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Identification of Biomolecular Information in Rotenone-Induced Cellular Model of Parkinson's Disease by Public Microarray Data Analysis.
Journal of Computational Biology ( IF 1.4 ) Pub Date : 2020-06-05 , DOI: 10.1089/cmb.2019.0151
Fan Yu 1 , Zhong-Sen Le 2 , Li-Hua Chen 3 , Hong Qian 3 , Bo Yu 1 , Wen-Hua Chen 1
Affiliation  

To explore the expression changes of genes and the pathological processes-related genetic information in Parkinson's disease (PD) model induced by rotenone. The microarray data set “GSE37178” was downloaded from Gene Expression Omnibus database. Differentially expression genes (DEGs) at different concentration and time points were examined and clustered using Mfuzz. Functional enrichment was analyzed with The Database for Annotation, Visualization and Integrated Discovery. Search Tool for the Retrieval of Interacting Genes was used to perform the protein–protein interaction (PPI) networks, and functional module analysis of PPI was constructed with Cytoscape. Moreover, transcription factors (TFs) and microRNA (miRNA) target were screened with TRRUST and WebGestalt GAST, respectively. In total, 680 DEGs were examined in the group with rotenone treatment. Clustering analysis revealed that 115 genes presented a consistent rising trend, and 138 genes presented a falling trend. Functional enrichment analysis uncovered that the upregulated genes associated with “type I interferon signaling pathway,” and the downregulated genes were related to “proteasome-mediated ubiquitin-dependent protein catabolic process.” The PPI network included 156 nodes and 298 interactions, and ISG15, RRM2, FBXW11, and FOXM1 were the hub genes. Meanwhile, 38 TF-target and 269 miRNA-target interactions were obtained; the mRNAs of the MIR-181 family have more target genes, such as TRIM13. Our study showed that aberrant expression of ISG15, RRM2, FBXW11, FOXM1, and MIR-181 family were associated with pathological processes in PD, and they could be the research focuses to further investigate the mechanism of PD.

中文翻译:

通过公共微阵列数据分析鉴定鱼藤酮诱导的帕金森病细胞模型中的生物分子信息。

探讨鱼藤酮诱导的帕金森病(PD)模型中基因的表达变化及病理过程相关的遗传信息。从基因表达综合数据库下载微阵列数据集“GSE37178”。使用 Mfuzz 检查并聚类不同浓度和时间点的差异表达基因 (DEG)。使用 The Database for Annotation、Visualization 和 Integrated Discovery 分析了功能丰富度。用于检索相互作用基因的搜索工具用于执行蛋白质 - 蛋白质相互作用(PPI)网络,并使用Cytoscape构建PPI的功能模块分析。此外,转录因子 (TFs) 和 microRNA (miRNA) 目标分别用 TRRUST 和 WebGestalt GAST 进行筛选。总共,在鱼藤酮治疗组中检查了680个DEG。聚类分析显示,115个基因呈现一致上升趋势,138个基因呈现下降趋势。功能富集分析发现,上调基因与“I型干扰素信号通路”相关,下调基因与“蛋白酶体介导的泛素依赖性蛋白质分解代谢过程”相关。PPI 网络包括 156 个节点和 298 个交互,以及ISG15RRM2FBXW11FOXM1是枢纽基因。同时,获得了 38 个 TF-target 和 269 个 miRNA-target 相互作用;MIR-181家族的mRNA有更多的靶基因,如TRIM13。我们的研究表明ISG15RRM2FBXW11FOXM1MIR-181家族的异常表达与PD的病理过程有关,可作为进一步探讨PD机制的研究重点。
更新日期:2020-06-05
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