scholarly journals Random walks on mutual microRNA-target gene interaction network improve the prediction of disease-associated microRNAs

2017 ◽  
Vol 18 (1) ◽  
Author(s):  
Duc-Hau Le ◽  
Lieven Verbeke ◽  
Le Hoang Son ◽  
Dinh-Toi Chu ◽  
Van-Huy Pham
2021 ◽  
Vol 12 ◽  
Author(s):  
Genís Calderer ◽  
Marieke L. Kuijjer

Networks are useful tools to represent and analyze interactions on a large, or genome-wide scale and have therefore been widely used in biology. Many biological networks—such as those that represent regulatory interactions, drug-gene, or gene-disease associations—are of a bipartite nature, meaning they consist of two different types of nodes, with connections only forming between the different node sets. Analysis of such networks requires methodologies that are specifically designed to handle their bipartite nature. Community structure detection is a method used to identify clusters of nodes in a network. This approach is especially helpful in large-scale biological network analysis, as it can find structure in networks that often resemble a “hairball” of interactions in visualizations. Often, the communities identified in biological networks are enriched for specific biological processes and thus allow one to assign drugs, regulatory molecules, or diseases to such processes. In addition, comparison of community structures between different biological conditions can help to identify how network rewiring may lead to tissue development or disease, for example. In this mini review, we give a theoretical basis of different methods that can be applied to detect communities in bipartite biological networks. We introduce and discuss different scores that can be used to assess the quality of these community structures. We then apply a wide range of methods to a drug-gene interaction network to highlight the strengths and weaknesses of these methods in their application to large-scale, bipartite biological networks.


2020 ◽  
Vol 2020 ◽  
pp. 1-10
Author(s):  
Hao Yu ◽  
Yang Liu ◽  
Chao Li ◽  
Jianhao Wang ◽  
Bo Yu ◽  
...  

Background. Neuropathic pain (NP) is a devastating complication following nerve injury, and it can be alleviated by regulating neuroimmune direction. We aimed to explore the neuroimmune mechanism and identify some new diagnostic or therapeutic targets for NP treatment via bioinformatic analysis. Methods. The microarray GSE18803 was downloaded and analyzed using R. The Venn diagram was drawn to find neuroimmune-related differentially expressed genes (DEGs) in neuropathic pain. Gene Ontology (GO), pathway enrichment, and protein-protein interaction (PPI) network were used to analyze DEGs, respectively. Besides, the identified hub genes were submitted to the DGIdb database to find relevant therapeutic drugs. Results. A total of 91 neuroimmune-related DEGs were identified. The results of GO and pathway enrichment analyses were closely related to immune and inflammatory responses. PPI analysis showed two important modules and 8 hub genes: PTPRC, CD68, CTSS, RAC2, LAPTM5, FCGR3A, CD53, and HCK. The drug-hub gene interaction network was constructed by Cytoscape, and it included 24 candidate drugs and 3 hub genes. Conclusion. The present study helps us better understand the neuroimmune mechanism of neuropathic pain and provides some novel insights on NP treatment, such as modulation of microglia polarization and targeting bone resorption. Besides, CD68, CTSS, LAPTM5, FCGR3A, and CD53 may be used as early diagnostic biomarkers and the gene HCK can be a therapeutic target.


10.1186/gm404 ◽  
2012 ◽  
Vol 4 (12) ◽  
Author(s):  
Raymond J Louie ◽  
Jingyu Guo ◽  
John W Rodgers ◽  
Rick White ◽  
Najaf A Shah ◽  
...  

2018 ◽  
Vol 78 (1) ◽  
pp. 36-42 ◽  
Author(s):  
Hong Zhu ◽  
Long-Fei Wu ◽  
Xing-Bo Mo ◽  
Xin Lu ◽  
Hui Tang ◽  
...  

ObjectivesTo identify novel DNA methylation sites significant for rheumatoid arthritis (RA) and comprehensively understand their underlying pathological mechanism.MethodsWe performed (1) genome-wide DNA methylation and mRNA expression profiling in peripheral blood mononuclear cells from RA patients and health controls; (2) correlation analysis and causal inference tests for DNA methylation and mRNA expression data; (3) differential methylation genes regulatory network construction; (4) validation tests of 10 differential methylation positions (DMPs) of interest and corresponding gene expressions; (5) correlation between PARP9 methylation and its mRNA expression level in Jurkat cells and T cells from patients with RA; (6) testing the pathological functions of PARP9 in Jurkat cells.ResultsA total of 1046 DNA methylation positions were associated with RA. The identified DMPs have regulatory effects on mRNA expressions. Causal inference tests identified six DNA methylation–mRNA–RA regulatory chains (eg, cg00959259-PARP9-RA). The identified DMPs and genes formed an interferon-inducible gene interaction network (eg, MX1, IFI44L, DTX3L and PARP9). Key DMPs and corresponding genes were validated their differences in additional samples. Methylation of PARP9 was correlated with mRNA level in Jurkat cells and T lymphocytes isolated from patients with RA. The PARP9 gene exerted significant effects on Jurkat cells (eg, cell cycle, cell proliferation, cell activation and expression of inflammatory factor IL-2).ConclusionsThis multistage study identified an interferon-inducible gene interaction network associated with RA and highlighted the importance of PARP9 gene in RA pathogenesis. The results enhanced our understanding of the important role of DNA methylation in pathology of RA.


2015 ◽  
Vol 8 (1) ◽  
Author(s):  
Huanchun Ying ◽  
Jing Lv ◽  
Tianshu Ying ◽  
Shanshan Jin ◽  
Jingru Shao ◽  
...  

2016 ◽  
Vol 7 (1) ◽  
Author(s):  
Jingshan Huang ◽  
Fernando Gutierrez ◽  
Harrison J. Strachan ◽  
Dejing Dou ◽  
Weili Huang ◽  
...  

2022 ◽  
Author(s):  
Wei-Zhen Zhou ◽  
Wenke Li ◽  
Huayan Shen ◽  
Ruby W. Wang ◽  
Wen Chen ◽  
...  

Congenital heart disease (CHD) is the most common cause of major birth defects, with a prevalence of 1%. Although an increasing number of studies reporting the etiology of CHD, the findings scattered throughout the literature are difficult to retrieve and utilize in research and clinical practice. We therefore developed CHDbase, an evidence-based knowledgebase with CHD-related genes and clinical manifestations manually curated from 1114 publications, linking 1124 susceptibility genes and 3591 variations to more than 300 CHD types and related syndromes. Metadata such as the information of each publication and the selected population and samples, the strategy of studies, and the major findings of study were integrated with each item of research record. We also integrated functional annotations through parsing ~50 databases/tools to facilitate the interpretation of these genes and variations in disease pathogenicity. We further prioritized the significance of these CHD-related genes with a gene interaction network approach, and extracted a core CHD sub-network with 163 genes. The clear genetic landscape of CHD enables the phenotype classification based on the shared genetic origin. Overall, CHDbase provides a comprehensive and freely available resource to study CHD susceptibility, supporting a wide range of users in the scientific and medical communities. CHDbase is accessible at http://chddb.fwgenetics.org/.


Sign in / Sign up

Export Citation Format

Share Document