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亲环蛋白1(TaCyp1)与宿主细胞MED21相互作用。

Cyclophilin1 (TaCyp1) Interacts With Host Cell MED21.

作者信息

Zhao Shuaiyang, Liu Junlong, Guan Guiquan, Liu Aihong, Li Youquan, Yin Hong, Luo Jianxun

机构信息

State Key Laboratory of Veterinary Etiological Biology, Key Laboratory of Veterinary Parasitology of Gansu Province, Lanzhou Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Lanzhou, China.

Jiangsu Co-innovation Center for Prevention and Control of Important Animal Infectious Diseases and Zoonoses, Yangzhou, China.

出版信息

Front Microbiol. 2018 Dec 3;9:2973. doi: 10.3389/fmicb.2018.02973. eCollection 2018.

Abstract

Host cells infected by schizonts show the character of permanent proliferation , also named transformation. To explore the molecular mechanism a Cyp1 (TaCyp1) protein potentially involved in regulating cell transformation was used as bait to screen for its interacting proteins by yeast-two-hybrid assay. Additional GST-pull down experiments confirmed that only MED21 specifically interacted with TaCyp1. Moreover, the distribution of TaCyp1 around schizonts facilitated interaction with host cell MED21. As a component of mediator complex, MED21 is normally involved in regulating the transcription of nearly all RNA polymerase II-dependent genes. Therefore, to explore its influence on NF-κB signaling MED21 RNA interference and parasite killing with BW720c treatment were performed. Knock down of MED21 resulted in a significant decrease in NF-κB1/2 mRNA expressions, but no significant change in P105, P52 levels, nor detectable alteration in levels of phosphorylated IκBα/β. By contrast, BW720c treatment induced an obvious decrease in the phosphorylation status of P52 and IκBα/β, but no obvious change in that of P105. This suggests that BW720c-induced parasite death had a significant negative influence on NF-κB signaling, whereas knock down of MED21 had no obvious effect on NF-κB signaling. Characterization of TaCyp1 provides information on the function of parasite cyclophilins and leads to a better understanding of the interactions between and its host leukocytes.

摘要

被裂殖体感染的宿主细胞表现出永久增殖的特征,也称为转化。为了探究其分子机制,将一种可能参与调节细胞转化的Cyp1(TaCyp1)蛋白用作诱饵,通过酵母双杂交试验筛选其相互作用蛋白。另外的GST下拉实验证实只有MED21能与TaCyp1特异性相互作用。此外,TaCyp1在裂殖体周围的分布促进了其与宿主细胞MED21的相互作用。作为中介体复合物的一个组成部分,MED21通常参与调节几乎所有RNA聚合酶II依赖性基因的转录。因此,为了探究其对NF-κB信号传导的影响,进行了MED21 RNA干扰和用BW720c处理杀死寄生虫的实验。敲低MED21导致NF-κB1/2 mRNA表达显著下降,但P105、P52水平没有显著变化,磷酸化的IκBα/β水平也没有可检测到的改变。相比之下,BW720c处理导致P52和IκBα/β的磷酸化状态明显下降,但P105的磷酸化状态没有明显变化。这表明BW720c诱导的寄生虫死亡对NF-κB信号传导有显著的负面影响,而敲低MED21对NF-κB信号传导没有明显影响。TaCyp1的特性为寄生虫亲环蛋白的功能提供了信息,并有助于更好地理解寄生虫与其宿主白细胞之间的相互作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/05d0/6286986/6056a47bb86c/fmicb-09-02973-g001.jpg

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