Interaction between proteins of the PPARγ and NFκB immune response pathways and rotavirus non-structural proteins.

IF 1.1 4区 医学 Q4 VIROLOGY
Dory Gómez, C. Guerrero
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引用次数: 0

Abstract

Cells infected with MA104 rotavirus and/or transfected with plasmids expressing NSP proteins, were analyzed for expression of cellular proteins related to NFκB and PPARγ pathways and evaluated through the ELISA, luminescence, flow cytometry and Western blot techniques. The association between cellular and viral (NSPs) proteins was examined by ELISA, epifluorescence and confocal microscopy techniques. It was observed that NSP1 protein interacts with RXR, NSP1, and NSP3 with PPARγ, NSP2 with p-IKKα/β and NSP5 with NFκB proteins. We have found that phosphorylated PPARγ is localized in cytoplasm and transcriptional activity of PPRE is diminished. These results lead to the conclusion, that RRV activates the proinflammatory pathway, increasing the expression of NFκB and possibly by PPARγ phosphorylation, its translocation to the nucleus is impeded, thus inactivating the proinflammatory pathway. Keywords: rotavirus; PPARγ; NFκB; NSPs; RRV.
PPARγ和NFκB免疫反应通路蛋白与轮状病毒非结构蛋白的相互作用。
对感染MA104轮状病毒和/或转染表达NSP蛋白的质粒的细胞进行NFκB和PPARγ通路相关蛋白的表达分析,并通过ELISA、发光、流式细胞术和Western blot技术进行评估。通过ELISA、荧光和共聚焦显微镜技术检测细胞和病毒(NSPs)蛋白之间的关联。NSP1蛋白与RXR、NSP1、NSP3蛋白与PPARγ、NSP2蛋白与p-IKKα/β、NSP5蛋白与NFκB蛋白相互作用。我们发现磷酸化的PPRE γ定位于细胞质中,PPRE的转录活性降低。这些结果可以得出结论,RRV激活促炎途径,增加NFκB的表达,并可能通过PPARγ磷酸化,阻碍其向细胞核的易位,从而使促炎途径失活。关键词:轮状病毒;PPARγ;NFκB;NSPs;RRV。
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来源期刊
Acta virologica
Acta virologica 医学-病毒学
CiteScore
3.10
自引率
11.80%
发文量
43
审稿时长
>12 weeks
期刊介绍: Acta virologica is an international journal of predominantly molecular and cellular virology. Acta virologica aims to publish papers reporting original results of fundamental and applied research mainly on human, animal and plant viruses at cellular and molecular level. As a matter of tradition, also rickettsiae are included. Areas of interest are virus structure and morphology, molecular biology of virus-cell interactions, molecular genetics of viruses, pathogenesis of viral diseases, viral immunology, vaccines, antiviral drugs and viral diagnostics.
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