麻疹病毒磷蛋白与 STAT1 的连接域相互作用。
The measles virus phosphoprotein interacts with the linker domain of STAT1.
机构信息
Department of Molecular Medicine, and Virology and Gene Therapy Graduate Track, Mayo Clinic College of Medicine, Rochester, MN 55905, USA.
出版信息
Virology. 2013 Sep;444(1-2):250-6. doi: 10.1016/j.virol.2013.06.019. Epub 2013 Jul 13.
Abstract
The measles virus (MV) phosphoprotein (P) and V proteins block the interferon (IFN) response by impeding phosphorylation of the signal transducer and activator of transcription 1 (STAT1) by the Janus kinase 1 (JAK1). We characterized how STAT1 mutants interact with P and JAK1 phosphorylation. Certain mutants of the linker, the Src-homology 2 domain (SH2), or the transactivation domain had reduced or abolished phosphorylation through JAK1 after IFN treatment. Other mutants, mainly localized in the linker, failed to interact with P as documented by the lack of interference with nuclear translocation. Thus the functional footprint of P on STAT1 localizes mainly to the linker domain; there is also some overlap with the STAT1 phosphorylation functional footprint on the SH2 domain. Based on these observations, we discuss how the MV-P might operate to inhibit the JAK/STAT pathway.
摘要
麻疹病毒（MV）的磷蛋白（P）和 V 蛋白通过阻碍 Janus 激酶 1（JAK1）对信号转导和转录激活子 1（STAT1）的磷酸化来阻断干扰素（IFN）反应。我们研究了 STAT1 突变体与 P 和 JAK1 磷酸化的相互作用方式。连接子、Src 同源性 2 结构域（SH2）或反式激活结构域的某些突变体在 IFN 处理后通过 JAK1 的磷酸化减少或丧失。其他突变体主要定位于连接子，缺乏与 P 的相互作用，这可通过缺乏核易位的干扰来证明。因此，P 对 STAT1 的功能足迹主要定位于连接子结构域；在 SH2 结构域上，STAT1 磷酸化的功能足迹也有一些重叠。基于这些观察结果，我们讨论了 MV-P 如何抑制 JAK/STAT 途径。
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本文引用的文献
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J Virol. 2011 Jan;85(1):348-56. doi: 10.1128/JVI.00802-10. Epub 2010 Oct 27.
2
Nipah virus sequesters inactive STAT1 in the nucleus via a P gene-encoded mechanism.尼帕病毒通过一种由P基因编码的机制将无活性的信号转导和转录激活因子1（STAT1）隔离在细胞核中。
J Virol. 2009 Aug;83(16):7828-41. doi: 10.1128/JVI.02610-08. Epub 2009 Jun 10.
3
Inhibition of IFN-alpha/beta signaling by two discrete peptides within measles virus V protein that specifically bind STAT1 and STAT2.麻疹病毒V蛋白内两条特异性结合STAT1和STAT2的离散肽对IFN-α/β信号传导的抑制作用。
Virology. 2009 Jan 5;383(1):112-20. doi: 10.1016/j.virol.2008.10.014. Epub 2008 Nov 12.
4
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J Virol. 2009 Jan;83(2):961-8. doi: 10.1128/JVI.01669-08. Epub 2008 Nov 12.
5
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Immunol Rev. 2008 Oct;225:46-67. doi: 10.1111/j.1600-065X.2008.00669.x.
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J Virol. 2008 Sep;82(17):8330-8. doi: 10.1128/JVI.00831-08. Epub 2008 Jun 25.
7
Measles virus circumvents the host interferon response by different actions of the C and V proteins.麻疹病毒通过C蛋白和V蛋白的不同作用规避宿主的干扰素反应。
J Virol. 2008 Sep;82(17):8296-306. doi: 10.1128/JVI.00108-08. Epub 2008 Jun 18.
8
Measles virus V protein blocks Jak1-mediated phosphorylation of STAT1 to escape IFN-alpha/beta signaling.麻疹病毒V蛋白阻断Jak1介导的STAT1磷酸化以逃避I型干扰素信号传导。
Virology. 2007 Nov 25;368(2):351-62. doi: 10.1016/j.virol.2007.06.037. Epub 2007 Aug 7.
9
Tyrosine 110 in the measles virus phosphoprotein is required to block STAT1 phosphorylation.麻疹病毒磷蛋白中的酪氨酸110是阻断STAT1磷酸化所必需的。
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