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吞噬作用中延伸因子1α与半乳糖/ N - 乙酰半乳糖胺凝集素中间亚基及肌动蛋白相互作用的评估

Evaluation on Elongation Factor 1 Alpha of Interaction with the Intermediate Subunit of the Gal/GalNAc Lectin and Actin in Phagocytosis.

作者信息

Zhou Hang, Guan Yue, Feng Meng, Fu Yongfeng, Tachibana Hiroshi, Cheng Xunjia

机构信息

Department of Medical Microbiology and Parasitology, School of Basic Medical Sciences, Fudan University, Shanghai 200032, China.

Department of Infectious Diseases, Tokai University School of Medicine, Kanagawa 259-1193, Japan.

出版信息

Pathogens. 2020 Aug 27;9(9):702. doi: 10.3390/pathogens9090702.

DOI:10.3390/pathogens9090702
PMID:32867020
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7558290/
Abstract

is the causative agent of amoebiasis. This disease results in 40,000 to 100,000 deaths annually. The pathogenic molecules involved in the invasion of trophozoites had been constantly being clarified. This study explored the role of elongation factor 1 alpha (EF1a) in pathogenicity. Biolayer interferometry binding and pull-down assays suggest that EF1a and intermediate subunit of lectin (Igl) binding are specific. Submembranous distribution of EF1a closely aligns with the localization of Igl, which appear in abundance on membranes of trophozoites. Messenger RNA (mRNA) expression of EF1a is positively correlated with trends in Igl levels after co-incubation with Chinese hamster ovary (CHO) cells in vitro, suggesting a regulatory linkage between these proteins. Erythrophagocytosis assays also imply a role for EF1a in phagocytosis. Finally, EF1a and actin are collocated in trophozoites. These results indicated elongation factor 1a is associated with phagocytosis, and the relationships between EF1a, Igl, and actin are worth further study to better understand the pathogenic process.

摘要

是阿米巴病的病原体。这种疾病每年导致4万至10万人死亡。参与滋养体侵袭的致病分子一直在不断被阐明。本研究探讨了延伸因子1α(EF1a)在致病性中的作用。生物膜干涉术结合和下拉试验表明EF1a与凝集素中间亚基(Igl)的结合是特异性的。EF1a的膜下分布与Igl的定位紧密对齐,Igl在滋养体膜上大量出现。在体外与中国仓鼠卵巢(CHO)细胞共孵育后,EF1a的信使核糖核酸(mRNA)表达与Igl水平的变化趋势呈正相关,表明这些蛋白质之间存在调节联系。红细胞吞噬试验也暗示EF1a在吞噬作用中发挥作用。最后,EF1a和肌动蛋白在滋养体中并置。这些结果表明延伸因子1a与吞噬作用有关,EF1a、Igl和肌动蛋白之间的关系值得进一步研究,以更好地理解致病过程。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d849/7558290/2dc6a788a75d/pathogens-09-00702-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d849/7558290/7f75830c3658/pathogens-09-00702-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d849/7558290/05521b631441/pathogens-09-00702-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d849/7558290/c10598b6b9fe/pathogens-09-00702-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d849/7558290/da9e6c220522/pathogens-09-00702-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d849/7558290/932a08eecd0e/pathogens-09-00702-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d849/7558290/2dc6a788a75d/pathogens-09-00702-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d849/7558290/7f75830c3658/pathogens-09-00702-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d849/7558290/05521b631441/pathogens-09-00702-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d849/7558290/c10598b6b9fe/pathogens-09-00702-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d849/7558290/da9e6c220522/pathogens-09-00702-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d849/7558290/932a08eecd0e/pathogens-09-00702-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d849/7558290/2dc6a788a75d/pathogens-09-00702-g006.jpg

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