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从微阵列和结构域-结构域蛋白质相互作用推断感染机制的R脚本方法。

R Script Approach to Infer Infection Mechanisms From Microarrays and Domain-Domain Protein Interactions.

作者信息

Arenas Ailan F, Salcedo Gladys E, Gomez-Marin Jorge E

机构信息

Grupo de Estudio en Parasitología Molecular (GEPAMOL), Universidad del Quindío, Armenia, Colombia.

Grupo de Investigación y Asesoría en Estadística, Universidad del Quindío, Armenia, Colombia.

出版信息

Bioinform Biol Insights. 2017 Dec 17;11:1177932217747256. doi: 10.1177/1177932217747256. eCollection 2017.

Abstract

Pathogen-host protein-protein interaction systems examine the interactions between the protein repertoires of 2 distinct organisms. Some of these pathogen proteins interact with the host protein system and may manipulate it for their own advantages. In this work, we designed an R script by concatenating 2 functions called rowDM and rowCVmed to infer pathogen-host interaction using previously reported microarray data, including host gene enrichment analysis and the crossing of interspecific domain-domain interactions. We applied this script to the -host system to describe pathogen survival mechanisms from human, mouse, and Gene Expression Omnibus series. Our outcomes exhibited similar results with previously reported microarray analyses, but we found other important proteins that could contribute to toxoplasma pathogenesis. We observed that ROP38 is the most differentially expressed protein among toxoplasma strains. Enrichment analysis and KEGG mapping indicated that the human retinal genes most affected by infections are those related to antiapoptotic mechanisms. We suggest that proteins PIK3R1, PRKCA, PRKCG, PRKCB, HRAS, and c-JUN could be the possible substrates for differentially expressed kinase ROP38. Likewise, we propose that causes overexpression of apoptotic suppression human genes.

摘要

病原体-宿主蛋白质-蛋白质相互作用系统研究两种不同生物体蛋白质组之间的相互作用。其中一些病原体蛋白质与宿主蛋白质系统相互作用,并可能为自身利益对其进行操纵。在这项工作中,我们通过拼接名为rowDM和rowCVmed的两个函数设计了一个R脚本,以利用先前报道的微阵列数据推断病原体-宿主相互作用,包括宿主基因富集分析和种间结构域-结构域相互作用的交叉。我们将此脚本应用于病原体-宿主系统,以描述来自人类、小鼠和基因表达综合数据库系列的病原体生存机制。我们的结果与先前报道的微阵列分析结果相似,但我们发现了其他可能有助于弓形虫发病机制的重要蛋白质。我们观察到ROP38是弓形虫菌株中差异表达最显著的蛋白质。富集分析和KEGG映射表明,受弓形虫感染影响最大的人类视网膜基因是那些与抗凋亡机制相关的基因。我们认为蛋白质PIK3R1、PRKCA、PRKCG、PRKCB、HRAS和c-JUN可能是差异表达的弓形虫激酶ROP38的潜在底物。同样,我们提出弓形虫会导致人类凋亡抑制基因的过表达。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9b58/5753922/c6066bcd78ae/10.1177_1177932217747256-fig1.jpg

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