that the mengovirus leader protein can be phosphorylated by CK-2 in vitro. Expression of a recombinant leader protein in which the consensus CK-2 sequence around threonine 47 was disturbed resulted in a mutant protein that could no longer be phosphorylated. The CK-2 consensus sequence was modified by site-directed mutagenesis and subsequently introduced into a mengovirus cDNA clone to investigate the effect of the phosphorylation of the leader protein on virus replication and on the host cell response. Modifications by which the CK-2 consensus sequence was disturbed resulted in mutant viruses with reduced growth kinetics. We demonstrated that the integrity of the CK-2 phosphorylation site of the mengovirus leader protein was specifically related to the suppression of NF-kappa B activation and subsequent suppression of alpha/beta interferon production in infected cells. We also found that the integrity of the CK-2 phosphorylation site of the leader protein coincided with an increase of ferritin expression in the infected cell. These data indicate that the leader protein suppresses the iron-mediated activation of NF-kappa B and thereby inhibits alpha/beta interferon expression in the infected cell.

摘要

在我们对脑心肌炎病毒前导蛋白生物学功能的研究中，我们在该蛋白中鉴定出一个酪蛋白激酶II（CK-2）磷酸化位点。在此我们报告，脑心肌炎病毒前导蛋白在体外可被CK-2磷酸化。苏氨酸47周围的CK-2共有序列被打乱的重组前导蛋白的表达产生了一种不再能被磷酸化的突变蛋白。通过定点诱变修饰CK-2共有序列，随后将其引入脑心肌炎病毒cDNA克隆中，以研究前导蛋白磷酸化对病毒复制和宿主细胞反应的影响。打乱CK-2共有序列的修饰导致生长动力学降低的突变病毒。我们证明，脑心肌炎病毒前导蛋白的CK-2磷酸化位点的完整性与感染细胞中NF-κB激活的抑制以及随后α/β干扰素产生的抑制特异性相关。我们还发现，前导蛋白的CK-2磷酸化位点的完整性与感染细胞中铁蛋白表达的增加相一致。这些数据表明，前导蛋白抑制铁介导的NF-κB激活，从而抑制感染细胞中α/β干扰素的表达。