iLIR@viral: A web resource for LIR motif-containing proteins in viruses.

iLIR@viral: A web resource for LIR motif-containing proteins in viruses.
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DOI:
10.1080/15548627.2017.1356978
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发表时间:
2017-10-03
期刊:
影响因子:
13.3
通讯作者:
Nezis IP
Nezis IP
中科院分区:
生物学1区
文献类型:
--
作者:
Jacomin AC;Samavedam S;Charles H;Nezis IP

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巨自噬/自噬已被证明可以介导病原细菌和病毒的选择性溶酶体降解(异体自噬),并有助于激活先天性和适应性免疫反应。自噬可以作为一种抗病毒防御机制,也可以作为感染过程中的前病毒过程。 Atg8 家族蛋白在自噬过程中发挥着核心作用,因为它们能够与自噬机制的组件以及选择性自噬受体和接头蛋白相互作用。这种相互作用通常是通过 LC3 相互作用区 (LIR) 基序介导的。到目前为止,只有一种病毒蛋白被实验证明具有功能性 LIR 基序,这为研究留下了广阔的空间。在这里,我们开发了 iLIR@viral 数据库 (http://ilir.uk/virus/) 作为可免费访问的网络资源,列出了病毒蛋白中识别的所有假定的规范 LIR 基序。此外,我们对文献进行了精心策划的文本挖掘分析,以识别病毒中新型推定的包含 LIR 基序的蛋白质 (LIRCP)。我们预计 iLIR@viral 将有助于阐明病毒中 LIRCP 的完整补充。
Macroautophagy/autophagy has been shown to mediate the selective lysosomal degradation of pathogenic bacteria and viruses (xenophagy), and to contribute to the activation of innate and adaptative immune responses. Autophagy can serve as an antiviral defense mechanism but also as a proviral process during infection. Atg8-family proteins play a central role in the autophagy process due to their ability to interact with components of the autophagy machinery as well as selective autophagy receptors and adaptor proteins. Such interactions are usually mediated through LC3-interacting region (LIR) motifs. So far, only one viral protein has been experimentally shown to have a functional LIR motif, leaving open a vast field for investigation. Here, we have developed the iLIR@viral database (http://ilir.uk/virus/) as a freely accessible web resource listing all the putative canonical LIR motifs identified in viral proteins. Additionally, we used a curated text-mining analysis of the literature to identify novel putative LIR motif-containing proteins (LIRCPs) in viruses. We anticipate that iLIR@viral will assist with elucidating the full complement of LIRCPs in viruses.
口蹄疫病毒感染通过 3C(pro) 降解 ATG5-ATG12 抑制自噬和 NF-kappa B 抗病毒反应
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