Viruses exploit the function of epidermal growth factor receptor

Viruses exploit the function of epidermal growth factor receptor
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病毒利用表皮生长因子受体的功能

DOI:
10.1002/rmv.1796
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发表时间:
2014-07
影响因子:
11.1
通讯作者:
Wang, Yifei
Wang, Yifei
中科院分区:
医学2区
文献类型:
--
作者:
Zheng, Kai;Kitazato, Kaio;Wang, Yifei

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表皮生长因子受体(EGFR)是一种调节细胞稳态过程的受体酪氨酸激酶。配体结合后,EGFR激活不同的下游信号级联,促进细胞存活、增殖、运动和血管生成,并诱导F-肌动蛋白依赖性EGFR内吞作用,使活化的受体重新定位以进行降解或再循环。由配体与EGFR结合诱导的应答,包括细胞信号传导激活、蛋白激酶磷酸化和细胞骨架网络重排,类似于由病毒感染诱导的应答。越来越多的证据表明,许多病毒篡夺EGFR内吞作用或EGFR介导的信号传导,以进入、复制、炎症和病毒拮抗宿主抗病毒系统。此外,病毒已经获得了复杂的机制,通过中断EGFR再循环过程和调节EGFR表达来调节EGFR功能。在这篇综述中,我们提供了一个概述的机制,病毒改变EGFR信号有利于他们的继续生存。版权所有© 2014约翰威利父子有限公司.
Epidermal growth factor receptor (EGFR) is a receptor tyrosine kinase that regulates cellular homeostatic processes. Following ligand binding, EGFR activates different downstream signalling cascades that promote cell survival, proliferation, motility, and angiogenesis and induces F‐actin‐dependent EGFR endocytosis, which relocalises the activated receptors for degradation or recycling. The responses that are induced by ligand binding to EGFR, including cell signalling activation, protein kinase phosphorylation and cytoskeletal network rearrangement, resemble those induced by virus infection. Increasing evidence demonstrates that many viruses usurp EGFR endocytosis or EGFR‐mediated signalling for entry, replication, inflammation, and viral antagonism to the host antiviral system. In addition, viruses have acquired sophisticated mechanisms to regulate EGFR functions by interrupting the EGFR‐recycling process and modulating EGFR expression. In this review, we provide an overview of the mechanisms by which viruses alter EGFR signalling in favour of their continued survival. Copyright © 2014 John Wiley & Sons, Ltd.
DOI: 10.1038/emboj.2013.212
发表时间: 2013-10-16
期刊: EMBO JOURNAL
影响因子: 11.4
作者:
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期刊: Journal of experimental & clinical cancer research : CR
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DOI: 10.1128/jvi.70.1.612-616.1996
发表时间: 1996-01
影响因子: 5.4
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